Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1
By R. M. Costa, N. B. Federov, J. Kogan, G. Murphy, Joel N.H. Stern, M. Ohno, R. Kucherlapati, T. Jacks, Alcino J. Silva. Nature, 2002
602 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/81c47cc1f89a2c454988b3ad2757b0a7d011dac2
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In Cellular and Molecular Neuroscience
- O. Marín
- R. Malinow
- Ronald L. Davis
- Michael D. Ehlers
- Yi Zhong
- S. Farris
- R. Nicoll
- Richard L. Huganir
In Molecular Biology
In Neurology
Citations in the corpus
- Olfactory memory formation in Drosophila: from molecular to systems neuroscience. (2005, background): “Although there exist several possible mechanisms for these deficiencies (Costa et al. 2002), the gene product neurofibromin has been shown to activate G protein–stimulated adenylyl cyclase activity (Tong et al. 2002), so one possibility is that NF1 works partly through adenylyl cyclases (Tong et…”
- Ras and Rap control AMPA receptor trafficking during synaptic plasticity. (2002, background): “…have been shown toUniversity of Virginia School of Medicine Charlottesville, Virginia 22908 control important neuronal functions (Dolmetsch et al., 2001; Pak et al., 2001; Wu et al., 2001; Ye et al., 2000) and have significant effects on behavior (Brambilla et al., 1997; Costa et al., 2002).”
- Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits (2011, neutral): “, 2007), neurofibromatosis type 1 (Costa et al., 2002), Down’s syndrome (Fernandez et al.”
- Optetrode: a multichannel readout for optogenetic control in freely moving mice (2011, neutral): “, mice provide a very diverse genetic platform for the investigation of behaviors ranging from learning to social performanc”
- Interneuron dysfunction in psychiatric disorders (2012, background): “Like patients with this disease, mice with mutations in Nf1 display spatial-learning deficits, and this impairment seems to be caused by enhanced inhibitory activity in the hippocampu”