Open AccessProtein Kinase C is Essential for Kainate‐Induced Anxiety‐Related Behavior and Glutamatergic Synapse Upregulation in Prelimbic Cortex
Author(s) -
Liu Bei,
Feng Jing,
Wang JinHui
Publication year - 2014
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12313
Subject(s) - infralimbic cortex , neuroscience , kainate receptor , downregulation and upregulation , glutamatergic , synapse , chemistry , microbiology and biotechnology , ampa receptor , glutamate receptor , biology , prefrontal cortex , cognition , receptor , biochemistry , gene
Summary Aim Anxiety is one of common mood disorders, in which the deficit of serotonergic and GABA ergic synaptic functions in the amygdala and prefrontal cortex is believed to be involved. The pathological changes at the glutamatergic synapses and neurons in these brain regions as well as their underlying mechanisms remain elusive, which we aim to investigate. Methods An agonist of kainate‐type glutamate receptors, kainic acid, was applied to induce anxiety‐related behaviors. The morphology and functions of glutamatergic synapses in the prelimbic region of mouse prefrontal cortex were analyzed using cellular imaging and electrophysiology. Results After kainate‐induced anxiety is onset, the signal transmission at the glutamatergic synapses is upregulated, and the dendritic spine heads are enlarged. In terms of the molecular mechanisms, the upregulated synaptic plasticity is associated with the expression of more protein kinase C ( PKC ) in the dendritic spines. Chelerythrine, a PKC inhibitor, reverses kainate‐induced anxiety and anxiety‐related glutamatergic synapse upregulation. Conclusion The activation of glutamatergic kainate‐type receptors leads to anxiety‐related behaviors and glutamatergic synapse upregulation through protein kinase C in the prelimbic region of the mouse prefrontal cortex.