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Protein kinase C is essential for kainate-induced anxiety-related behavior and glutamatergic synapse upregulation in prelimbic cortex.

ABSTRACT: AIM:Anxiety is one of common mood disorders, in which the deficit of serotonergic and GABAergic 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.

SUBMITTER: Liu B

PROVIDER: S-EPMC6493007 | biostudies-other | 2014 Nov

REPOSITORIES: biostudies-other

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Protein kinase C is essential for kainate-induced anxiety-related behavior and glutamatergic synapse upregulation in prelimbic cortex.

Liu Bei B Feng Jing J Wang Jin-Hui JH

CNS neuroscience & therapeutics 20140902 11

<h4>Aim</h4>Anxiety is one of common mood disorders, in which the deficit of serotonergic and GABAergic 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.<h4>Methods</h4>An agonist of kainate-type glutamate receptors, kainic acid, was applied to induce anxiety-related behaviors. The morpholo ...[more]

PMID: 25180671

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Project description:Acute exposure to a salient stressor, such as in post-traumatic stress disorder, can have lasting impacts upon an individual and society. To study stress in rodents, some naturalistic methods have included acute exposure to a predator odor, such as the synthetic fox odor 2,4,5, trimethyl-3-thiazoline (TMT). These experiments explore the stress-related behaviors and cortical activity induced by TMT exposure in adult male C57BL/6J mice and the influence of the stress neuropeptide corticotropin-releasing factor (CRF) on these responses. Compared to H2O and a novel odorant, vanilla, mice exposed to TMT in the home cage showed increased avoidance and defensive burying indicative of evident stress responses. Consistent with stress-induced activation of the medial prefrontal cortex (mPFC), we found that the prelimbic (PL) and infralimbic (IL) subregions of the mPFC had elevated c-Fos immunolabeling after TMT and vanilla compared to H2O. Slice physiology recordings were performed in layers 2/3 and 5 of the PL and IL, following TMT, vanilla, or H2O exposure. In TMT mice, but not vanilla or H2O mice, PL layers 2/3 showed heightened spontaneous excitatory post-synaptic currents and synaptic drive, suggesting TMT enhanced excitatory transmission. Synaptic drive in PL was increased in both TMT and H2O mice following bath application of 300?nM CRF, but only H2O mice increased excitatory currents with 100?nM CRF, suggesting dose-effect curve shifts in TMT mice. Further, systemic pretreatment with the CRF-R1 antagonist CP154526 and bath application with the CRF-R1 antagonist NBI27914 reduced excitatory transmission in TMT mice, but not H2O mice. CP154526 also reduced stress-reactive behaviors induced by TMT. Taken together, these findings suggest that exposure to TMT leads to CRF-R1 driven changes in behavior and changes in synaptic function in layer 2/3 neurons in the PL, which are consistent with previous findings that CRF-R1 in the mPFC plays an important role in predator odor-related behaviors.

Dataset Information

Protein kinase C is essential for kainate-induced anxiety-related behavior and glutamatergic synapse upregulation in prelimbic cortex.

Publications

Protein kinase C is essential for kainate-induced anxiety-related behavior and glutamatergic synapse upregulation in prelimbic cortex.

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