Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett syndrome.

By Vardhan S Dani, Q. Chang, A. Maffei, Gina G. Turrigiano, R. Jaenisch, Sacha B. Nelson. Proceedings of the National Academy of Sciences of the United States of America, 2005

648 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/395393131649556807952ef9f71defe5af13af33

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Citations in the corpus

Interneuron dysfunction in psychiatric disorders (2012, result): “These results are consistent with previous work showing that the cortex of Mecp2 -null mice has deficient inhibitory function and might be prone to hyperexcitabilit”
From synapse to nucleus: calcium-dependent gene transcription in the control of synapse development and function. (2008, background): “Recently, the activity-regulated transcriptional regulator MeCP2 has been shown to specifically control the strength of excitatory synaptic connections (Dani et al., 2005).”
The story of Rett syndrome: from clinic to neurobiology. (2007, positive): “In addition, loss of MeCP2 in mice results in reduced spontaneous activity in cortical slices due to a decrease in the total excitatory synaptic drive and an increase in the total inhibitory drive (Dani et al., 2005).”
A synaptic trek to autism. (2009, background): “Current Opinion in Neurobiology 2009, 19:231–234 knockout [33] and in several mice proposed as model of autism such as the Caps2 knockout [34] or mice subject to prenatal valproate treatment [35].”
Structural plasticity of GABAergic axons is regulated by network activity and GABAA receptor activation (2013, methodology): “First, we recorded spontaneous excitatory and inhibitory currents in hippocampal CA1 pyramidal cells and determined total synaptic input as a measure of the activity of the slice (Maffei et al., 2004; Dani et al., 2005).”
Brain-specific phosphorylation of MeCP2 regulates activity-dependent Bdnf transcription, dendritic growth, and spine maturation. (2006, background): “Although our model posits that activity- or neurotrophin-dependent MeCP2 S421 phosphorylation relieves its transcriptional repressor function on Bdnf promoter IV and would predict an increase in BDNF levels in Mecp2 null mice, the decreased levels of the activity-dependent gene product BDNF that are”
The autistic neuron: troubled translation? (2008, background): “…of mutations that cause ASDs in humans consistently point to disrupted synaptic function: excessive or diminished excitatory synaptic connectivity (Chao et al., 2007; Hanson and Madison, 2007) and alterations in the balance of excitation and inhibition (Dani et al., 2005; Tabuchi et al., 2007).”
Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Additionally, defects in inhibitory synaptic transmission were detected in the cortex, hippocampus, and brain stem of Mecp2-null mutants (Dani et al. 2005; Medrihan et al. 2008; Zhang et al. 2008).”