Astrocytic Hydrogen Sulfide Regulates Supraoptic Cellular Activity in the Adaptive Response of Lactating Rats to Chronic Social Stress

• Main Authors: Dongyang Li, Haitao Liu, Hongyang Wang, Shuwei Jia, Xiaoran Wang, Shuo Ling, Guichuan Chen, Xiaoyu Liu, Yu-Feng Wang
• Format: Article
• Language: English
• Published: SAGE Publishing 2021-09-01
• Series: ASN Neuro
• Online Access: https://doi.org/10.1177/17590914211043087

Maternal social stress among breastfeeding women can be adapted in chronic process. However, neuroendocrine mechanisms underlying such adaptation remain to be identified. Here, we report the effects of 2 hr/day unfamiliar male rat invasion (UMI) stress on maternal behaviors in lactating rats during postpartum day 8 (UMI8) to postpartum day 12 (UMI12). Rat dams at UMI8 presented signs of maternal anxiety, depression, and attacks toward male intruder. These changes partially reversed at UMI12 except the sign of anxiety. In the supraoptic nucleus (SON), UMI12 but not UMI8 significantly increased the expression of c-Fos and phosphorylated extracellular signal-regulated protein kinase 1/2. At UMI8 but not UMI12, length of glial fibrillary acidic protein (GFAP, astrocytic cytoskeletal element) filaments around oxytocin (OT) neurons was significantly longer than that of their controls; the amount of GFAP fragments at UMI12 was significantly less than that at UMI8. Expression of cystathionine β-synthase (CBS, enzyme for H 2 S synthesis) at UMI12 was significantly higher than that at UMI8. CBS expression did not change significantly in the somatic zone of the SON but decreased significantly at the ventral glia lamina at UMI8. In brain slices of the SON, aminooxyacetate (a CBS blocker) significantly increased the expression of GFAP proteins that were molecularly associated with CBS. Aminooxyacetate also reduced the firing rate of OT neurons whereas Na 2 S, a donor of H 2 S, increased it. The adaptation during chronic social stress is possibly attributable to the increased production of H 2 S by astrocytes and the subsequent retraction of astrocytic processes around OT neurons.