Ritger Alexandra C, Loh Maxine K, Stickling Courtney P, Padival Mallika, Ferrara Nicole C, Rosenkranz J Amiel
Department of Foundational Sciences and Humanities, Discipline of Neuroscience, Rosalind Franklin University, North Chicago, Illinois, United States.
Center for Neurobiology of Stress Resilience and Psychiatric Disorders, Rosalind Franklin University, North Chicago, Illinois, United States.
J Neurophysiol. 2025 Feb 1;133(2):582-597. doi: 10.1152/jn.00215.2024. Epub 2025 Jan 7.
The medial amygdala (MeA) is activated by social stimuli and manipulations of the MeA disrupt a wide range of social behaviors. Social stress can shift social behaviors and may accomplish this partly via effects on the MeA. However, very little is known about the effects of social stress on the electrophysiological activity of MeA neurons. The posterior division of the MeA (MeAp) has been implicated in driving social engagement. We hypothesized that repeated social stress would cause parallel changes in in vivo activity of MeAp neurons and social behavior. The resident-intruder paradigm was used to produce repeated social stress in adult male rats. After repeated social stress, MeAp neurons were recorded with in vivo single-unit electrophysiology in anesthetized rats. MeAp neurons, specifically those in the posterodorsal subnucleus (MeApd), fired faster in stressed rats than in controls, and this effect was directly associated with stressor intensity. The MeAp sends dense projections to the posterior bed nucleus of stria terminalis (pBNST) and ventromedial hypothalamus (VMH), and both regions are essential for social engagement and are sensitive to social stressors. MeAp projections to pBNST had higher activity after stress, whereas projections to the VMH were not affected. These effects were significant only in rats that displayed susceptibility to this social stressor, as demonstrated by lower weight gain. Furthermore, the effect of stress on MeApd and MeAp-pBNST neuronal firing was correlated with lower social interaction. These results indicate that heightened MeApd and MeA-pBNST activity may contribute to alterations in social behaviors following social stress. Social stress contributes to psychiatric disorders and impacts multiple brain regions. However, effects on a crucial area for social function, the medial amygdala (MeA), are unclear. We found that social stress increased firing of posterior MeA neurons, and particularly neurons that project to bed nucleus of the stria terminalis, a region implicated in anxiety. Effects of stress on this circuit were associated with diminished social interaction and help clarify how stress can impact social functions.
内侧杏仁核(MeA)会被社交刺激激活,对MeA的操控会扰乱多种社交行为。社会压力会改变社交行为,且可能部分是通过对MeA的影响来实现的。然而,关于社会压力对MeA神经元电生理活动的影响,我们知之甚少。MeA的后部分(MeAp)被认为与推动社交参与有关。我们假设反复的社会压力会导致MeAp神经元的体内活动和社交行为发生平行变化。采用居住者-入侵者范式在成年雄性大鼠中产生反复的社会压力。反复的社会压力后,在麻醉的大鼠中用体内单单位电生理学记录MeAp神经元。MeAp神经元,特别是后背部亚核(MeApd)中的那些神经元,在应激大鼠中比在对照大鼠中放电更快,且这种效应与应激源强度直接相关。MeAp向终纹床核后部(pBNST)和腹内侧下丘脑(VMH)发出密集投射,这两个区域对于社交参与都至关重要,且对社会压力源敏感。应激后,MeAp向pBNST的投射具有更高的活性,而向VMH的投射则未受影响。这些效应仅在对这种社会压力源表现出易感性的大鼠中显著,体重增加较低证明了这一点。此外,压力对MeApd和MeAp-pBNST神经元放电的影响与社交互动减少相关。这些结果表明,MeApd和MeA-pBNST活性增强可能导致社会压力后社交行为的改变。社会压力会导致精神疾病并影响多个脑区。然而,对社交功能的关键区域内侧杏仁核(MeA)的影响尚不清楚。我们发现社会压力增加了MeA后部神经元的放电,特别是那些投射到终纹床核的神经元,该区域与焦虑有关。压力对该神经回路的影响与社交互动减少相关,并有助于阐明压力如何影响社交功能。