1. Academic Validation
  2. Hydrogen sulfide mitigates memory impairments via the restoration of glutamatergic neurons in a mouse model of hemorrhage shock and resuscitation

Hydrogen sulfide mitigates memory impairments via the restoration of glutamatergic neurons in a mouse model of hemorrhage shock and resuscitation

  • Exp Neurol. 2024 Mar 19:376:114758. doi: 10.1016/j.expneurol.2024.114758.
Rong-Xin Song 1 Ting-Ting Zhou 2 Shi-Yan Jia 2 Wen-Guang Li 3 Jun Wang 4 Bao-Dong Li 5 Yu-Dong Shan 2 Li-Min Zhang 6 Xiao-Ming Li 7
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China.
  • 2 Department of Anesthesia and Trauma Research, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China.
  • 3 Graduate School, Hebei Medical University, Shijiazhuang, China.
  • 4 Department of Orthopedics, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China.
  • 5 Department of Neurology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China.
  • 6 Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China. Electronic address: azai2010@126.com.
  • 7 Department of Orthopedics, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou No.2 Hospital, Cangzhou, China; Hebei Key Laboratory of Integrated Traditional and Western Medicine in Osteoarthrosis Resrearch, Cangzhou, China. Electronic address: 258976836@qq.com.
Abstract

Impaired long-term memory, a complication of traumatic stress including hemorrhage shock and resuscitation (HSR), has been reported to be associated with multiple neurodegenerations. The ventral tegmental area (VTA) participates in both learned appetitive and aversive behaviors. In addition to being prospective targets for the therapy of addiction, depression, and Other stress-related diseases, VTA glutamatergic neurons are becoming more widely acknowledged as powerful regulators of reward and aversion. This study revealed that HSR exposure induces memory impairments and decreases the activation in glutamatergic neurons, and decreased β power in the VTA. We also found that optogenetic activation of glutamatergic neurons in the VTA mitigated HSR-induced memory impairments, and restored β power. Moreover, hydrogen sulfide (H2S), a gasotransmitter with pleiotropic roles, has neuroprotective functions at physiological concentrations. In vivo, H2S administration improved HSR-induced memory deficits, elevated c-fos-positive vesicular glutamate transporters (Vglut2) neurons, increased β power, and restored the balance of γ-aminobutyric acid (GABA) and glutamate in the VTA. This work suggests that glutamatergic neuron stimulation via optogenetic assay and exogenous H2S may be useful therapeutic approaches for improving memory deficits following HSR.

Keywords

Glutamate; Hemorrhage shock and resuscitation; Hydrogen sulfide; Optogenetic activation; Ventral tegmental area.

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