Abstract:
:The medial prefrontal cortex (mPFC) is thought to exert inhibitory control over stress-induced activation of the amygdala and neurocognitive effects. As evidence to support this, we examined how exposure to either a brief or prolonged stress affected on amygdalar c-Fos levels and recognition memory of animals with mPFC chemical lesions. mPFC-lesioned and sham-operated animals were subjected to either a brief 20-min restraint+20 tailshocks or a prolonged 60-min restraint+60 tailshocks. Post-stress performances in the object recognition memory and c-Fos immunoreactivity in the amygdala were then assessed. In sham-operated animals, the object recognition memory was reliably impaired following the prolonged, but not following the brief stress exposure. On the other hand, in mPFC-lesioned animals, the brief stress significantly impaired recognition memory and enhanced c-Fos expression in the amygdala. Present findings of loss of mPFC activity exacerbating stress effects provide causal evidence that the mPFC exerts inhibitory control on stress.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Park JC,Jeon YJ,Kim JJ,Cho J,Choi DH,Han JSdoi
10.1016/j.neulet.2020.135245subject
Has Abstractpub_date
2020-09-14 00:00:00pages
135245eissn
0304-3940issn
1872-7972pii
S0304-3940(20)30515-2journal_volume
735pub_type
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