Electroacupuncture at SP6 Modulates Functional Brain Networks and Reduces Plasma Norepinephrine to Ameliorate Premature Ejaculation in Rats.

Authors

Ning Wu, Tong Wang, Dawei Ni, Yutian Dai, Yanxin Song, Hongchao Wang, Qinggui Zhong, Jianhuai Chen, Chunlu Xu

Published in

Andrology. Sep 04, 2026. Epub Sep 04, 2026.

Abstract

The brain plays a critical role in premature ejaculation (PE), but the specific regions involved remain unclear. This study aimed to identify functional brain network alterations in PE-like rats and investigate the modulatory effects of electroacupuncture (EA) at SP6.
Sixteen male Sprague-Dawley rats were divided into PE-like (n = 8) and control (n = 8) groups based on ejaculation frequency (EF). Copulatory behavior (EF, ejaculation latency [EL]), resting-state fMRI, and plasma norepinephrine (NE) were assessed at baseline and after 4 weeks of daily EA at SP6. Functional brain networks were constructed using graph theory, and nodal measures were compared between groups.
PE-like rats exhibited significantly shortened EL and elevated plasma NE. Global network measures did not differ between groups. However, PE-like rats showed: (1) decreased nodal strength and betweenness centrality in hypothalamus; (2) decreased betweenness centrality in retrosplenial granular cortex zone a/postsubiculum; (3) increased clustering coefficient and global efficiency in RSD/RSGa; (4) decreased local efficiency in primary somatosensory and dorsal thalamic nucleus. EF and NE were negatively associated with dorsal thalamic nucleus local efficiency, while EL was negatively associated with hypothalamus strength and betweenness centrality. EA treatment significantly reduced EF and NE, prolonged EL, and normalized most nodal abnormalities; the improvement in dorsal thalamic nucleus local efficiency survived FDR correction.
PE-like behavior in rats is associated with specific nodal alterations in hypothalamus, thalamus, and somatosensory cortex, alongside elevated NE. EA at SP6 was associated with partial normalization of these abnormalities, suggesting potential neuromodulatory mechanisms for PE, though causal relationships require further investigation.

PMID:
42698290
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.

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