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.
Bibliographical noteFunding Information:
This work was supported by the Korea Research Foundation Grants funded by the Korean Government ( NRF-2017R1A2B4011540 and NRF-2015M3C7A1031395 to J.S.H.; NRF - 2014R1A2A1A11050236 and NRF-2019R1A2C1006285 to D.H.C; and NRF- 2015M3C7A1028392 to J.W.C), and the National Institutes of Health Grant MH099073 to J.J.K.). The authors have no conflicts of interest to declare.
© 2020 Elsevier B.V.
- Medial prefrontal cortex
- Recognition memory