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BDNF and glucocorticoids regulate corticotrophin-releasing hormone (CRH) homeostasis in the hypothalamus
Open accessAbstract
Regulation of the hypothalamic–pituitary–adrenal (HPA) axis is critical for adaptation to environmental changes. The principle regulator of the HPA axis is corticotrophin-releasing hormone (CRH), which is made in the parventricular nucleus and is an important target of negative feedback by glucocorticoids. However, the molecular mechanisms that regulate CRH are not fully understood. Disruption of normal HPA axis activity is a major risk factor of neuropsychiatric disorders in which decreased expression of the glucocorticoid receptor (GR) has been documented. To investigate the role of the GR in CRH neurons, we have targeted the deletion of the GR, specifically in the parventricular nucleus. Impairment of GR function in the parventricular nucleus resulted in an enhancement of CRH expression and an up-regulation of hypothalamic levels of BDNF and disinhibition of the HPA axis. BDNF is a stress and activity-dependent factor involved in many activities modulated by the HPA axis. Significantly, ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor TrkB, decreased CRH expression and normal HPA functions. We find the differential regulation of CRH relies upon the cAMP response-element binding protein coactivator CRTC2, which serves as a switch for BDNF and glucocorticoids to direct the expression of CRH.
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“Additional evidence for CORT acting directly on PVN neurons comes from studies where targeted deletion of GR in the PVN increased CRH expression and CORT and ACTH levels in male mice (Jeanneteau et al., 2012).”
From Hypothalamic–pituitary–adrenal and hypothalamic–pituitary–gonadal axes: sex differences in regulation of stress responsivity (2017) · cites this paper as Jeanneteau et al., 2012
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“This cross-talk between BDNF and CRH may be at least partly mediated by the CREB and MAPK pathway and is involved in the enhancement of fear memory under stress (187).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
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“The administration of BDNF in vivo induces increased CRH level and reduction of BDNF or its receptor normalizes the CRH level and thus, the HPA axis.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
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“Moreover, there is a feedback loop whereby directly regulates CRH, and thus, the HPA axis (187).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
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“For BDNF, its expression level responds to stress-related HPA axis activation.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
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“BDNF directly regulates the HPA axis.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
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“Finally, the broad disruption of the GR allele in the CNS [GRNesCre (5)] and its targeted deletion in the forebrain [forebrain-specific GR knock-out; FBGRKO mice] (119), or the PVN all resulted in the disinhibition of the HPA axis (120).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [120]
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“In vivo, the GR-mediated control of Crh transcription is strikingly opposite in the hypothalamus and in the amygdala of the same mouse depending on the behavioral context (Jeanneteau et al., 2012; Zalachoras et al., 2016).”
BackgroundInfluentialSelf-citationMicroRNA-132 may play a role in coexistence of depression and cardiovascular disease: A hypothesis
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Considering the Microbiome in Stress-Related and Neurodevelopmental Trajectories to Schizophrenia
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“Because GC receptors and TrkB are co-expressed in the hippocampus, important crosstalk between GCs and BDNF occurs here, as threat appraisal relies on both current stress and appropriate context from memory (34).”
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Autry, A. E. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1028223 · Cited by 20
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BackgroundInfluentialGao, J., Chen, Y., Su, D., Marshall, C., & Xiao, M. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2018.07.007 · Cited by 25
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An example of DNA methylation as a means to quantify stress in wildlife using killer whales
Crossman, C. A., Barrett-Lennard, L. G., & Frasier, T. R. (2021) · Scientific Reports · doi:10.1038/s41598-021-96255-1 · Cited by 20
Targeting osteoblastic 11β-HSD1 to combat high-fat diet-induced bone loss and obesity
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Azogu, I., & Plamondon, H. (2017) · Hormones and Behavior · doi:10.1016/j.yhbeh.2017.02.012 · Cited by 20
“Notably, BDNF exerts important regulatory influences on the brain stress and reward systems (Martinowich et al., 2007) as a stress and activity-dependent neurotrophin involved in the activity of the hypothalamic-pituitary-adrenal (HPA) axis (Jeanneteau et al., 2012).”
High activity of the stress promoter contributes to susceptibility to stress in the tree shrew
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“Because the transcription factors CREB 24 and GR 25,26 are involved in the regulation of CRH gene expression, we first determined the activity of the promoters in response to CRH transcription activation by forskolin-induced CREB activation and CRH transcription inhibition by dexamethasone-induced…”
Effects of crack cocaine addiction and stress-related genes on peripheral BDNF levels.
Rovaris, D., Schuch, J., Grassi-Oliveira, R., Sanvicente-Vieira, B., da Silva, B. D., Walss-Bass, C., Müller, D., Stolf, A., von Diemen, L., Ceresér, K. M., et al. (2017) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2017.02.011 · Cited by 19
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“stress response, including: (1) CNS and PNS responses and neurochemical plasticity to chronic stress; (2) comorbidity of stress-related disorders; and (3) the role of the limbic system and neuroendocrine cascade in chronic stress (Herman et al., 1996, 2003, 2005, 2012, 2016; Jankord and Herman, 2008; Jeanneteau et al.…”
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Nagarajan, G., Jurkevich, A., Kang, S. W., & Kuenzel, W. J. (2017) · Journal of Neuroendocrinology · doi:10.1111/jne.12494 · Cited by 17
Thorsdottir, D., Cruickshank, N. C., Einwag, Z., Hennig, G. W., & Erdös, B. (2019) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00478.2019 · Cited by 18
Expression of NGF, BDNF and their receptors in subcutaneous adipose tissue of lactating cows
Colitti, M., Loor, J. J., & Stefanon, B. (2015) · Research in Veterinary Science · doi:10.1016/j.rvsc.2015.08.016 · Cited by 17
Sotelo-Rivera, I., Cote-Vélez, A., Uribe, R.-M., Charli, J., & Joseph‐Bravo, P. (2017) · Endocrine · doi:10.1007/s12020-016-1223-z · Cited by 17
“The latter is exemplified by the lack of effect of Gc to inhibit BDNF-induced CREB phorphorylation or its recruitment to Crh promoter since BDNF activates the ERK-MAPK pathway [55] in contrast to the Cort or Dex interference of cAMP-PKA-induced CREB phosphorylation or pCREB recruitment to Trh or Gr (Nr3c1) promoter [t…”
Central Neuroepigenetic Regulation of the Hypothalamic–Pituitary–Adrenal Axis
Dick, A. L. W., & Provençal, N. (2018) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2018.04.006 · Cited by 17
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“One such mechanism could be the activation of the hypothalamic-pituitary-adrenal axis, since BDNF stimulates corticotropin-releasing hormone expression in the PVN, while elevated glucocorticoid levels downregulate BDNF synthesis in the PVN (Givalois et al. 2004; Jeanneteau et al. 2012).”
BackgroundWassink, L., Bussy, U., Li, W., & Scribner, K. T. (2019) · Animal Behaviour · doi:10.1016/j.anbehav.2019.09.005 · Cited by 16
“Dysregulation can occur when sustained elevated cortisol levels result in downregulation of corticosteroid receptors in brain tissue (Meaney, Sapolsky,&McEwen, 1985), which impairs the negative feedback loop of the HPI axis and perpetuates chronic cortisol elevation (Jeanneteau et al., 2012).”
BackgroundGlucocorticoid Receptor Genetic Variants and Response to Fluoxetine in Major Depressive Disorder
Nouraei, H., Firouzabadi, N., Mandegary, A., Zomorrodian, K., Bahramali, E., Shayesteh, M. R. H., & Ansari, S. (2017) · Journal of Neuropsychiatry · doi:10.1176/appi.neuropsych.16120322 · Cited by 15
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“Persisting effects have been shown even 6 months after termination of continuous infusion of AONs for 7 days in the ventricles of the brain [10], and even single administration may have longlasting effects [32].”
BackgroundRisk and Resilience: The Role of Brain-derived Neurotrophic Factor in Alcohol Use Disorder
Ceballos, N. A., & Sharma, S. (2016) · AIMS neuroscience · doi:10.3934/neuroscience.2016.4.398 · Cited by 14
“It is well known that stressful experiences, and the resulting release of glucocorticoids such as cortisol, impact neuroplasticity in the brain through BDNF-related mechanisms [5,53,54], though it is important to recognize that other molecules are also involved in stress-induced neuroplasticity [55].”
BackgroundPolycystic Ovary Syndrome Pathophysiology: Integrating Systemic, CNS and Circadian Processes
Anderson, G. (2024) · Frontiers in Bioscience-Landmark · doi:10.31083/j.fbl2901024 · Cited by 16
“TrkB activation in the paraventricular nucleus (PVN) enhances corticotrophin-releasing hormone (CRH) release and therefore increases hypothalamic-pituitary-adrenal (HPA) axis activation via cortisol effects at the glucocorticoid receptor (GR) [38].”
Backgroundde, M. A. P.-M., Gutiérrez-Mariscal, M., Salmerón-Jiménez, M. F., Jaimes-Hoy, L., Charli, J., & Joseph‐Bravo, P. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00418 · Cited by 13
“Higher expression of Gr may contribute to overcome the reduced levels of corticosterone to lower Crh expression (57).”
BackgroundOxytocin Signaling as a Target to Block Social Defeat-Induced Increases in Drug Abuse Reward
Perez, C. F., Reguilón, M. D., Miñarro, J., & Rodríguez‐Arias, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052372 · Cited by 15
“This occurs due to the negative response of GC in the CRF promoter, which inhibits the binding of the transcriptional machinery to the CRF promoter, reducing the transcription of the CRF gene [98].”
BackgroundWang, Y., Han, J., Zhu, J., Zhang, M., Ju, M., Du, Y., & Tian, Z. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.703044 · Cited by 15
Childhood adverse events and BDNF promoter methylation in later-life
Zhou, A., Ancelin, M., Ritchie, K. A., & Ryan, J. L. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1108485 · Cited by 15
“BDNF levels have been shown to be highly dynamic in response to stress (18), and interacts directly with the hypothalamic-pituitary-adrenal (HPA) axis in regulating the stress response (19).”
BackgroundErdös, B., Clifton, R. R., Liu, M., Li, H., McCowan, M. L., Sumners, C., & Scheuer, D. A. (2015) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00207.2015 · Cited by 16
Increased neuroplasticity may protect against cardiovascular disease
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“BDNF is a stress- and activity-dependent factor [27].”
BackgroundInfluentialInvestigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia
Katz-Barber, M. W., Hollins, S. L., Cuskelly, A., Leong, A. J. W., Dunn, A. L., Harms, L. R., & Hodgson, D. M. (2020) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2020.100048 · Cited by 13
Nugent, N. R., Armey, M. F., Boker, S. M., Brick, L. A. D., Knopik, V. S., McGeary, J. E., Spirito, A., & Mehl, M. R. (2022) · BMJ Open · doi:10.1136/bmjopen-2021-056063 · Cited by 12
Acute stress enhances synaptic plasticity in male mice via a microbiota-dependent mechanism
Rosell‐Cardona, C., Collins, M., O’Riordan, K. J., Goodson, M. S., Kelley‐Loughnane, N., Cryan, J. F., & Clarke, G. A. (2025) · Neuropharmacology · doi:10.1016/j.neuropharm.2025.110434 · Cited by 12
“Our data align with different recent studies showing that BDNF can be modulated by both the HPA axis and the gut microbiota (Jeanneteau et al., 2012; Bistoletti et al., 2019).”
Candemir, E., Post, A. M., Dischinger, U., Palme, R., Slattery, D. A., O’Leary, A., & Reif, A. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.111927 · Cited by 14
Adachi, N., Suzuki, S., Matsuoka, H., Fushimi, S., Ono, J., Ohta, K., Hirai, Y., Miki, T., & Koshimizu, H. (2018) · Journal of Neurochemistry · doi:10.1111/jnc.14310 · Cited by 12
Azogu, I., Liang, J., & Plamondon, H. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2018.05.002 · Cited by 12
Koopmans, Y., Nelemans, S. A., Bosmans, G., Noortgate, W. V. D., Leeuwen, K. G. V., & Goossens, L. (2023) · Journal of Youth and Adolescence · doi:10.1007/s10964-023-01822-6 · Cited by 17
“There is evidence that BDNF is involved in HPA axis functioning, probably through its influence on the release of corticotropin-releasing hormone, which like cortisol plays a major role in HPA axis activity (Jeanneteau et al., 2012).”
BackgroundBurenkova, O. V., & Grigorenko, E. L. (2024) · Developmental Psychobiology · doi:10.1002/dev.22479 · Cited by 11
Al‐Zoubi, R. M., Abuhijleh, H., Zarour, A. M., Zakaria, Z. Z., Yassin, A. A., Al-Ansari, A. A., Al‐Asmakh, M., & Bawadi, H. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094895 · Cited by 11
“The expression of the bdnf gene in the brain is under the control of GRs [103–106], and BDNF, in turn, regulates CRH homeostasis [107].”
BackgroundUnderwood, M. D., Galfalvy, H., Hsiung, S., Liu, Y., Simpson, N. R., Bakalian, M. J., Rosoklija, G. B., Dwork, A. J., Arango, V., & Mann, J. J. (2023) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyad025 · Cited by 10
“We did not see an association between CRH and ELA or suicide despite reports in the literature of glucocorticoids repressing CRH transcription via the GR receptor (Malkoski et al., 1997; Jeanneteau et al., 2012; Evans et al., 2013).”
BackgroundBhave, S., & Uht, R. M. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.06.024 · Cited by 10
“…glucocorticoids down regulate CRH gene activation are fairly well understood, (Guardiola-Diaz et al 1996,Malkoski et al 1997,Malkoski and Dorin 1999,Jeanneteau et al 2012,Aguilera M AN US CR IP T AC CE PT ED and Liu 2012); however, mechanisms that maintain low levels of CRH gene expression are not.”
Li, X., Ma, J., Xu, J., Zhu, D., Li, A., Che, Y., Chen, D., & Feng, X. (2017) · Neurochemical Research · doi:10.1007/s11064-017-2366-x · Cited by 10
“This association is explained by glucocorticoid activation of the BDNF pathway via feedback mechanisms and enhancement of GR gene expression to recruit the CREBBDNF pathway and mediate memory consolidation [9, 22].”
BackgroundStröher, R., de Oliveira, C., Stein, D. J., de Macedo, I. C., Goularte, J. F., da Silva, L. S., Regner, G. G., Medeiros, H. R., Caumo, W., & Torres, I. L. D. S. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2019.12.027 · Cited by 10
Kadhim, H. J., Kang, S. W., & Kuenzel, W. J. (2021) · Stress · doi:10.1080/10253890.2021.1929163 · Cited by 11
“, 2013) and CRH neurons (Jeanneteau et al., 2012) could be involved in the regulation of stress, since the BDNF gene promotor site has many binding sites for cyclic adenosine monophosphate (cAMP) response element protein (CREB) (Blendy, 2006; Tardito et al.”
BackgroundRezg, R., Mornagui, B., Santos, J. S. O., Dulin, F., El‐Fazâa, S., El-Hadj, N. B., Bureau, R., & Gharbi, N. (2014) · Environmental Science and Pollution Research · doi:10.1007/s11356-014-3824-5 · Cited by 10
“Indeed, it has been reported that ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor TrkB, decreased CRH expression and normal HPA function (Jeanneteau et al. 2012).”
BackgroundMolecular and functional mapping of the neuroendocrine hypothalamus: a new era begins
Lee, T. H., Nicolas, J.-C., & Quarta, C. (2024) · Journal of Endocrinological Investigation · doi:10.1007/s40618-024-02411-5 · Cited by 12
“The latter has yet to be studied, but the CRH Nr3c1 population expresses glucocorticoid receptors to facilitate feedback mechanisms to suppress HPA axis overactivation [220].”
Zimmer, C., Taff, C. C., Ardia, D. R., Rosvall, K. A., Kallenberg, C., Bentz, A. B., Taylor, A. R., Johnson, L. S., & Vitousek, M. N. (2022) · Hormones and Behavior · doi:10.1016/j.yhbeh.2022.105280 · Cited by 10
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Neurobehavioral and molecular changes in a rodent model of ACTH-induced HPA axis dysfunction
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“GRs, mineralocorticoid receptors (MRs), and Trkb are co-expressed on hippocampal neurons highlighting the interplay between the GC-BDNF pathways (Jeanneteau et al., 2012).”
Advances in epigenetic mechanisms of chick embryo heat acclimation
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“Glucocorticoids can neutralise the effect of CREB-regulated transcription coactivator 2 (CRTC2) and inhibit CREB-mediated CRH induction through glucocorticoid receptors (GR) (Jeanneteau et al. 2012).”
BackgroundIwasa, T., Matsuzaki, T., Yano, K., Munkhzaya, M., Tungalagsuvd, A., Yiliyasi, M., Kuwahara, A., & Irahara, M. (2016) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2016.08.001 · Cited by 8
“As hypothalamic BDNF mRNA levels are also regulated by other factors, such as glucocorticoids (Jeanneteau et al., 2012), it is possible that these factors also affect the developmental changes in hypothalamic BDNF mRNA expression.”
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“This is due to the direct influence of this neurotrophin on the HPA [73, 154].”
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“…Givalois et al. (2004) found an interesting location of BDNF and its receptors in the median eminence, suggesting that these are presumably involved in dynamic processes such as hormone release and may be involved in the regulation of CRH homeostasis in the hypothalamus ( Jeanneteau et al. 2012).”
BackgroundTsimpolis, A., Kokkali, M., Logothetis, A., Kalafatakis, K., & Charalampopoulos, I. (2022) · Biomolecules · doi:10.3390/biom12091322 · Cited by 6
“Over the past 15 years, various sources of evidence indicate that the molecular biology of GCs interacts with that of the major neurotrophin in the central nervous system (CNS), the brain-derived neurotrophic factor (BDNF), regulating important aspects of neuronal cell physiology and impacting cellular viability, memo…”
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Irritable bowel syndrome may be induced by decreased neuroplasticity.
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“Furthermore, BDNF in the PVN has been shown to directly regulate corticotropin-releasing hormone production (77), and corticotrophin-releasing hormone receptor signaling pathways have been implicated to mediate the affects of BDNF on energy balance (78).”
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“…disinhibits the HPA axis, and that increased BDNF and its binding to TrkB receptors enhance CRH mRNA levels through activation of cAMP response-ele-ment binding protein (CREB), which can also be inhibited by decreased nuclear localization of the CREB coactivator CRT2 due to GC-GR activation [41].”
Molecular mechanism underlying stress response and adaptation
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Neuroplasticity in Post-Traumatic Stress Disorder
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“Igualmente, BDNF regula la expresión de CRH en el núcleo paraventricular del hipotálamo, lo que supone un vínculo con el estrés [27].”
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“expression in mouse models has been previously reported to increase CRH expression in the hypothalamus [65].”
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“11 Stress induced NGFs mediated dysregulation of HPA axis may end up as a psychiatric disorder (if stress causing factors persist) (2,114).”
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“Thus, BDNF is a stress-dependent factor [19].”
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“EE also promotes secretion of several neurotrophic factors [i.e., brain-derived-(BDNF), nerve-(NGF), and insulin-like growth factors (IGF) and neurotrophin-3 (NT-3)] [26] shown to impact mood regulation [27,28].”
BackgroundAnimal Models of Altered Glucocorticoid Signaling
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“With respect to GR several different fl oxed mice have been generated with loxP sites fl anking different exons of GR genomic locus [ 21 – 25 ].”
MethodAnorexic action of fusarenon-x in the hypothalamus and intestine
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Paeoniflorin and depression: a comprehensive review of underlying molecular mechanisms
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“Moreover, the serum levels of adrenocorticotropic hormone (ACTH) and CORT were found to be elevated in the homozygous KD mice (Jeanneteau et al. 2012).”
Leggieri, A., García‐González, J., Hosseinian, S., Ashdown, P., Anagianni, S., Wang, X., Havelange, W., Fernàndez‐Castillo, N., Cormand, B., & Brennan, C. H. (2025) · Translational Psychiatry · doi:10.1038/s41398-025-03703-x · Cited by 3
“BDNF levels often increase during stress to promote neuronal survival and plasticity, buffering negative effects of stress on the brain via TRKB [10, 11, 13, 58 – 60].”
Deinhardt, K., & Jeanneteau, F. D. (2012) · InTech eBooks · doi:10.5772/50420 · Cited by 4
“expressed, BDNF signaling did not elicit CRTC2 translocation to the nucleus, while cAMPelevating drugs or drugs that elevate intracellular calcium did (41).”
BackgroundSelf-citationPost-transcriptional Regulation by Brain-Derived Neurotrophic Factor in the Nervous System
Amen, A. M., Pham, D. L., & Meffert, M. K. (2015) · Springer eBooks · doi:10.1007/978-3-319-25124-0_14 · Cited by 3
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Metadata
- Authors
- Jeanneteau, F. D., Lambert, W. M., Ismaili, N., Bath, K. G., Lee, F. S., Garabedian, M. J., & Chao, M. V.
- Affiliations
- New York University (US)
- Department of Microbiology, New York University School of Medicine, New York, NY 10016;
- Brown University (US)
- Weill Cornell Medicine (US)
- Department of Cell Biology, Department of Physiology, Department of Neuroscience, and Department of Psychiatry, Skirball Institute of Biomolecular Medicine, and
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2012-01-09
- Volume
- 109
- Issue
- 4
- Pages
- 1305-1310
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3268297
- OpenAlex
- W2021067562
- Cited by
- 252
- References
- 38
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 18 · 2023: 12 · 2022: 12 · 2021: 17 · 2020: 18 · 2019: 18 · 2018: 18 · 2017: 27 · 2016: 19 · 2015: 17 · 2014: 15 · 2013: 24 · 2012: 15
- FWCI
- 9.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Biomedical Innovation
- National Institutes of Health (NS-21072)
- National Institute of Mental Health (R01MH086651, MH086651)
- National Institute of Allergy and Infectious Diseases (5T32 AI07180-29, T32AI007180)
- National Institute of Neurological Disorders and Stroke (R01NS021072, NS-21072, R56NS021072)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- brain-derived neurotrophic factor, glucocorticoids, corticotropin-releasing factor, hypothalamic-pituitary-adrenal axis, hypothalamus, glucocorticoid receptor, CRTC2, TrkB receptor, CREB, stress response, negative feedback
- MeSH terms
- Analysis of Variance, Animals, Corticotropin-Releasing Hormone, Glucocorticoids, Homeostasis, Hypothalamo-Hypophyseal System, Hypothalamus, Immunohistochemistry, Mice, Inbred C57BL, Neurons, Pituitary-Adrenal System, Receptors, Glucocorticoid, Transcription Factors, Trans-Activators, Mutagenesis, Site-Directed, Rats, Sprague-Dawley, Mice, Knockout, Microscopy, Confocal, Brain-Derived Neurotrophic Factor, Chromatin Immunoprecipitation, Mice, Rats, Real-Time Polymerase Chain Reaction
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