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Pharmacol Biochem Behav. 2017 Apr;155:16-23. doi: 10.1016/j.pbb.2017.03.002. Epub 2017 Mar 8.

Cystathionine-β-synthase-derived hydrogen sulfide is required for amygdalar long-term potentiation and cued fear memory in rats.

Author information

1
Department of Psychiatry and Medical Experimental Center, Jiangxi Mental Hospital/Affiliated Mental Hospital of Nanchang University, Nanchang 330029, PR China.
2
Department of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, PR China.
3
Department of Neurology, Second Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
4
Department of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, PR China.
5
Department of Psychiatry and Medical Experimental Center, Jiangxi Mental Hospital/Affiliated Mental Hospital of Nanchang University, Nanchang 330029, PR China. Electronic address: jxmh_wb@163.com.
6
Department of Psychiatry and Medical Experimental Center, Jiangxi Mental Hospital/Affiliated Mental Hospital of Nanchang University, Nanchang 330029, PR China. Electronic address: yuanjimyang@yeah.net.

Abstract

Hydrogen sulfide (H2S) is an endogenous gaseous molecule that functions as a neuromodulator in the brain. We previously reported that H2S regulated amygdalar synaptic plasticity and cued fear memory in rats. However, whether endogenous H2S is required for amygdalar long-term potentiation (LTP) induction and cued fear memory formation remains unclear. Here, we show that cystathionine-β-synthase (CBS), the predominant H2S-producing enzyme in the brain, was highly expressed in the amygdala of rats. Suppressing CBS activity by inhibitor prevented activity-triggered generation of H2S in the lateral amygdala (LA) region. Incubating brain slices with CBS inhibitor significantly prevented the induction of NMDA receptors (NMDARs)-dependent LTP in the thalamo-LA pathway, and intra-LA infusion of CBS inhibitor impaired cued fear memory in rats. Notably, treatment with H2S donor, but not CBS activator, significantly reversed the impairments of LTP and fear memory caused by CBS inhibition. Mechanismly, inhibition of CBS activity led to a reduction in NMDAR-mediated synaptic response in the thalamo-LA pathway, and treatment with H2S donor restored the function of NMDARs. Collectively, these results indicate that CBS-derived H2S is required for amygdalar synaptic plasticity and cued fear memory in rats, and the effects of endogenous H2S might involve the regulation of NMDAR function.

KEYWORDS:

Amygdala; Cystathionine-β-synthase; Fear memory; Hydrogen sulfide; Long-term potentiation; NMDA receptors

PMID:
28283345
DOI:
10.1016/j.pbb.2017.03.002
[Indexed for MEDLINE]

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