• Ryo Kawabata, Hiroki Yamanaka, Kimiko Kobayashi, Yoshihiko Oke, Ayumi Fujita, Yoshitaka Oku, Ikuko Yao, and Kohei Koga.
• Biomedical Chemistry Major, Graduate School of Science and Technology, Kwansei Gakuin University, Sanda, Hyogo 669-1330, Japan; Department of Neurophysiology, Faculty of Medicine, Hyogo Medical University, Nishinomiya, Hyogo 663-8501, Japan.
• Neuroscience. 2023 Jul 15; 523: 476047-60.

AbstractStress can be categorized according to physical, psychological and social factors. Exposure to stress produces stress-induced hypersensitivity and forms negative emotions such as anxiety and depression. For example, acute physical stress induced by the elevated open platform (EOP) causes prolonged mechanical hypersensitivity. The anterior cingulate cortex (ACC) is a cortical region involved in pain and negative emotions. Recently, we showed that mice exposed to the EOP changed spontaneous excitatory, but not inhibitory transmission in layer II/III pyramidal neurons of the ACC. However, it is still unclear whether the ACC is involved in the EOP induced mechanical hypersensitivity, and how the EOP alters evoked synaptic transmission on excitatory and inhibitory synaptic transmission in the ACC. In this study, we injected ibotenic acid into the ACC to examine if it was involved in stress-induced mechanical hypersensitivity induced by EOP exposure. Next, by using whole-cell patch-clamp recording from brain slice preparation, we analyzed action potentials and evoked synaptic transmission from layer II/III pyramidal neurons within the ACC. Lesion of the ACC completely blocked the stress-induced mechanical hypersensitivity induced by EOP exposure. Mechanistically, EOP exposure mainly altered evoked excitatory postsynaptic currents such as input-output and paired pulse ratio. Intriguingly, the mice exposed in the EOP also produced low-frequency stimulation induced short-term depression on excitatory synapses in the ACC. These results suggest that the ACC plays a critical role in the modulation of stress-induced mechanical hypersensitivity, possibly through synaptic plasticity on excitatory transmission.Copyright © 2023 IBRO. Published by Elsevier Ltd. All rights reserved.

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