Chewing rescues stress-attenuated hippocampal memory by reducing stress

Objectives: Chewing has been suggested to restore impaired cognitive functions in the hippocampus. To address how chewing involves acute stress-attenuated hippocampal function, we measured the long-term potentiation (LTP), a cellular mechanism underlying hippocampal memory, in rats that underwent stress exposure with or without chewing.

Methods: Adult male rats were divided into three experimental conditions of: 1) restraint stress without chewing (ST), 2) restraint stress with chewing (SC), and 3) no treatment (CT). Rats in group SC were allowed to chew a wooden stick during the stress period. We prepared hippocampal slices for LTP recording and collected trunk blood from all experimental animals for assaying the plasma level of stress hormones. For rats in the two stressed groups, we collected tissue and blood immediately after, 24h after or 48h after exposure to the stressor.

Results: The rats in group SC required 24h for the stress-attenuated magnitude of LTP to return to the control level, while those in group ST required 48h. The rapid recovery of LTP in group SC was associated with a larger number of functioning NMDA receptors, one of the glutamate ionotropic receptors that are essential to initiate LTP and readily impaired by stress, suggesting that most NMDA receptors had already become functionally restored in group SC by 24h post-stress survival time. We also found that the plasma concentration of adrenocorticotropic hormone in group SC was 59% of that of rats in group ST immediately after exposure to the stressor, which indicates suppressed activation in the hypothalamic-pituitary-adrenal (HPA) axis of the rats exposed to stress with chewing.

Conclusion: Chewing may suppress stress responses in the HPA axis and the subsequent corticosterone secretion, leading to the rapid recovery of stress-attenuated hippocampal memory process. MEXT provided an Open Research Center subsidy (H18) to support this work.