Recent studies have showed that ketamine is a rapid and efficient antidepressant, but the mechanism of its antidepressant effect is not fully clear. It is still lack of the research investigating the relation between depressive-like behaviors and neuronal activities in specific brain area after administration of ketamine in vivo. Medial prefrontal cortex (mPFC) involved in the pathogenesis of depression. As a result of effective assessments after behavioral test, most studies lack of direct evidence of the relation between efficacy and the activity of specific brain area. Therefore, we used fiber photometry to explore the alteration of Ca2+ transient in the prelimbic (PrL) area of mPFC during behavioral tests in freely moving mice. Our results showed that the chronic corticosterone (CORT) protocol induced depressive-like behaviors. Administration of ketamine reversed these effects. The activation of Ca2+ transients was associated with some behaviors during behavioral tests. Struggling, rearing and exploring evoked strong Ca2+ transients, but moving and grooming did not. The Ca2+ transients amplitude reductions of struggling, rearing and exploring induced by CORT were reversed by ketamine. The results indicated that ketamine ameliorated depressive-like behaviors via mediating neural activation in PrL.
Keywords: Ca(2+) transients; Depression; Fiber photometry; Ketamine; Medial prefrontal cortex; Neuron.
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