Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms
Open accessAbstract
Bisphenol A (BPA), an environmental xenoestrogen, has been reported to induce learning and memory impairments in rodent animals. However, effects of BPA exposure on synaptic plasticity and the underlying physiological mechanisms remain elusive. Our behavioral and electrophysiological analyses show that BPA obviously perturbs hippocampal spatial memory of juvenile Sprague–Dawley rats after four weeks exposure, with significantly impaired long‐term potentiation (LTP) in the hippocampus. These effects involve decreased spine density of pyramidal neurons, especially the apical dendritic spine. Further presynaptic findings show an overt inhibition of pulse‐paired facilitation during electrophysiological recording, which suggest the decrease of presynaptic transmitter release and is consistent with reduced production of presynaptic glutamate after BPA exposure. Meanwhile, LTP‐related glutamate receptors, NMDA receptor 2A (NR2A) and AMPA receptor 1 (GluR1), are significantly downregulated in BPA‐exposed rats. Excitatory postsynaptic currents (EPSCs) results also show that EPSC NMDA , but not EPSC AMPA , is declined by 40% compared to the baseline in BPA‐perfused brain slices. Taken together, these findings reveal that juvenile BPA exposure has negative effects on synaptic plasticity, which result from decreases in dendritic spine density and excitatory synaptic transmission. Importantly, this study also provides new insights into the dynamics of BPA‐induced memory deterioration during the whole life of rats.
AI snapshot
Written from the paper’s full text.
TL;DR
Juvenile BPA exposure in male Sprague–Dawley rats impaired hippocampus-dependent spatial memory and hippocampal CA1 synaptic plasticity, with both presynaptic and postsynaptic deficits. The authors link these effects to decreased dendritic spine density, reduced glutamate release/synthesis, and downregulated NR2A and GluR1.
Key findings
- BPA crossed the blood–brain barrier: CSF BPA was 4.36 ± 2.28 ng mL−1 in exposed rats versus 0.17 ± 0.07 ng mL−1 in controls (n = 8 per group, p < 0.05).
- BPA-exposed rats showed spatial memory impairment without learning deficit: less time in the MWM target quadrant (p < 0.05) and less novel-arm time/entries in the Y maze (p < 0.05 and p < 0.01), with no swimming speed/distance differences.
- LTP was impaired in CA1: BPA produced 133.11 ± 16.17% fEPSP slope potentiation versus 199.63 ± 39.51% in controls 60 min after HFS (p < 0.01).
- Synaptic mechanisms included ~20% lower total dendritic spine density (p < 0.01), apical spine density reduced to two thirds of control (p < 0.01), decreased PPF ratio (141 ± 11% vs 191.83 ± 23%, p < 0.01), 22.47% lower glutamate release (p < 0.05), and ~40% lower EPSCNMDA after acute BPA (282.13 ± 10.32 pA to 151.88 ± 8.73 pA, p < 0.01), while EPSCAMPA did not significantly change.
Methods
- Male Sprague–Dawley rats were orally treated with BPA (1 mg kg−1 d−1 in DMSO) or vehicle from postnatal 21–24 to 49–52 d; controls received equivalent DMSO.
- Behavioral testing used Morris water maze, Y maze, and open field; electrophysiology measured Sch–CA1 fEPSP input/output, paired-pulse facilitation, and LTP after high-frequency stimulation; Golgi–Cox staining assessed dendritic length and spine density; Western blot measured glutamate receptor subunits; patch clamp measured EPSCNMDA and EPSCAMPA in acute BPA-treated slices; ELISA/activity assays measured glutamate release and glutaminase activity.
- Data are expressed as mean ± S.E.M.; unpaired two-tailed t-tests and repeated measures ANOVA were used, with p < 0.05 considered significant.
Limitations
- The paper states that future studies are required to investigate dose-dependent effects of BPA on juvenile behaviors and to explore molecular mechanisms of BPA-induced synaptic changes.
- Evident from the text: only male rats were used, only one BPA dose (1 mg kg−1 d−1) was tested, and exposure was limited to the juvenile period, so sex differences, dose–response relationships, and other developmental windows are not addressed.
- Evident from the text: several experiments used small group sizes (8–10 rats per group), and the study reports associative physiological and morphological changes rather than direct causal molecular pathways.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
7 of 24 cited sources checked · 1 supported · 0 flagged · accuracy not yet measured
- Premisecitation
A positive relationship between spine morphology and LTP induction has been demonstrated.
“A positive relationship between spine morphology and LTP induction has been demonstrated.14”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [14] X. Yu, Y. Zuo, Curr. Opin. Neurobiol. 2011, 21, 169. 20728341 PMC2991530 source
The Methods (Spine Synapses; page unavailable) describe counting asymmetric spine synapses, and the Discussion (page unavailable) links synapse number to working-memory performance. Searches for LTP induction, long-term potentiation, and potentiation found no passage addressing a relationship between spine morphology and LTP induction. (LLM, conf=0.76)
Experimental — accuracy not yet measured
- Premisecitation
17β-estradiol interaction with estrogen receptors has the potential to heighten the magnitude of LTP at hippocampal CA3-CA1 synapses in rats.
“It has been found that 17β‐estradiol interaction with estrogen receptors has potential to heighten the magnitude of LTP at hippocampal CA3–CA1 synapses in rats.24”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [24] a) C. C. Smith, L. C. Vedder, L. L. McMahon, Psychoneuroendocrinology 2009, 34, S130; 19596521 PMC2796081 b) J. L. Spencer, E. M. Waters, R. D. Romeo, G. E. Wood, T. A. Milner, B. S. McEwen, Front. Neuroendocrinol. 2008, 29, 219; 18078984 PMC2440702 c) C. C. Smith, L. L. McMahon, J. Neurosci. 2005, 25, 7780. 16120779 PMC6725261 source
The Molecular mechanisms of synaptic function in vivo section discusses LTP studies in hippocampal cultured slices, but not estradiol, estrogen receptors, or LTP magnitude at rat CA3–CA1 synapses. Searches for those terms and their paraphrases found no passage addressing the claim. Page numbers were unavailable in our copy. (LLM, conf=0.73)
Experimental — accuracy not yet measured
- Interpretationown data
BPA crosses the blood-brain barrier in the CNS.
“This confirms that BPA could pass across the BBB,17”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [17] Y. Sun, M. N. Nakashima, M. Takahashi, N. Kuroda, K. Nakashima, Biomed. Chromatogr. 2002, 16, 319. 12210505 source
The paper’s Abstract discusses possible effects of BPA exposure on brain development, and the Discussion mentions potential brain-related mechanisms, but neither passage addresses whether BPA crosses the blood-brain barrier. Searches for “blood-brain barrier,” “BBB,” and entry into the CNS found no passage establishing that point. Page numbers were not available in our copy. (LLM, conf=0.70)
Experimental — accuracy not yet measured
- Premisecitation
Decrease of synapsin I phosphorylation can enable less vesicles to be released during presynaptic depolarization.
“which can enable less vesicles to be released during the presynaptic depolarization.34”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [34] R. Llinas, J. A. Gruner, M. Sugimori, T. L. McGuinness, P. Greengard, J. Physiol. 1991, 436, 257. 1676419 PMC1181504 source
The Discussion describes changes in proteins involved in synaptic signaling and vesicle trafficking, but does not address whether reduced synapsin I phosphorylation limits vesicle release during presynaptic depolarization. A References entry calls synapsin I a synaptic vesicle protein; searches for synapsin I phosphorylation and presynaptic vesicle release found no passage making the claimed connection. No page numbers are available in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
- Premisecitation
Developmental BPA exposure in cultured hypothalamic cells causes a decrease of synapsin I phosphorylation.
“developmental BPA exposure in cultured hypothalamic cells causes decrease of synapsin I phosphorylation,33”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [33] T. Iwakura, M. Iwafuchi, D. Muraoka, M. Yokosuka, T. Shiga, C. Watanabe, R. Ohtani‐Kaneko, Toxicology 2010, 272, 52. 20399245 source
The Neuronal cultures and Western blotting assay sections describe lead-treated hippocampal neurons and measurement of β-catenin phosphorylation, not BPA-treated hypothalamic cells or synapsin I phosphorylation. Searches for BPA, hypothalamic cells, and synapsin phosphorylation found no passage addressing the attributed claim. (LLM, conf=0.78)
Experimental — accuracy not yet measured
- Findingown data
BPA-induced spine regressive alterations were restricted to the apical dendrite, not the basal dendrite.
“Interestingly, BPA‐induced spine regressive alterations were restricted to the apical dendrite, not the basal dendrite (Figure 4B).”
Quote in the paperSubstantial claim - Findingown data
Basal spines were not affected by BPA treatments (p > 0.05).
“However, basal spines were not affected by BPA treatments (p > 0.05, Figure 4B).”
Quote in the paperSubstantial claim - Findingown data
In the Morris water maze probe test, BPA-treated rats spent significantly less swimming time in the target quadrant than control animals (p < 0.05).
“BPA‐treated rats spent significantly less swimming time in the target quadrant (location of platform) than the control animals (p < 0.05).”
Quote in the paperSubstantial claim - Findingown data
Total branch lengths in control and BPA-exposed rats were 76.47 ± 5.24 and 76 ± 3.16 μm, respectively.
“According to Sholl analysis, total branch lengths in control and BPA‐exposed rats were 76.47 ± 5.24 and 76 ± 3.16 µm, respectively.”
Quote in the paperNot a substantial claim - Findingown data
Locomotion of rats (moving distance and velocity) in the open field test was similar between control and BPA groups.
“Additionally, the locomotion of rats (moving distance and velocity) in open field test was similar between the two groups (Supporting Information)”
Quote in the paperSubstantial claim - Findingown data
Apical spine density was decreased to two thirds of that of the control group (p < 0.01).
“We found that the apical spines density was decreased to two third of that of the control group (p < 0.01, Figure 4B).”
Quote in the paperSubstantial claim - Findingown data
There was a significant decrease in total spine density in BPA-exposed rats, about a 20% decrease in dendritic spine number compared with control (p < 0.01).
“there was a significant decrease in total spine density in BPA‐exposed rats, about 20% decrease in dendritic spine number compared with the control groups (p < 0.01, Figure 4B).”
Quote in the paperSubstantial claim - Findingown data
In the Y maze test, the BPA group spent less time in the novel arm than the control group (p < 0.05).
“the BPA group spent less time in the novel arm than the control group (p < 0.05, Figure 2H).”
Quote in the paperSubstantial claim - Findingown data
BPA exposure of juvenile rats for 38 d resulted in a mean CSF BPA level of 4.36 ± 2.28 ng/mL, compared with 0.17 ± 0.07 ng/mL in controls (n = 8 rats per group, p < 0.05).
“exposure of juvenile rats for 38 d to BPA resulted in a mean CSF level of 4.36 ± 2.28 ng mL−1; BPA concentration in control group was 0.17 ± 0.07 ng mL−1 (n = 8 rats per group, p < 0.05).”
Quote in the paperSubstantial claim - Findingown data
BPA led to a slight but nonsignificant increase of EPSCAMPA (−310.94 ± 8.23 pA pre-BPA; −644.59 ± 15.78 pA post-BPA, p > 0.05).
“In contrast, BPA specifically led to a slight but nonsignificant increase of EPSCAMPA (−310.94 ± 8.23 pA in pre‐BPA‐treated neurons; −644.59 ± 15.78 pA in post‐BPA‐treated neurons, p > 0.05, Figure 5D).”
Quote in the paperNot a substantial claim - Findingown data
Juvenile BPA exposure decreased NR2A expression in the hippocampus (Figure 5A).
“decreased NR2A expression after juvenile BPA exposure (Figure 5A)”
Quote in the paperSubstantial claim - Findingown data
EPSCNMDA was significantly decreased by about 40% after BPA treatment (10 × 10−6 M) compared with baseline (282.13 ± 10.32 pA pre-BPA, 151.88 ± 8.73 pA post-BPA, p < 0.01).
“the EPSCNMDA of synaptic responses was significantly decreased by about 40% after BPA treatment (10 × 10−6 m) compared with baseline values (282.13 ± 10.32 pA in pre‐BPA‐treated neurons, 151.88 ± 8.73 pA in post‐BPA‐treated neurons, p < 0.01).”
Quote in the paperSubstantial claim - Findingown data
Glutaminase activity for glutamate synthesis was significantly inhibited after chronic BPA exposure (n = 8 rats per group, p < 0.05).
“glutaminase activity for glutamate synthesis was significantly inhibited after chronic BPA exposure (n = 8 rats per group, p < 0.05).”
Quote in the paperSubstantial claim - Findingown data
BPA exposure produced 133.11 ± 16.17% potentiation of fEPSP slope, whereas control LTP was 199.63 ± 39.51% of fEPSP in 60 min after HFS (p < 0.01).
“BPA exposure produced a 133.11 ± 16.17% potentiation of fEPSP slope, whereas control LTP was 199.63 ± 39.51% of fEPSP in 60 min after HFS (p < 0.01).”
Quote in the paperSubstantial claim - Findingown data
Juvenile BPA exposure downregulated AMPA receptors (GluR1) in the hippocampus (Figure 5B).
“the downregulation of AMPA receptors (GluR1) (Figure 5B)”
Quote in the paperSubstantial claim - Findingown data
In Morris water maze training, there was no significant difference in time to find the escape platform between control and BPA-exposed rats (p > 0.05).
“During training (four times a day, at 10 min intervals), there is no significant difference on the time for finding the escape platform between control and BPA‐exposed rats (p > 0.05, Figure 2 B).”
Quote in the paperSubstantial claim - Findingown data
The input/output curve of fEPSP slope in the BPA exposure group was significantly depressed across stimulus intensities of 0.1-1.4 mA (n = 10 rats per group, p < 0.01).
“Compared to the control group, the I/O curve of field excitatory postsynaptic potential (fEPSP) slope in BPA exposure group was significantly depressed with a range of stimulus intensities (0.1–1.4 mA) (n = 10 rats per group, p < 0.01, Figure 3 A).”
Quote in the paperSubstantial claim - Findingown data
There was no significant difference in intersection between dendrites and Sholl circles (dendritic arborization) in control and BPA-exposed rats (p > 0.05).
“There was no significant difference in intersection between dendrites and Sholl circles (dendritic arborization) in control and BPA‐exposed rats (p > 0.05, Figure 4 A)”
Quote in the paperNot a substantial claim - Findingown data
Glutamate release in BPA-treated rats was decreased by 22.47% compared with control (n = 8 rats per group, p < 0.05).
“glutamate release in BPA‐treated rats was decreased by 22.47% as compared to control (n = 8 rats per group, p < 0.05, Figure 6D).”
Quote in the paperSubstantial claim - Findingown data
The PPF ratio at the peak of synaptic enhancement was significantly decreased to 141 ± 11% compared with 191.83 ± 23% in the control group (p < 0.01, n = 10 rats per group).
“The PPF ratio at the peak of the synaptic enhancement was significantly decreased to 141 ± 11% compared to 191.83 ± 23% of control group (p < 0.01, n = 10 rats per group, Figure 6B).”
Quote in the paperSubstantial claim - Findingown data
Juvenile BPA exposure decreased the paired-pulse facilitation (PPF) ratio in hippocampal CA1 areas (Figure 6).
“obviously decreased PPF ratio, glutamate release and glutaminase activity were observed after juvenile BPA exposure (Figure 6).”
Quote in the paperSubstantial claim - Findingown data
AMPA current had a nonsignificant increase in acute BPA-treated slices.
“AMPA current had a nonsignificant increase in acute BPA‐treated slices”
Quote in the paperNot a substantial claim - Findingown data
Acute BPA perfusion significantly declined NMDA-dependent current.
“we also found significantly declined NMDA‐dependent current after acute BPA perfusion.”
Quote in the paperSubstantial claim - Findingown data
Juvenile BPA exposure decreased glutaminase activity in the hippocampus (Figure 6).
“obviously decreased PPF ratio, glutamate release and glutaminase activity were observed after juvenile BPA exposure (Figure 6).”
Quote in the paperSubstantial claim - Findingown data
Juvenile BPA exposure decreased glutamate release in the hippocampus (Figure 6).
“obviously decreased PPF ratio, glutamate release and glutaminase activity were observed after juvenile BPA exposure (Figure 6).”
Quote in the paperSubstantial claim - Interpretationown data
Juvenile BPA exposure has negative effects on synaptic plasticity.
“Taken together, these findings reveal that juvenile BPA exposure has negative effects on synaptic plasticity”
Quote in the paperSubstantial claim - Interpretationown data
Downregulation of postsynaptic glutamate receptors may decrease LTP after BPA exposure.
“These findings indicate that downregulation of postsynaptic glutamate receptors may decrease LTP after BPA exposure.”
Quote in the paperSubstantial claim - Interpretationown data
BPA exposure during the juvenile period perturbs hippocampus-dependent spatial memory consolidation.
“These results lend a strong proof that BPA exposure during the juvenile period perturbs hippocampus‐dependent spatial memory consolidation.”
Quote in the paperSubstantial claim - Interpretationown data
BPA passing across the blood-brain barrier exerts toxic effects on the CNS.
“and thus exert toxic effect on the CNS.”
Quote in the paperSubstantial claim - Interpretationown data
BPA exposure could downregulate presynaptic transmitter release in the hippocampal CA1 areas.
“It suggests that BPA exposure could downregulate the presynaptic transmitter release in the hippocampal CA1 areas.”
Quote in the paperSubstantial claim - Interpretationown data
In the present study, BPA exposure during the whole juvenile phase affected only memory consolidation.
“In the present study, BPA exposure in whole juvenile phase just has effect on the memory consolidation.”
Quote in the paperSubstantial claim - Interpretationreasoning
The hippocampus in juvenile animals is less sensitive to BPA exposure than in the first developmental stage.
“It implies that the hippocampus in juvenile animals is less sensitive to BPA exposure than it in the first developmental stage”
Quote in the paperSubstantial claim - Premisecitation
In the hippocampus, spine head size can be increased after LTP induction through AMPA receptor recruitment at synapses.
“In the hippocampus, the spine head size could be increased after LTP induction through AMPA receptor recruitment at synapses.29”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [29] C. D. Kopec, B. Li, W. Wei, J. Boehm, R. Malinow, J. Neurosci 2006, 26, 2000. 16481433 PMC6674938 source
- Interpretationown data
The development of dendritic shafts was not affected by juvenile BPA exposure.
“suggesting that the development of dendritic shafts was not affected by juvenile BPA exposure.”
Quote in the paperNot a substantial claim - Interpretationown data
Decreased NR2A expression after juvenile BPA exposure explains the postsynaptic mechanism of memory and synaptic plasticity impairment.
“decreased NR2A expression after juvenile BPA exposure (Figure 5A) is proposed to explain the postsynaptic mechanism of memory and synaptic plasticity impairment.”
Quote in the paperSubstantial claim- Rests on an assumption: NR is one of the crucial synaptic elements for activity-dependent synaptic plasticity.
- Premisecitation
Memory changes in rodents and primates after BPA exposure are usually accompanied by loss of dendritic spines in the medial prefrontal cortex and hippocampus.
“These memory changes in rodents and primates are usually accompanied by loss of dendritic spines in the medial prefrontal cortex and hippocampus,[[qv: 5b,9]]”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites 5b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [9] a) J. D. Elsworth, J. D. Jentsch, C. A. Vandevoort, R. H. Roth, D. E. Jr. Redmond, C. Leranth, Neurotoxicology 2013, 35, 113; 23337607 PMC3660149 b) R. E. Bowman, V. Luine, H. Khandaker, J. J. Villafane, M. Frankfurt, Synapse 2014, 68, 498. 24975924 PMC6112112 source
- Interpretationown data
The negative effects of juvenile BPA exposure on synaptic plasticity result from decreases in dendritic spine density and excitatory synaptic transmission.
“which result from decreases in dendritic spine density and excitatory synaptic transmission.”
Quote in the paperSubstantial claim - Interpretationown data
The memory deficits observed after juvenile BPA exposure were not due to motor dysfunction.
“which strongly implicated that memory deficits were not due to motor dysfunction.”
Quote in the paperSubstantial claim - Interpretationown data
BPA exposure significantly impaired synaptic plasticity of the hippocampal CA1 areas.
“The normalized results indicate that BPA exposure significantly impaired synaptic plasticity of the hippocampal CA1 areas.”
Quote in the paperSubstantial claim - Interpretationcitation
Downregulation of AMPA receptors (GluR1) after juvenile BPA exposure suggests a lower regulative capability to control synaptic plasticity in the hippocampus.
“the downregulation of AMPA receptors (GluR1) (Figure 5B) suggests that there is a lower regulative capability to control synaptic plasticity in the hippocampus after juvenile BPA exposure.30”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30] G. G. Turrigiano, S. B. Nelson, Nat. Rev. Neurosci. 2004, 5, 97. 14735113 source
- Interpretationown data
Juvenile BPA exposure impaired basic synaptic transmission of the hippocampal CA1 areas.
“This result suggests that juvenile BPA exposure impaired the basic synaptic transmission of the hippocampal CA1 areas.”
Quote in the paperSubstantial claim - Interpretationreasoning
BPA-induced structure and function deterioration are dependent on perturbing the functions of estrogen receptors in the hippocampus.
“this finding further suggests that BPA‐induced structure and function deterioration are dependent on perturbing the functions of estrogen receptors on the hippocampus.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites 24a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationown data
Juvenile BPA-exposed rats have deficits of spatial memory for a familiar environment.
“These findings suggest the deficits of spatial memory for familiar environment in juvenile‐BPA‐exposed rats.”
Quote in the paperSubstantial claim - Interpretationown data
BPA can interfere with postsynaptic sites of excitatory synapses in pyramidal dendrites.
“This suggests that BPA can interfere with postsynaptic sites of excitatory synapses in pyramidal dendrites.”
Quote in the paperSubstantial claim - Premisecitation
BPA can exert hormone mimetic or antagonist activities through binding estrogen receptor α and β.
“As a xenoestrogen, BPA could exert hormone mimetic or antagonist activities through binding estrogen receptor α and β.4”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [4] N. J. MacLusky, T. Hajszan, C. Leranth, Environ. Health Perspect. 2005, 113, 675. 15929888 PMC1257590 source
- Interpretationown data
Decreased glutamate levels in the hippocampus provide a likely explanation for presynaptic impairment of physiological function in BPA-exposed rats.
“Decreased glutamate levels in the hippocampus also provide a likely explanation for presynaptic impairment of physiological function in BPA exposed rats.”
Quote in the paperSubstantial claim - Interpretationown data
Juvenile BPA exposure exerted a region-specific effect on spine protrusion of dendritic shafts.
“These results indicate that juvenile BPA exposure exerted a region specific effect on spine protrusion of dendritic shafts.”
Quote in the paperSubstantial claim - Premisecitation
Perinatal BPA exposure results in less glutamate release from presynaptic neurons.
“perinatal BPA exposure results in less glutamate release from presynaptic neurons.32”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [32] N. J. Cabaton, C. Canlet, P. R. Wadia, M. Tremblay‐Franco, R. Gautier, J. Molina, C. Sonnenschein, J. P. Cravedi, B. S. Rubin, A. M. Soto, D. Zalko, Environ. Health Perspect. 2013, 121, 586. 23425943 PMC3673190 source
- Interpretationreasoning
There may be an obvious decline of the EPSCNMDA/EPSCAMPA ratio in BPA-exposed rats.
“suggesting that there may be an obvious decline of EPSCNMDA/EPSCAMPA ratio in BPA‐exposed rats.”
Quote in the paperSubstantial claim - Interpretationown data
Decreased spine density, glutamate release, and NR2A and GluR1 expression may contribute to the functional deficits caused by juvenile BPA exposure.
“The decreased spine density, glutamate release, and NR2A and GluR1 expression may contribute to such functional deficits.”
Quote in the paperSubstantial claim - Interpretationreasoning
The presynaptic site in the hippocampus is susceptible to both perinatal and juvenile BPA exposure.
“Therefore, the presynaptic site in the hippocampus is susceptible to both perinatal and juvenile BPA exposure.”
Quote in the paperSubstantial claim - Interpretationown data
The declined NMDA-dependent current after acute BPA perfusion provides basal evidence for glutamatergic synaptic current in LTP and spatial memory deficits in juvenile BPA-exposed rats.
“this provided the basal evidence for glutamatergic synaptic current in LTP and spatial memory deficits in juvenile BPA‐exposed rats.”
Quote in the paperSubstantial claim - Interpretationcitation
BPA could directly perturb transmitter release from vesicles through regulating the activity of synapsins.
“These findings indicate that BPA could also directly perturb the transmitter release from vesicles through regulating the activity of synapsins.”
Quote in the paperSubstantial claim - Interpretationown data
Decreased PPF ratio, glutamate release, and glutaminase activity after juvenile BPA exposure provide the presynaptic mechanism of impaired LTP by BPA exposure.
“These alterations provide the presynaptic mechanism of impaired LTP by BPA exposure.”
Quote in the paperSubstantial claim- Rests on an assumption: PPF in hippocampal CA1 areas is an indicator of presynaptic transmitter release probability.
- Classified as probably not a substantial claim. 11
- May combine two claims. 13
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation17β-estradiol enhances dendritic apical spine density of CA1 pyramidal neurons in the hippocampus via ERK and mTOR activation.
“17β‐estradiol has been shown to enhance dendritic apical spine density of CA1 pyramidal neurons in the hippocampus, via ERK and mTOR activation.[[qv: 24a,26]]”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites 24a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [26] J. J. Tuscher, V. Luine, M. Frankfurt, K. M. Frick, J. Neurosci. 2016, 36, 1483. 26843632 PMC4737764 source
May combine two claims.
PremisecitationChronic BPA exposure during pregnancy and lactation can induce memory deficits later in the life of rats, including impaired spatial recognition memory in mid-adolescence and deficient spatial learning and memory in juvenile and adult rats.
“chronic BPA exposure in pregnancy and lactation (the critical periods of brain development) could induce memory deficits later in the life of rats, such as impaired spatial recognition memory in mid‐adolescence,6 and deficient spatial learning and memory in juvenile and adult.7”
Quote in the paperSubstantial claim1 of 2 sources checked- cites [6] A. Poimenova, E. Markaki, C. Rahiotis, E. Kitraki, Neuroscience 2010, 167, 741. 20219646 source
- cites [7] a) R. Kuwahara, S. Kawaguchi, Y. Kohara, H. Cui, K. Yamashita, J. Pharmacol. Sci. 2013, 123, 132; 24077108 b) M. E. Rebuli, L. Camacho, M. E. Adonay, D. M. Reif, D. L. Aylor, H. B. Patisaul, Toxicol. Sci. 2015, 148, 341. 26209558 PMC4683367 source
The Introduction says only that animal and human studies have associated BPA exposure with adverse neurodevelopmental effects. Searches for pregnancy and lactation exposure, rat spatial recognition, and spatial learning found no passage addressing the claimed memory deficits or ages; the paper assesses dietary BPA exposure instead. (LLM, conf=0.74)
Experimental — accuracy not yet measured
May combine two claims.
Findingown dataBPA-exposed rats had lower frequency of entry into the novel arm and higher frequency of entry into the home arm than the control group (p < 0.01).
“BPA‐exposed rats had lower frequency of entry into the novel arm and higher frequency of entry into the home arm than the control group (p < 0.01, Figure 2I).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataBPA-treated rats showed no difference in swimming speed and total swimming distance compared with control rats (p > 0.05).
“Notably, BPA‐treated rats showed no difference in swimming speed and total swimming distance with control rats (p > 0.05, Figure 2E,F).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataDuring the probe test, escape latency of BPA-treated rats showed no significant difference from control, but an increasing trend (p > 0.05).
“During probe test, escape latency of BPA‐treated rats showed no significant difference with the control group, but an increasing trend (p > 0.05, Figure 2D).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataThere was a significant decrease in NR2A and GluR1 expression levels (n = 8 rats per group, p < 0.05) but not in the remaining subunits.
“there was a significant decrease in NR2A and GluR1 expression levels (n = 8 rats per group, p < 0.05) but not in the remaining subunits.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataSynaptic transmissions mediated by NMDA receptors were deranged after BPA exposure, contributing to the reduced LTP.
“These results suggest that synaptic transmissions mediated by NMDA receptors (NR) were deranged after BPA exposure, contributing to the reduced LTP.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationThe presence of GluR1 and the deficiency of GluR2 in AMPA receptors contribute to LTP enhancement.
“the presence of GluR1 as well as the deficient of GluR2 in AMPA receptors has a contribution to LTP enhancement.[[qv: 15b]]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [[qv: 15b]]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationown dataAltered synaptic transmission contributed to BPA-induced cognitive impairment, with decreased presynaptic glutamate synthesis and release and excitatory receptor expression.
“Meanwhile, altered synaptic transmission also contributed to BPA‐induced cognitive impairment, with the decrease of presynaptic glutamate synthesis and release, and excitatory receptors expression.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
PremisecitationInduction of LTP at Sch-CA1 synapses is dependent on glutamate receptors, especially NR2A, NR2B, GluR1, and GluR2.
“Induction of LTP at Sch‐CA1 synapses is dependent on glutamate receptors, especially NR2A, NR2B, GluR1, and GluR2.15”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [15] a) K. Prybylowski, R. J. Wenthold, J. Biol. Chem. 2004, 279, 9673; 14742424 b) S. Rumpel, J. LeDoux, A. Zador, R. Malinow, Science 2005, 308, 83. 15746389 source
May combine two claims.
Interpretationown dataJuvenile BPA exposure resulted in hippocampal-dependent spatial memory impairment without a learning deficit.
“The current training and probe test results suggest that juvenile BPA exposure resulted in hippocampal‐dependent spatial memory impairment without learning deficit.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationOver-stimulating NMDA receptors (NRs) could increase Ca2+ influx, which then induces short- or long-term alterations in the hippocampus, such as LTP.
“Over‐stimulating of NRs could increase Ca2+ influx, which then induces short‐ or long‐term alterations in the hippocampus, e.g., LTP.[[qv: 15a]]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [[qv: 15a]]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationown dataJuvenile BPA exposure inhibited LTP induction in the hippocampal CA1 areas after HFS of Sch in the CA3 areas, which underlies BPA-related memory deficits involving synapse plasticity changes.
“Our results showed that juvenile BPA exposure inhibited LTP induction in the hippocampal CA1 areas after HFS of Sch in the CA3 areas (Figure 3B), which underlies BPA related memory deficits involving synapse plasticity changes.”
Quote in the paperSubstantial claim- Rests on an assumption: Synaptic plasticity, including LTP and LTD, is the cellular basis of learning and memory at the physiological level.
Classified as probably not a substantial claim.
PremisecitationThe different signaling properties of NMDA receptors (NRs) are mainly due to their different subunit compositions.
“The different signaling properties of NRs are mainly due to their different subunit compositions.28”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [28] V. R. Rao, S. Finkbeiner, Trends Neurosci. 2007, 30, 284. 17418904 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationDendritic spines of pyramidal neurons receive most excitatory connections from presynaptic glutamatergic projections.
“Dendritic spines of pyramidal neurons are small protrusions from the dendritic shafts and receive most excitatory connections from presynaptic glutamatergic projections.13”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [13] N. L. Rochefort, A. Konnerth, EMBO Rep. 2012, 13, 699. 22791026 PMC3410382 source
Classified as probably not a substantial claim.
PremisecitationPaired-pulse facilitation is a presynaptic form of short-term synaptic plasticity due to enhanced presynaptic transmitter release in response to the second of two closely spaced action potentials during field potential recording.
“Paired‐pulse facilitation (PPF) is a presynaptic form of short‐term synaptic plasticity due to enhanced presynaptic transmitter release in response to the second of two closely spaced action potentials during field potential recording.16”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [16] R. S. Zucker, W. G. Regehr, Annu. Rev. Physiol. 2002, 64, 355. 11826273 source
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenThe study was approved by the Institutional Animal Care and Use Committee of University of Science and Technology of China, P. R. China.
“The study was approved by the Institutional Animal Care and Use Committee of University of Science and Technology of China, P. R. China.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningBPA exerts estrogen antagonist activity to induce reestablishment of excitatory synaptic transmission and impairment of synaptic plasticity.
“which underlies BPA exerting estrogen antagonist activity to induce reestablishment of excitatory synaptic transmission and impairment of synaptic plasticity.”
Quote in the paperSubstantial claim- Rests on an assumption: BPA acts as an estrogen antagonist.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenAll animal experiments were performed according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals.
“All animal experiments were performed according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
PremisecitationLTP expression includes the presynaptic locus associated with paired-pulse facilitation (PPF) ratio changes.
“It is well known that LTP expression includes the presynaptic locus associated with PPF ratio changes.31”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [31] a) P. E. Schulz, E. P. Cook, D. Johnston, J. Neurosci. 1994, 14, 5325; 7916043 PMC6577083 b) S. S. Yu, M. Wang, X. M. Li, W. H. Chen, J. T. Chen, H. L. Wang, D. Y. Ruan, BMC Dev. Biol. 2007, 7, 51; 17511882 PMC1888697 c) G. Mereu, M. Cammalleri, M. Fa, W. Francesconi, P. Saba, M. Tattoli, L. Trabace, A. Vaccari, V. Cuomo, J. Pharmacol. Exp. Ther. 2000, 294, 728. 10900254 source
Classified as probably not a substantial claim.
Premisecitation17β-estrogen enhances learning and LTP magnitude by increasing the ratio of NMDA transmission to AMPA transmission.
“17β‐estrogen enhances learning and LTP magnitude by increasing the ratio of NMDA transmission to AMPA transmission,[[qv: 24c]]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [[qv: 24c]]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationown dataJuvenile BPA exposure caused profound neurocognitive deterioration in spatial memory and synaptic plasticity.
“the present study shows that juvenile BPA exposure caused profound neurocognitive deterioration in spatial memory and synaptic plasticity.”
Quote in the paperSubstantial claim
The paper relies on this without support.
Synaptic plasticity, including LTP and LTD, is the cellular basis of learning and memory at the physiological level.
“Synaptic plasticity, including long‐term potentiation and depression (LTP and LTD), has been recognized as the cellular basis of learning and memory at the physiological level.”
The paper relies on this without support.
Reports assessing how physiological functions degrade in BPA-exposed rodents are scarce.
“Currently, reports assessing how physiological functions degrade in BPA‐exposed rodents are scarce.”
The paper relies on this without support.
NR is one of the crucial synaptic elements for activity-dependent synaptic plasticity.
“NR is considered one of the crucial synaptic elements for activity‐dependent synaptic plasticity.”
The paper relies on this without support.
PPF in hippocampal CA1 areas is an indicator of presynaptic transmitter release probability.
“PPF in the hippocampal CA1 areas is a transient form of presynaptic plasticity, which is considered an indicator of presynaptic transmitter release probability.”
The paper relies on this without support.
BPA acts as an estrogen antagonist.
“which underlies BPA exerting estrogen antagonist activity to induce reestablishment of excitatory synaptic transmission and impairment of synaptic plasticity.”
The paper relies on this without support.
The exposure concentration used (1 mg/kg/day) is much lower than the currently accepted lowest observed adverse effect level (50 mg/kg/day).
“The exposure concentration mentioned above was much lower than the currently accepted lowest observed adverse effect level (50 mg kg−1 d−1).”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Spine-analysis rat count differs between results and methods
MajorThe morphology results specify 10 rats per group, whereas the Golgi-Cox staining method specifies eight per group.
“A total of 10–12 pyramidal neurons in each control and BPA‐exposed rats were included for final analysis (n = 10 rats per group).”
“After CSF collection, brain samples (with or without BPA exposure, n = 8 per group) were processed by the Golgi‐Cox staining method”
Electrophysiology sample size differs between results and methods
MajorThe field-potential results report 10 rats per group, but the corresponding in vivo recording method specifies eight per group.
“the I/O curve of field excitatory postsynaptic potential (fEPSP) slope in BPA exposure group was significantly depressed with a range of stimulus intensities (0.1–1.4 mA) (n = 10 rats per group, p < 0.01, Figure 3 A).”
“Briefly, 49–52 d old SD rats (n = 8 per group) were anesthetized”
Neuron counts per rat differ between results and methods
MajorThe results describe including 10-12 pyramidal neurons in each rat, but the morphology method says 5-6 neurons from each brain were used.
“A total of 10–12 pyramidal neurons in each control and BPA‐exposed rats were included for final analysis”
“About 2–3 neurons per section were chosen and then 5–6 neurons from each brain were used for morphological analyses.”
Exposure duration does not match the stated ages
MinorExposure from postnatal day 21 to day 49 spans 28 days, not the 38 days reported for juvenile exposure.
Reported 38 · recomputed 28
“exposure of juvenile rats for 38 d to BPA resulted in a mean CSF level of 4.36 ± 2.28 ng mL−1”
CSF sample size differs between results and methods
MinorThe CSF BPA result states eight rats per group, while the BPA-detection method states 16 rats per group.
“BPA concentration in control group was 0.17 ± 0.07 ng mL−1 (n = 8 rats per group, p < 0.05).”
“BPA detection: SD rats with or without juvenile BPA exposure (n = 16 per group) were deeply anesthetized”
Cites
Brain development during childhood and adolescence: a longitudinal MRI study
Giedd, J. N., Blumenthal, J., Jeffries, N. O., Castellanos, F. X., Liu, H., Zijdenbos, A., Paus, T., Evans, A. C., & Rapoport, J. L. (1999) · Nature Neuroscience · doi:10.1038/13158 · Cited by 5,552 · see citing works
Short-Term Synaptic Plasticity
Zucker, R. S., & Regehr, W. G. (2002) · Annual Review of Physiology · doi:10.1146/annurev.physiol.64.092501.114547 · Cited by 5,068 · see citing works
Rice, D., & Barone, S. (2000) · Environmental Health Perspectives · doi:10.1289/ehp.00108s3511 · Cited by 2,944 · see citing works
Human exposure to bisphenol A (BPA)
Vandenberg, L. N., Hauser, R. B., Marcus, M., Olea, N., & Welshons, W. V. (2007) · Reproductive Toxicology · doi:10.1016/j.reprotox.2007.07.010 · Cited by 2,897 · see citing works
Homeostatic plasticity in the developing nervous system
Turrigiano, G. G., & Nelson, S. B. (2004) · Nature Reviews Neuroscience · doi:10.1038/nrn1327 · Cited by 2,485 · see citing works
Bisphenol A and human health: A review of the literature
Rochester, J. R. (2013) · Reproductive Toxicology · doi:10.1016/j.reprotox.2013.08.008 · Cited by 2,018 · see citing works
Design and validation of a tool for neurite tracing and analysis in fluorescence microscopy images
Meijering, E. H. W., Jacob, M., Sarria, J. ‐. F., Steiner, P., Hirling, H., & Unser, M. A. (2004) · Cytometry Part A · doi:10.1002/cyto.a.20022 · Cited by 1,611 · see citing works
Bisphenol-A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption
Vandenberg, L. N., Maffini, M. V., Sonnenschein, C., Rubin, B. S., & Soto, A. M. (2009) · Endocrine Reviews · doi:10.1210/er.2008-0021 · Cited by 1,407 · see citing works
Postsynaptic receptor trafficking underlying a form of associative learning
Rumpel, S., LeDoux, J., Zador, A., & Malinow, R. (2005) · Science · doi:10.1126/science.1103944 · Cited by 775 · see citing works
Locally dynamic synaptic learning rules in pyramidal neuron dendrites
Harvey, C. D., & Svoboda, K. (2007) · Nature · doi:10.1038/nature06416 · Cited by 625 · see citing works
Glutamate Receptor Exocytosis and Spine Enlargement during Chemically Induced Long-Term Potentiation
Kopec, C. D., Li, B., Wei, W., Boehm, J., & Malinow, R. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.3918-05.2006 · Cited by 486 · see citing works
Changes in paired-pulse facilitation suggest presynaptic involvement in long-term potentiation
Schulz, P. E., Cook, E. P., & Johnston, D. (1994) · Journal of Neuroscience · doi:10.1523/jneurosci.14-09-05325.1994 · Cited by 460 · see citing works
The Politics of Plastics: The Making and Unmaking of Bisphenol A “Safety”
Vogel, S. A. (2009) · American Journal of Public Health · doi:10.2105/ajph.2008.159228 · Cited by 416 · see citing works
Uncovering the mechanisms of estrogen effects on hippocampal function
Spencer-Segal, J. L., Waters, E. M., Romeo, R. D., Wood, G. E., Milner, T. A., & McEwen, B. S. (2007) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2007.08.006 · Cited by 415 · see citing works
Llinas, R. H., Gruner, J. A., Sugimori, M., McGuinness, T. L., & Greengard, P. (1991) · The Journal of Physiology · doi:10.1113/jphysiol.1991.sp018549 · Cited by 317 · see citing works
Dellu, F., Contarino, A., Simon, H., Koob, G. F., & Gold, L. H. (2000) · Neurobiology of Learning and Memory · doi:10.1006/nlme.1999.3919 · Cited by 303 · see citing works
Dendritic spines: from structure to in vivo function
Rochefort, N. L., & Konnerth, A. (2012) · The EMBO Reports · doi:10.1038/embor.2012.102 · Cited by 299 · see citing works
Remodeling of Synaptic Actin Induced by Photoconductive Stimulation
Colicos, M. A., Collins, B., Sailor, M. J., & Goda, Y. (2001) · Cell · doi:10.1016/s0092-8674(01)00579-7 · Cited by 270 · see citing works
Wang, W., Abualnaja, K. O., Asimakopoulos, A. G., Covaci, A., Gevao, B., Johnson‐Restrepo, B., Kumosani, T., Malarvannan, G., Minh, T. B., Moon, H., et al. (2015) · Environment International · doi:10.1016/j.envint.2015.06.015 · Cited by 264 · see citing works
Geens, T., Roosens, L., Neels, H. M., & Covaci, A. (2009) · Chemosphere · doi:10.1016/j.chemosphere.2009.05.024 · Cited by 259 · see citing works
NMDA and AMPA receptors: old channels, new tricks
Rao, V. R., & Finkbeiner, S. M. (2007) · Trends in Neurosciences · doi:10.1016/j.tins.2007.03.012 · Cited by 250 · see citing works
Xu, X.-H., Zhang, J., Wang, Y.-M., Ye, Y.-P., & Luo, Q.-Q. (2010) · Hormones and Behavior · doi:10.1016/j.yhbeh.2010.02.012 · Cited by 211 · see citing works
Lorber, M., Schecter, A., Paepke, O., Shropshire, W., Christensen, K., & Birnbaum, L. (2015) · Environment International · doi:10.1016/j.envint.2015.01.008 · Cited by 198 · see citing works
The Environmental Estrogen Bisphenol A Inhibits Estradiol-Induced Hippocampal Synaptogenesis
MacLusky, N. J., Hajszan, T., & Leranth, C. (2005) · Environmental Health Perspectives · doi:10.1289/ehp.7633 · Cited by 196 · see citing works
Smith, C. C., & McMahon, L. L. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.0762-05.2005 · Cited by 189 · see citing works
The developmental stages of synaptic plasticity
Löhmann, C., & Kessels, H. W. H. G. (2013) · The Journal of Physiology · doi:10.1113/jphysiol.2012.235119 · Cited by 176 · see citing works
Poimenova, A., Markaki, E., Rahiotis, C., & Kitraki, E. (2010) · Neuroscience · doi:10.1016/j.neuroscience.2010.02.051 · Cited by 174 · see citing works
Levels of Bisphenol A in Canned Soft Drink Products in Canadian Markets
Cao, X.-L., Corriveau, J., & Popovic, S. (2009) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf803213g · Cited by 154 · see citing works
Xu, J., Wu, L., Chen, W., & Chang, A. C. (2008) · Journal of Chromatography A · doi:10.1016/j.chroma.2008.07.001 · Cited by 154 · see citing works
Tuscher, J. J., Luine, V., Frankfurt, M., & Frick, K. M. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.3135-15.2016 · Cited by 149 · see citing works
Effects of Low Doses of Bisphenol A on the Metabolome of Perinatally Exposed CD-1 Mice
Cabaton, N. J., Canlet, C., Wadia, P. R., Tremblay‐Franco, M., Gautier, R., Molina, J., Sonnenschein, C., Cravedi, J., Rubin, B. S., Soto, A. M., et al. (2013) · Environmental Health Perspectives · doi:10.1289/ehp.1205588 · Cited by 147 · see citing works
N-Methyl-D-aspartate Receptors: Subunit Assembly and Trafficking to the Synapse
Prybylowski, K., & Wenthold, R. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.r300029200 · Cited by 137 · see citing works
Elsworth, J. D., Jentsch, J. D., VandeVoort, C. A., Roth, R. H., Redmond, D. E., & Léránth, C. (2013) · NeuroToxicology · doi:10.1016/j.neuro.2013.01.001 · Cited by 132 · see citing works
Smith, C. C., Vedder, L. C., & McMahon, L. L. (2009) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2009.06.003 · Cited by 129 · see citing works
Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.
Eilam‐Stock, T., Serrano, P. A., Frankfurt, M., & Luine, V. N. (2011) · Behavioral Neuroscience · doi:10.1037/a0025959 · Cited by 121 · see citing works
Sun, Y., Nakashima, M. N., Takahashi, M., Kuroda, N., & Nakashima, K. (2002) · Biomedical Chromatography · doi:10.1002/bmc.161 · Cited by 118 · see citing works
Spine plasticity in the motor cortex
Yu, X., & Zuo, Y. (2010) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2010.07.010 · Cited by 106 · see citing works
Zhou, R., Bai, Y., Yang, R., Zhu, Y., Chi, X., Li, L., Chen, L., Sokabe, M., & Chen, L. (2011) · Neuropharmacology · doi:10.1016/j.neuropharm.2011.01.031 · Cited by 92 · see citing works
Chen, Z., Yang, X., Liu, H., Wei, W., Zhang, K.-S., Huang, H., Giesy, J. P., Liu, H., Du, J., & Wang, H. (2014) · Archives of Toxicology · doi:10.1007/s00204-014-1301-z · Cited by 91 · see citing works
Self-citationGonçalves, C. R., Cunha, R. W., Barros, D. M., & Martínez, P. E. (2010) · Environmental Toxicology and Pharmacology · doi:10.1016/j.etap.2010.06.003 · Cited by 80 · see citing works
Diaz Weinstein, S., Villafane, J. J., Juliano, N., & Bowman, R. E. (2013) · Brain Research · doi:10.1016/j.brainres.2013.07.018 · Cited by 73 · see citing works
Kimura, E., Matsuyoshi, C., Miyazaki, W., Benner, S., Hosokawa, M., Yokoyama, K., Kakeyama, M., & Tohyama, C. (2015) · Archives of Toxicology · doi:10.1007/s00204-015-1485-x · Cited by 71 · see citing works
Parameshwaran, K., Buabeid, M. A., Karuppagounder, S. S., Uthayathas, S., Thiruchelvam, K., Shonesy, B. C., Dityatev, A. E., Escobar, M. E., Dhanasekaran, M., & Suppiramaniam, V. D. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-011-0805-4 · Cited by 67 · see citing works
Rebuli, M. E., Camacho, L., Adonay, M. E., Reif, D. M., Aylor, D. L., & Patisaul, H. B. (2015) · Toxicological Sciences · doi:10.1093/toxsci/kfv163 · Cited by 64 · see citing works
Hu, F., Xu, L., Liu, Z.-H., Ge, M.-M., Ruan, D.-Y., & Wang, H.-L. (2014) · PLoS ONE · doi:10.1371/journal.pone.0101894 · Cited by 54 · see citing works
Self-citationPerinatal Exposure to Low-Dose Bisphenol A Impairs Spatial Learning and Memory in Male Rats
Kuwahara, R., Kawaguchi, S., Kohara, Y., Cui, H., & Yamashita, K. (2013) · Journal of Pharmacological Sciences · doi:10.1254/jphs.13093fp · Cited by 52 · see citing works
Elsworth, J. D., Jentsch, J. D., Groman, S. M., Roth, R. H., Redmond, E. D., & Leranth, C. (2015) · Journal of Comparative Neurology · doi:10.1002/cne.23735 · Cited by 51 · see citing works
Adolescent bisphenol‐A exposure decreases dendritic spine density: Role of sex and age
Bowman, R. E., Luine, V. N., Khandaker, H., Villafane, J. J., & Frankfurt, M. (2014) · Synapse · doi:10.1002/syn.21758 · Cited by 45 · see citing works
Kodavanti, P. R. S., Royland, J. E., Osorio, C., Winnik, W. M., Ortiz, P., Lei, L., Ramabhadran, R., & Alzate, O. (2015) · Environmental Health Perspectives · doi:10.1289/ehp.1408504 · Cited by 45 · see citing works
Kovanecz, I., Gelfand, R., Masouminia, M., Gharib, S. K., Segura, D., Vernet, D., Rajfer, J., Li, D., Kannan, K., & González-Cadavid, N. F. (2013) · International Journal of Impotence Research · doi:10.1038/ijir.2013.37 · Cited by 42 · see citing works
Analyzing the influence of BDNF heterozygosity on spatial memory response to 17β-estradiol
Wu, Y., Du, X., van den Buuse, M., & Hill, R. (2015) · Translational Psychiatry · doi:10.1038/tp.2014.143 · Cited by 36 · see citing works
Mereu, G., Cammalleri, M., Fà, M., et al. (2000) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)39128-1 · Cited by 32 · see citing works
In vitro effects of bisphenol A on developing hypothalamic neurons
Iwakura, T., Iwafuchi, M., Muraoka, D., Yokosuka, M., Shiga, T., Watanabe, C., & Ohtani‐Kaneko, R. (2010) · Toxicology · doi:10.1016/j.tox.2010.04.005 · Cited by 27 · see citing works
Yu, S., Wang, M., Li, X., Chen, W., Chen, J., Wang, H.-L., & Ruan, D. (2007) · BMC Developmental Biology · doi:10.1186/1471-213x-7-51 · Cited by 25 · see citing works
Self-citationChen, L., Miao, Y., Chen, L., Xu, J., Wang, X., Zhao, H., Shen, Y., Hu, Y. B., Bian, Y., Shen, Y., et al. (2014) · Biomaterials · doi:10.1016/j.biomaterials.2014.07.030 · Cited by 20 · see citing works
Self-citationHu, F., Ge, M.-M., & Chen, W. (2015) · Synapse · doi:10.1002/syn.21873 · Cited by 12 · see citing works
Self-citation
Flagged first, then by citations
Research works printed but not linked: 3
- Wang Z., 2016, Adv. Sci., 1600248, 1
- Amaral D., 2006, The Hippocampus Book
- 10.1016/j.biomaterials.2014.07.030 · DOI
Cited by
Sorted by citations
Neuro-toxic and Reproductive Effects of BPA
Santoro, A., Chianese, R., Troisi, J., Richards, S. M., Nori, S. L., Fasano, S., Guida, M., Plunk, E. C., Viggiano, A., Pierantoni, R., et al. (2019) · Current Neuropharmacology · doi:10.2174/1570159x17666190726112101 · Cited by 281 · see citing works
Mustieles, V., D’Cruz, S. C., Couderq, S., Rodríguez‐Carrillo, A., Fini, J., Hofer, T., Steffensen, I., Dirven, H. A. A. M., Barouki, R., Olea, N., et al. (2020) · Environment International · doi:10.1016/j.envint.2020.105811 · Cited by 269 · see citing works
Zhang, H., Kuang, H., Luo, Y., Liu, S., Meng, L., Pang, Q., & Fan, R. (2019) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2019.134036 · Cited by 77 · see citing works
Thongkorn, S., Kanlayaprasit, S., Jindatip, D., Tencomnao, T., Hu, V. W., & Sarachana, T. (2019) · Scientific Reports · doi:10.1038/s41598-019-39386-w · Cited by 66 · see citing works
Welch, C. J., & Mulligan, K. A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23052894 · Cited by 74 · see citing works
Jakaria, M., Park, S., Haque, M. E., Karthivashan, G., Kim, I., Ganesan, P., & Choi, D. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00307 · Cited by 70 · see citing works
Suresh, S., Ankul Singh, S., & Vellapandian, C. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104939 · Cited by 61 · see citing works
Shi, Y., Wang, H., Zhu, Z., Ye, Q., Lin, F., & Cai, G. (2022) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2022.160129 · Cited by 56 · see citing works
Wu, D., Wu, F., Lin, R., Meng, Y., Wei, W., Sun, Q., & Jia, L. (2020) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2020.04.023 · Cited by 56 · see citing works
Gao, Y., Wang, F., Tang, J., et al. (2024) · Chemical Engineering Journal · doi:10.1016/j.cej.2024.153651 · Cited by 51 · see citing works
Wang, G., Li, H., Li, N., et al. (2022) · Angewandte Chemie International Edition · doi:10.1002/anie.202210619 · Cited by 50 · see citing works
Bisphenol A inhibits autophagosome-lysosome fusion and lipid droplet degradation
Song, D., Chen, Y., Wang, B., et al. (2019) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2019.109492 · Cited by 49 · see citing works
Mu, X., Liu, J., Wang, H., Yuan, L., Wang, C., Li, Y., & Qiu, J. Y. (2022) · Environmental Science & Technology · doi:10.1021/acs.est.2c01531 · Cited by 46 · see citing works
Bisphenol A (BPA) and neurological disorders: An overview
Hyun, S., & Ka, M. (2024) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2024.106614 · Cited by 45 · see citing works
Elkader, H. A. E. A., Abdou, H. M., Khamiss, O., & Essawy, A. E. (2021) · Environmental Science and Pollution Research · doi:10.1007/s11356-021-12927-5 · Cited by 45 · see citing works
“For each rat, the ambulation frequency, number of grooming events, number of rearings, latency time (sec), freezing time, number of faecal boli and total time in the inner and outer zones (sec) during the exploration period were recorded manually from video camera footage (Hu et al. 2017).”
MethodResultMeng, L., Gui, S., Ouyang, Z., Wu, Y., Zhuang, Y., Pang, Q., & Fan, R. (2023) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2023.132074 · Cited by 41 · see citing works
Yin, Z., Hua, L., Chen, L., Hu, D., Li, J., An, Z., Tian, T., Ning, H., & Ge, Y. (2020) · Toxicology in Vitro · doi:10.1016/j.tiv.2020.104911 · Cited by 38 · see citing works
Henriksen, A. D. P., Andrade, A., Harris, E. P., Rissman, E. F., & Wolstenholme, J. T. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21093129 · Cited by 37 · see citing works
“Direct exposure to BPA alters synaptic spine morphology [27–30] and synaptic plasticity [33].”
BackgroundWolstenholme, J. T., Drobná, Z., Henriksen, A. D. P., Goldsby, J. A., Stevenson, R. J., Irvin, J. W., Flaws, J. A., & Rissman, E. F. (2019) · Endocrinology · doi:10.1210/en.2019-00196 · Cited by 34 · see citing works
Bisphenols exert detrimental effects on neuronal signaling in mature vertebrate brains
Schirmer, E., Schuster, S., & Machnik, P. (2021) · Communications Biology · doi:10.1038/s42003-021-01966-w · Cited by 32 · see citing works
Chen, Z., Li, T., Zhang, L., Wang, H., & Hu, F. (2018) · Toxicology · doi:10.1016/j.tox.2018.10.002 · Cited by 33 · see citing works
Self-citationYu, H., Ma, L., Liu, D., Wang, Y., Pei, X., Duan, Z., Ma, M., & Zhang, Y. (2020) · Environmental Pollution · doi:10.1016/j.envpol.2020.115055 · Cited by 31 · see citing works
Xiong, L., Xue, L., Du, R., Zhou, H.-L., Tan, Y., Ma, Z., Jin, Y., Zhang, Z., Xu, Y. X. Z., Hu, Q., et al. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.529544 · Cited by 32 · see citing works
Self-citationWu, D., Liu, H., Liu, Y., Wei, W., Sun, Q., Wen, D., & Jia, L. (2021) · Food and Chemical Toxicology · doi:10.1016/j.fct.2021.112307 · Cited by 32 · see citing works
Wang, R., Liu, Z., Bi, N., Gu, X., Huang, C., Zhou, R., Liu, H., & Wang, H.-L. (2023) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2023.115034 · Cited by 30 · see citing works
Lee, C. Y., Hyun, S., Ko, M. Y., Kim, H. R., Rho, J., Kim, K. K., Kim, W.-Y., & Ka, M. (2021) · Cerebral Cortex · doi:10.1093/cercor/bhab183 · Cited by 28 · see citing works
Liu, J., Wang, R., Wang, B., et al. (2022) · Applied Surface Science · doi:10.1016/j.apsusc.2022.154625 · Cited by 27 · see citing works
Al‐Shami, A. S., Elkader, H. A. E. A., Moussa, N., Essawy, A. E., & Haroun, M. (2024) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-024-05039-4 · Cited by 26 · see citing works
Xu, Z., Wang, A., Hu, J., Li, Z., Zheng, Y., Liu, Y., Xiang, Q., Wang, J., Yao, W., Ding, C., et al. (2025) · Environmental Pollution · doi:10.1016/j.envpol.2025.126591 · Cited by 26 · see citing works
Liu, H., Lin, H., Xu, T., et al. (2023) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2023.166890 · Cited by 26 · see citing works
Essawy, A. E., Elkader, H. A. E. A., Khamiss, O., Eweda, S. M., & Abdou, H. M. (2021) · PeerJ · doi:10.7717/peerj.11930 · Cited by 25 · see citing works
“Suppression of GA activity in the present study may be due to the presynaptic mechanism of impaired long-term potentiation (LTP) by BPA intoxication (Hu et al., 2017).”
BackgroundMeng, L., Ouyang, Z., Chen, Y., Huang, C., Yu, Y., & Fan, R. (2024) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2024.172655 · Cited by 25 · see citing works
Hu, F., Liang, W., Zhang, L., Wang, H., Li, Z., & Zhou, Y. (2021) · Chemosphere · doi:10.1016/j.chemosphere.2021.132044 · Cited by 22 · see citing works
Self-citationHealth risks of Bisphenol-A exposure: From Wnt signaling perspective
Liu, Z., Xia, Y., Ai, S., & Wang, H.-L. (2024) · Environmental Research · doi:10.1016/j.envres.2024.118752 · Cited by 20 · see citing works
Wang, G., Li, H., Li, N., et al. (2022) · Angewandte Chemie · doi:10.1002/ange.202210619 · Cited by 20 · see citing works
Bowman, R. E., Hagedorn, J., Madden, E., & Frankfurt, M. (2018) · Hormones and Behavior · doi:10.1016/j.yhbeh.2018.11.004 · Cited by 19 · see citing works
“, 2015) suggests that the mechanism underlying the behavioral effects of BPA also involve synaptic plasticity, which is supported in the literature (Elsworth et al., 2015; Hu et al., 2017; Mhaouty-Kodja et al., 2018; Ogiue-Ikeda et al., 2008).”
Leguizamón, C. R. R., Elnagar, M. R., Kristiansen, U., & Kohlmeier, K. A. (2019) · Scientific Reports · doi:10.1038/s41598-018-37606-3 · Cited by 16 · see citing works
Risk of Alzheimer's disease and environmental bisphenol A exposure
Engin, A. B., & Engin, A. (2021) · Current Opinion in Toxicology · doi:10.1016/j.cotox.2021.03.003 · Cited by 16 · see citing works
Xu, G., Hu, F., Wang, X., Zhang, B., & Zhou, Y. (2017) · Archives of Toxicology · doi:10.1007/s00204-017-2047-1 · Cited by 16 · see citing works
“1 3 can influence synaptic plasticity and cause deficits in dendritic spines in rats and non-human primates (Eilam-Stock et al. 2012; Elsworth et al. 2015; Hu et al. 2017; Leranth et al. 2008; MacLusky et al. 2005).”
BackgroundSelf-citationBi, N., Ding, J.-J., Zou, R.-X., Gu, X., Liu, Z., & Wang, H.-L. (2021) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2021.115641 · Cited by 15 · see citing works
Bisphenol analogues induced social defects and neural impairment in zebrafish
Mu, X., Liu, Z., Zhao, X., Chen, L., Jia, Q., Wang, C., Li, T., Guo, Y., Qiu, J. Y., & Qian, Y. (2023) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2023.166307 · Cited by 15 · see citing works
Self-citationBisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo
Flores, A., Moyano, P. M., Solà, E., García, J. M., García, J., Frejo, M. T., Guerra-Menéndez, L., Labajo-González, E., Lobo, I., Abascal, L., et al. (2023) · Biology · doi:10.3390/biology12060782 · Cited by 15 · see citing works
“However, BPA was also reported to reduce the content of glutamate by decreasing the activity of glutaminase, which mediates the synthesis of glutamate [15].”
BackgroundSuresh, S., & Vellapandian, C. (2024) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2024.116953 · Cited by 13 · see citing works
Yang, Y., Wang, Y. Y., Wang, Y. Y., et al. (2024) · Inorganic Chemistry · doi:10.1021/acs.inorgchem.4c01342 · Cited by 13 · see citing works
Hassani, F. V., Masjedi, E., Hosseinzadeh, H., Bedrood, Z., Abnous, K., & Mehri, S. (2020) · PubMed Central · doi:10.22038/ijbms.2020.41097.9714 · Cited by 13 · see citing works
“It was recently reported that postnatal treatment of male Sprague–Dawley rats with BPA (1 mg/kg/day, 21–24 to 49–52 day) resulted in significant neurocognitive disorder in synaptic plasticity and spatial memory and reduced NMDA receptor 2A (NR2A) and AMPA receptor subunit GluR1 expression contributing to memory defici…”
BackgroundBisphenol A Activates Calcium Influx in Immortalized GnRH Neurons
Ruffinatti, F. A., Gilardino, A., Secchi, V., Cottone, E., Lovisolo, D., & Bovolin, P. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20092160 · Cited by 13 · see citing works
Nayan, N. M., Husin, A., Kadir, S. H. S. A., Aziz, C. B. A., Mazlan, M., & Siran, R. (2022) · Brain Science Advances · doi:10.26599/bsa.2022.9050009 · Cited by 11 · see citing works
Wu, D., Sun, Q., Wei, W., Bai, Y., Zhai, L., & Jia, L. (2023) · Food and Chemical Toxicology · doi:10.1016/j.fct.2023.114112 · Cited by 9 · see citing works
Fallahnezhad, S., Ghorbani-Taherdehi, F., Sahebkar, A., Nadim, A., Kafashzadeh, M., Kafashzadeh, M., & Valokola, M. G. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01257-9 · Cited by 8 · see citing works
“Administration of BPA significantly also decreased synaptic plasticity and expression of NR1, NR2A, NR2B, GluR1, and ERβ in mice and rat hippocampus, hence impairing learning and memory (Cabaton et al. 2013; Hu et al. 2017; Xu et al. 2013).”
BackgroundHu, F., Liu, J., Xu, G., et al. (2020) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2020.01.015 · Cited by 8 · see citing works
Self-citationBi, N., Huang, C., Gu, X., et al. (2025) · Environment & Health · doi:10.1021/envhealth.5c00110 · Cited by 7 · see citing works
Al‐Shami, A. S., Haroun, M., Essawy, A. E., Moussa, N., & Elkader, H. A. E. A. (2024) · NeuroToxicology · doi:10.1016/j.neuro.2024.11.006 · Cited by 7 · see citing works
Huang, J., Tan, Y., Xue, L., et al. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.15428 · Cited by 6 · see citing works
“Two researchers blinded to the experimental design recorded the number of each arm entered by rats within 5 min as well as residence time in each arm (Hu et al., 2017).”
BackgroundMethodSelf-citationHu, F., Zhang, L., Li, T., Wang, H., Liang, W., & Zhou, Y. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2020.03.035 · Cited by 6 · see citing works
Self-citationProtective effect of isoflurane preconditioning on neurological function in rats with HIE
Fei‐Sun, Y., Huang, M., Qin, H., de Souza, S. C., Han, X., Wang, Y., & Wang, Y. (2022) · Ibrain · doi:10.1002/ibra.12081 · Cited by 4 · see citing works
“1,2 It can reduce or even interrupt cerebrovascular blood flow and is one of the common causes in disabled children after the neonatal period.”
BackgroundLi, J., Wu, D., Mu, Y., Wang, Y., Zhai, L., & Jia, L. (2025) · Environmental Research · doi:10.1016/j.envres.2025.121538 · Cited by 5 · see citing works
GGA1 participates in spermatogenesis in mice under stress
Jiao, H., Chen, Y., Han, T., et al. (2023) · PeerJ · doi:10.7717/peerj.15673 · Cited by 4 · see citing works
“BPA, the main chemical monomer of epoxy resins and polycarbonate plastics, is often used to make food containers, water bottles, children’s toys, and medical devices ( Hu et al., 2017 ).”
Qin, M., Guo, X., Xu, N., et al. (2025) · Toxics · doi:10.3390/toxics13030162 · Cited by 4 · see citing works
“All authors have read and agreed to the published version of the manuscript.”
Obesity aggravates neuroinflammatory and neurodegenerative effects of bisphenol A in female rats
Mangla, A., Goswami, P., Sharma, B., Suramya, S., Jindal, G., Javed, M., Saifi, M. A., Parvez, S., Nag, T. C., & Raisuddin, S. (2024) · Toxicology Mechanisms and Methods · doi:10.1080/15376516.2024.2349538 · Cited by 4 · see citing works
“…hormonal balance can eventually have a negative impact on brain function (Röhr et al. 2020). another issue of concern nowadays is that the world is facing the exposure to endocrine-disrupting chemicals (eDcs) which have the ability to act as obesogens (hu et al. 2017; egusquiza and Blumberg 2020).”
InfluentialNayan, N. M., Kadir, S. S. A., Husin, A., & Siran, R. (2024) · Physiology and Behavior · doi:10.1016/j.physbeh.2024.114546 · Cited by 3 · see citing works
Logeshwari, B., Jeyabalan, S., Veeraraghavan, G., Krishnaraj, K., Ashok, C., Rajasekaran, N. K., Wong, L. S., Subramaniyan, V., & Sekar, M. (2025) · Toxicology Reports · doi:10.1016/j.toxrep.2025.102161 · Cited by 4 · see citing works
“BPA may influence synaptic plasticity and HPI axis signaling, whereas AlCl ₃ could involve mitochondrial dysfunction and tauopathy, as suggested by previous reports [52 – 55].”
Baykal, S., & Nalbantoğlu, A. (2023) · Clinical Neuropharmacology · doi:10.1097/wnf.0000000000000574 · Cited by 3 · see citing works
Frankfurt, M., Luine, V. N., & Bowman, R. E. (2020) · Vitamins and hormones · doi:10.1016/bs.vh.2020.04.004 · Cited by 3 · see citing works
Hu, F., Xu, G., Zhang, L., et al. (2021) · Archives of Toxicology · doi:10.1007/s00204-021-03192-z · Cited by 2 · see citing works
“Additionally, long-term BPA exposure can markedly induce cognitive and emotional deficits in rodents and non-human primates, accompanied by impairment of synaptic plasticity in the prefrontal cortex and hippocampus (Elsworth et al. 2015; Hu et al. 2017; Hua et al. 2010).”
BackgroundSelf-citationZhang, W., Zhang, L., Liang, W., Wang, H., & Hu, F. (2023) · Toxicology · doi:10.1016/j.tox.2023.153718 · Cited by 2 · see citing works
Self-citationJamka, M., Kurek, S., Makarewicz-Bukowska, A., et al. (2024) · Metabolites · doi:10.3390/metabo14050271 · Cited by 2 · see citing works
“Furthermore, BPA’s neurotoxicity has been associated with inhibition of neurogenesis [65] and reduced synaptic plasticity in rats [66].”
BackgroundRecording from an Identified Neuron Efficiently Reveals Hazard for Brain Function in Risk Assessment
Machnik, P., & Schuster, S. (2021) · Molecules · doi:10.3390/molecules26226935 · Cited by 2 · see citing works
Ren, J., Bai, W., Guo, Y., Liu, Q., Wang, Y., & Wang, C. (2025) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70100 · Cited by 1 · see citing works
Zhang, L., Li, X., Zhao, Y., Wang, P., Shi, M., Xiao, L., Pei, X., Duan, Z., Ma, M., & Yu, H. (2025) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2025.118651 · Cited by 1 · see citing works
Bisphenol A Treatment Impairs Synaptic Function in Human Cholinergic Neurons
Carrese, A. M., Vitale, R., Turco, M., Aniello, F., Petecca, N., Cigliano, L., Vitale, E., & Donizetti, A. (2025) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70558 · Cited by 1 · see citing works
“Although several studies have shown that postnatal BPA exposure impairs synaptic plasticity in the prefrontal cortex and hippocampus of nonhuman primates [20, 21], rats [22, 23], and mice [24], these findings are primarily derived from animal models.”
Sukjamnong, S., Saeliw, T., Panjabud, P., Thongkorn, S., Kanlayaprasit, S., Lertpeerapan, P., Hu, V. W., & Sarachana, T. (2026) · Biology Direct · doi:10.1186/s13062-026-00803-6 · Cited by 1 · see citing works
“…impairments in synaptic plasticity and spatial memory in rats, characterized by disrupted hippocampal synaptic transmission and long-term potentiation (LTP), reduced dendritic spine density in pyramidal neurons, and impaired synaptic transmission at both presynaptic and postsynaptic levels [56].”
Adigun, K. O., Ehinmowo, M. I., Folarin, O. R., & Adebiyi, O. E. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.17.603899 · Cited by 1 · see citing works
Protective effect of isoflurane preconditioning on neurological function in rats with HIEPreprint
Wang, Y., Chen, T., Huangfu, L., Zhou, H., Xiao, Q., Xu, F., Xiong, L., & Wang, T. (2022) · Research Square · doi:10.21203/rs.3.rs-1561903/v1
Protective effect of isoflurane preconditioning on neurological function in rats with HIEPreprint
Wang, Y., Chen, T., Huangfu, L., Zhou, H., Xiao, Q., Xu, F., Xiong, L., & Wang, T. (2022) · Research Square · doi:10.21203/rs.3.rs-1561903/v2
Sanannam, B., Jindatip, D., & Sarachana, T. (2021) · doi:10.58837/chula.the.2021.261
Kourat, D., Adli, D. E. H., Brahmi, M., Alkholifi, F. K., Dayel, F. F. B., Arabi, W., Fauconnier, M., Bouzouira, B., Kahloula, K., Slimani, M., et al. (2025) · Pharmaceuticals · doi:10.3390/ph18040509
“Most of these investigations, particularly those conducted with animal models exposed to low doses of BPA near the current fixed daily limit, have indicated that perinatal, postnatal, prepubertal, and pubertal exposure to BPA may adversely affect learning and memory [25,26].”
Yang, T. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04570-0
“This suggests that EDCs may disrupt synaptic structural stability by interfer - ing with the expression and function of synaptic membrane proteins, potentially acting as environmental triggers for early cognitive impairment in AD [71–73].”
Wang, W., Peng, Z., Feng, X., Chen, Z., Zhang, J., Huang, T., Zhang, Q., Wu, D., & Liu, Q. (2025) · NeuroToxicology · doi:10.1016/j.neuro.2025.103340
Self-citationAcute inhibition of NMDA receptor function by bisphenol A and bisphenol F in adult rat brain
Krausová, B. H., Radostová, D., Malenínská, K., et al. (2026) · NeuroToxicology · doi:10.1016/j.neuro.2026.103430
Lin, N., Li, Z., Zhang, L., Tang, H., Feng, Y., Zhu, X., Liu, H., Wang, M., & Hu, F. (2026) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2026.120126
Self-citationAzmi, S. K., Ali, N. F., & Siran, R. (2026) · Toxicology Reports · doi:10.1016/j.toxrep.2026.102278
“Several studies demonstrated that BPA exposure disrupts the normal GluN2A/GluN2B balance, leading to impaired synaptic transmission and destabilisation of hippocampal circuitry [34,35,40].”
InfluentialWang, L., Zhu, G., Luo, G., Yang, L., Ren, W., Wang, R., & Xu, H. (2026) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-026-10297-8
“The arm entries of each rat were observed and recorded and the number of times the rats entered each arm within 5 min and the residence time in each arm were recorded to analyze the ability of spatial memory in rats (Hu et al. 2017).”
Liu, Z. H., Chang, M., WANG, Z. M., et al. (2026) · Progress in Natural Science Materials International · doi:10.1016/j.pnsc.2026.06.010
Rabby, T., Rafi, M. T. H., Sultana, N., Saha, S., Naziha, I. J., Islam, S., Chen, U., Sumi, S. A., Hussain, M. S., ., D., et al. (2026) · Environmental Reviews · doi:10.1139/er-2025-0245
Hyun, S.-A., Ko, M. Y., Jang, S., Lee, B.-S., Rho, J., Kim, K. K., Kim, W.-Y., & Ka, M. (2022) · Disease Models & Mechanisms · doi:10.1242/dmm.049177 · Cited by 40 · see citing works
“Moreover, BPA exposure decreases glutamate receptor expression and synaptic transmission (Hu et al., 2017).”
InfluentialShen, Y., Li, X., Wang, H., Wang, Y., Tao, L., Wang, P., & Zhang, H. (2023) · Toxicology · doi:10.1016/j.tox.2023.153678 · Cited by 22 · see citing works
- Authors
- Hu, F., Li, T., Gong, H., Chen, Z., Jin, Y., Xu, G., & Wang, M.
- Affiliations
- Hefei University of Technology (CN)
- CAS Key Laboratory of Brain Function and Diseases School of Life Sciences University of Science and Technology of China Hefei Anhui 230027 P. R. China
- University of Science and Technology of China (CN)
- Corresponding author
- Hu, Fan
- Wang, Ming
- Venue
- Advanced Science
- Publisher
- Wiley
- Published
- 2017-04-19
- Volume
- 4
- Issue
- 8
- Pages
- 1600493-1600493
- ISSN
- 2198-3844 (ISSN-L)
- PMC
- PMC5566242
- OpenAlex
- W2606968215
- Semantic Scholar
- 18355311cc9bdbbf2ff7b6d20989484ef0178e17
- Cited by
- 87
- References
- 56
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 12 · 2023: 11 · 2022: 13 · 2021: 12 · 2020: 10 · 2019: 7 · 2018: 3 · 2017: 1
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Advanced Science (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (submittedVersion, cc-by)
- PubMed Central (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (21307024)
- China Postdoctoral Science Foundation (2013M531500)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- bisphenol A, synaptic plasticity, long-term potentiation, dendritic spine density, presynaptic neurotransmitter release, excitatory postsynaptic currents, xenoestrogens, learning and memory impairment, juvenile exposure, glutamate
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-12.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-12.
Cited sources are checked by gpt-6-sol.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
