The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Cognitive deficits in Tsc1+/−mice in the absence of cerebral lesions and seizures
Abstract
Objective: Tuberous sclerosis complex (TSC) is characterized by brain lesions, epilepsy, increased incidence of mental retardation and autism. The causal link between lesion load and epilepsy on cognitive disabilities has been debated, and these factors explain only part of the intelligence quotient variability. A Tsc2 rat model of the disease provided evidence that the TSC genes are directly involved in neuronal function. However, these lesion‐ and epilepsy‐free animals did not show learning deficits, leaving open the possibility that the presence of brain lesions or epilepsy is a prerequisite for the cognitive deficits to fully develop. Here, we reinvestigated the relation among cerebral lesions, epilepsy, and cognitive function using Tsc1+/−mice. Methods: We used immunocytochemistry and high‐resolution magnetic resonance imaging to study the presence of neuronal pathology in Tsc1+/−mice. We used the Morris water maze, fear conditioning, social interaction, and nest building test to study the presence of cognitive and social deficits. Results: We observed no spontaneous seizures or cerebral lesions in the brains of Tsc1+/−mice. In addition, giant dysmorphic cells were absent, and spine number and dendritic branching appeared to be normal. Nevertheless, Tsc1+/−mice showed impaired learning in the hippocampus‐sensitive versions of the learning tasks and impaired social behavior. Interpretation: Tsc1+/−mice show social and cognitive deficits in the absence of apparent cerebral pathology and spontaneous seizures. These findings support a model in which haploinsufficiency for the TSC genes leads to aberrations in neuronal functioning resulting in impaired learning and social behavior. Ann Neurol 2007
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“our studies show that tuberous sclerosis–related cognitive deficits emerged in the absence of spontaneous seizures and neuropathology”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
In the citing paper
“Unlike *Tsc2*+/− mutants, however, *Tsc1*+/− mice also show abnormal social behavior.”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
In the citing paper
“Because there is a close functional interaction between the Tsc1 and Tsc2 proteins, it is more likely that genetic background[8](#R8),[11](#R11) accounts for the differences in social behavior.”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
In the citing paper
“A recent study reported hippocampal-dependent learning deficits in *Tsc1*+/− mice[11](#R11).”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
In the citing paper
“a result consistent with the idea that modifier genes in the genetic background influence the expressivity of tuberous sclerosis phenotypes[5](#R5),[8](#R8),[11](#R11).”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
In the citing paper
“our data show that tuberous sclerosis–related cognitive deficits are not necessarily the consequence of neuroanatomical abnormalities (that is, tubers) or seizures.”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [11]
Citations
Cites
Place navigation impaired in rats with hippocampal lesions
Morris, R. G. M., Garrud, P., Rawlins, J. N. P., & O'Keefe, J. (1982) · Nature · doi:10.1038/297681a0 · Cited by 6,340
Differential contribution of amygdala and hippocampus to cued and contextual fear conditioning.
Phillips, R. G., & LeDoux, J. E. (1992) · Behavioral Neuroscience · doi:10.1037/0735-7044.106.2.274 · Cited by 3,292
Regulation of neuronal morphology and function by the tumor suppressors Tsc1 and Tsc2
Tavazoie, S. F., Alvarez, V. A., Ridenour, D. A., Kwiatkowski, D. J., & Sabatini, B. L. (2005) · Nature Neuroscience · doi:10.1038/nn1566 · Cited by 497
Meikle, L., Talos, D. M., Onda, H., Pollizzi, K., Rotenberg, A., Sahin, M., Jensen, F. E., & Kwiatkowski, D. J. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.5540-06.2007 · Cited by 462
Specific Genetic Disorders and Autism: Clinical Contribution Towards their Identification
Cohen, D., Pichard, N., Tordjman, S., Baumann, C., Burglen, L., Excoffier, E., Lazar, G., Mazet, P., Pinquier, C., Verloes, A., et al. (2005) · Journal of Autism and Developmental Disorders · doi:10.1007/s10803-004-1038-2 · Cited by 316
Research works printed but not linked: 26
- 10.1017/S0033291702007092 · DOI · Paper page
- 10.1007/BF01046223 · DOI
- 10.1093/cercor/bhj144 · DOI · Paper page
- 10.1017/S0033291701004561 · DOI
- 10.1177/08830738060210020901 · DOI
- 10.1177/08830738040190090501 · DOI
- 10.1111/j.1528-1167.2007.01035.x · DOI
- 10.1136/adc.2003.026815 · DOI
- 10.1056/NEJMc062928 · DOI · Paper page
- 10.1016/j.tibs.2003.09.003 · DOI · Paper page
- 10.1385/MN:34:3:205 · DOI · Paper page
- 10.1016/j.molmed.2007.06.003 · DOI · Paper page
- 10.1111/j.1460-9568.2006.04594.x · DOI · Paper page
- 10.1111/j.1471-4159.2005.03538.x · DOI · Paper page
- 10.1093/hmg/ddi190 · DOI
- 10.1038/35010550 · DOI
- 10.1007/s00401-004-0865-8 · DOI
- 10.1046/j.1460-9568.2002.02100.x · DOI
- 10.1172/JCI7319 · DOI · Paper page
- 10.1073/pnas.95.26.15629 · DOI
- 10.1006/mcne.2002.1184 · DOI
- 10.2310/7010.2006.00046 · DOI
- 10.1073/pnas.91.24.11413 · DOI
- 10.1038/ng0195-70 · DOI
- Kobayashi T, 1999, Renal carcinogenesis, hepatic hemangiomatosis, and embryonic lethality caused by a germ‐line Tsc2 mutation in mice, Cancer Res, 59, 1206
- 10.1093/hmg/11.5.525 · DOI
Cited by
Sorted by citations
Behavioural phenotyping assays for mouse models of autism
Silverman, J. L., Yang, M., Lord, C., & Crawley, J. N. (2010) · Nature Reviews Neuroscience · doi:10.1038/nrn2851 · Cited by 1,462
Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits
Tang, G., Gudsnuk, K., Kuo, S.-H., Cotrina, M. L., Rosoklija, G., Sosunov, A., Sonders, M. S., Kanter, E., Castagna, C., Yamamoto, A., et al. (2014) · Neuron · doi:10.1016/j.neuron.2014.07.040 · Cited by 1,146
mTOR signaling: At the crossroads of plasticity, memory and disease
Hoeffer, C. A., & Klann, E. (2010) · Trends in Neurosciences · doi:10.1016/j.tins.2009.11.003 · Cited by 1,128
Translational control of long-lasting synaptic plasticity and memory
Costa-Mattioli, M., Sossin, W. S., Klann, E., & Sonenberg, N. (2009) · Neuron · doi:10.1016/j.neuron.2008.10.055 · Cited by 944
Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis
Ehninger, D., Han, S., Shilyansky, C., Zhou, Y., Li, W., Kwiatkowski, D. J., Ramesh, V., & Silva, A. J. (2008) · Nature Medicine · doi:10.1038/nm1788 · Cited by 882
Zoghbi, H. Y., & Bear, M. F. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a009886 · Cited by 797
Disentangling the heterogeneity of autism spectrum disorder through genetic findings
Jeste, S. S., & Geschwind, D. H. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2013.278 · Cited by 644
The Autistic Neuron: Troubled Translation?
Kelleher, R. J., & Bear, M. F. (2008) · Cell · doi:10.1016/j.cell.2008.10.017 · Cited by 598
Mutations causing syndromic autism define an axis of synaptic pathophysiology
Auerbach, B. D., Osterweil, E. K., & Bear, M. F. (2011) · Nature · doi:10.1038/nature10658 · Cited by 592
Zhou, J., Blundell, J., Ogawa, S., Kwon, C.-H., Zhang, W., Sinton, C., Powell, C. M., & Parada, L. F. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.5685-08.2009 · Cited by 441
Antoine, M. W., Langberg, T., Schnepel, P., & Feldman, D. E. (2019) · Neuron · doi:10.1016/j.neuron.2018.12.026 · Cited by 413
mTOR complexes in neurodevelopmental and neuropsychiatric disorders
Costa-Mattioli, M., & Monteggia, L. M. (2013) · Nature Neuroscience · doi:10.1038/nn.3546 · Cited by 367
Translational control in synaptic plasticity and cognitive dysfunction
Buffington, S. A., Huang, W., & Costa-Mattioli, M. (2014) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-071013-014100 · Cited by 348
Cognitive impairment in epilepsy: the role of network abnormalities
Holmes, G. L. (2015) · Epileptic Disorders · doi:10.1684/epd.2015.0739 · Cited by 334
The genomic landscape of tuberous sclerosis complex
Martin, K. R., Zhou, W., Bowman, M. J., Shih, J., Au, K. S., Dittenhafer-Reed, K. E., Sisson, K. A., Koeman, J., Weisenberger, D. J., Cottingham, S. L., et al. (2017) · Nature Communications · doi:10.1038/ncomms15816 · Cited by 238
An epigenetic framework for neurodevelopmental disorders: From pathogenesis to potential therapy
Millan, M. J. (2013) · Neuropharmacology · doi:10.1016/j.neuropharm.2012.11.015 · Cited by 229
Loss of Tsc1 In Vivo Impairs Hippocampal mGluR-LTD and Increases Excitatory Synaptic Function
Bateup, H. S., Takasaki, K. T., Saulnier, J. L., Denefrio, C. L., & Sabatini, B. L. (2011) · Journal of Neuroscience · doi:10.1523/jneurosci.1617-11.2011 · Cited by 204
Reversing Neurodevelopmental Disorders in Adults
Ehninger, D., Li, W., Fox, K., Stryker, M. P., & Silva, A. J. (2008) · Neuron · doi:10.1016/j.neuron.2008.12.007 · Cited by 196
Neuronal and glia abnormalities in Tsc1-deficient forebrain and partial rescue by rapamycin
Carson, R. P., Van Nielen, D. L., Winzenburger, P. A., & Ess, K. C. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.08.024 · Cited by 165
Enhanced synapse remodelling as a common phenotype in mouse models of autism
Isshiki, M., Tanaka, S., Kuriu, T., Tabuchi, K., Takumi, T., & Okabe, S. (2014) · Nature Communications · doi:10.1038/ncomms5742 · Cited by 152
Everolimus for treatment of tuberous sclerosis complex‐associated neuropsychiatric disorders
Krueger, D. A., Sadhwani, A., Byars, A. W., de Vries, P. J., Franz, D. N., Whittemore, V. H., Filip‐Dhima, R., Murray, D., Kapur, K., & Sahin, M. (2017) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.494 · Cited by 133
Ehninger, D., De Vries, P. J., & Silva, A. J. (2009) · Journal of Intellectual Disability Research · doi:10.1111/j.1365-2788.2009.01208.x · Cited by 120
Santini, E., & Klann, E. (2014) · Science Signaling · doi:10.1126/scisignal.2005832 · Cited by 118
Rapamycin reverses status epilepticus-induced memory deficits and dendritic damage
Brewster, A. L., Lugo, J. N., Patil, V. V., Lee, W. L., Qian, Y., Vanegas, F., & Anderson, A. E. (2013) · PLoS ONE · doi:10.1371/journal.pone.0057808 · Cited by 112
Low sociability in BTBR T+tf/J mice is independent of partner strain
Yang, M., Abrams, D. N., Zhang, J. Y., Weber, M. D., Katz, A. M., Clarke, A. M., Silverman, J. L., & Crawley, J. N. (2012) · Physiology & Behavior · doi:10.1016/j.physbeh.2011.12.025 · Cited by 112
TSC1/TSC2 signaling in the CNS
Han, J. M., & Sahin, M. (2011) · FEBS Letters · doi:10.1016/j.febslet.2011.02.001 · Cited by 105
Tsai, P., & Sahin, M. (2011) · Current Opinion in Neurology · doi:10.1097/wco.0b013e32834451c4 · Cited by 84
Reijnders, M. R. F., Kousi, M., van Woerden, G. M., Klein, M., Bralten, J., Mancini, G. M. S., van Essen, T., Proietti-Onori, M., Smeets, E. E. J., van Gastel, M., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00933-6 · Cited by 76
Modeling autism-relevant behavioral phenotypes in rats and mice: Do ‘autistic’ rodents exist?
Servadio, M., Vanderschuren, L. J. M. J., & Trezza, V. (2015) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000163 · Cited by 76
Recent advances in gene therapy for neurodevelopmental disorders with epilepsy
Turner, T. J., Zourray, C., Schorge, S., & Lignani, G. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15168 · Cited by 71
The Gut-Immune-Brain Axis in Autism Spectrum Disorders; A Focus on Amino Acids
van Sadelhoff, J. H. J., Perez Pardo, P., Wu, J., Garssen, J., van Bergenhenegouwen, J., Hogenkamp, A., Hartog, A., & Kraneveld, A. D. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00247 · Cited by 71
Xie, Y.-C., Yao, Z.-H., Yao, X.-L., Pan, J.-Z., Zhang, S.-F., Zhang, Y., & Hu, J.-C. (2018) · Journal of Alzheimer's Disease · doi:10.3233/jad-180782 · Cited by 24
Metadata
- Authors
- Goorden, S. M. I., van Woerden, G. M., van der Weerd, L., Cheadle, J. P., & Elgersma, Y.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2007-12
- Volume
- 62
- Issue
- 6
- Pages
- 648-655
- ISSN
- 0364-5134
- 1531-8249
- Cited by
- 230
- References
- 5
- Language
- en
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.
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
