Brief stress impairs recognition memory through amygdalar activation in animals with medial prefrontal cortex lesions

• Published in: Neuroscience letters Vol. 735; p. 135245
• Main Authors: Park, Jung-Cheol, Jeon, Yong-Jae, Kim, Jeansok J., Cho, Jeiwon, Choi, Dong-Hee, Han, Jung-Soo
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 14.09.2020
• Subjects: Amygdala; Amygdala - metabolism; Animals; c-Fos; Male; Medial prefrontal cortex; Memory - physiology; Prefrontal Cortex - metabolism; Proto-Oncogene Proteins c-fos - metabolism; Rats; Rats, Sprague-Dawley; Recognition memory; Recognition, Psychology - physiology; Restraint, Physical - physiology; Restraint, Physical - psychology; Stress; Stress, Psychological - metabolism; Stress, Psychological - psychology; c-Fos; Medial prefrontal cortex; Recognition memory; Amygdala; Stress
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2020.135245

•A brief stress (20-min uncontrollable) does not impair recognition memory.•A prolonged stress (60-min uncontrollable) impairs recognition memory.•A brief stress induces higher c-Fos levels in the amygdala of the mPFC-lesioned animals.•A brief stress impairs recognition memory in the mPFC-lesioned animals.•No effects of mPFC lesions on pre-stress and post-stress CORT levels. 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.