Holman Parker J, Ellis Linda, Chao Amanda, Mitchell Cecilia, Raineki Charlis, Weinberg Joanne
Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Department of Psychology, Brock University, St. Catharines, Ontario, Canada.
Alcohol Clin Exp Res (Hoboken). 2025 Jul;49(7):1445-1458. doi: 10.1111/acer.70082. Epub 2025 May 20.
Social behavior relies on the dynamic, complex, and coordinated activity of a highly conserved "social behavior neural network," which includes the olfactory bulb (OB), piriform cortex (PCX), lateral septum, medial prefrontal cortex (mPFC), amygdala, paraventricular nucleus of the hypothalamus (PVN), and ventral hippocampus. Prenatal alcohol exposure (PAE) is known to disrupt social behavior development, leading to lifelong social functioning impairments. Individuals with PAE are at heightened risk of experiencing early-life adversity (ELA), which independently affects social behavior development; however, little is known about the combined effects of PAE and ELA on social behavior.
We previously demonstrated that PAE and ELA impact social recognition memory throughout adolescence; here, we combine animal models of PAE and ELA to gain insight into both independent and interactive effects of these insults on social behavior network neural activity in both early and late adolescent male and female rats. We measured neural activity (c-fos mRNA expression) across the network following social recognition memory testing.
Our findings indicate that both PAE and ELA are associated with altered neural activity in regions supporting social recognition memory, notably the OB, PCX, mPFC, amygdala, and PVN. The direction of these effects and specific regions impacted vary by sex and age at assessment. Importantly, different brain areas exhibit distinct sensitivities to each type of insult, with PAE generally resulting in hypoactivity of the amygdala and ELA altering mPFC activity.
These data contribute to a more complete social neurobehavioral profile, accounting for both PAE and ELA, to support earlier diagnoses and interventions.
社会行为依赖于一个高度保守的“社会行为神经网络”的动态、复杂且协调的活动，该网络包括嗅球（OB）、梨状皮质（PCX）、外侧隔、内侧前额叶皮质（mPFC）、杏仁核、下丘脑室旁核（PVN）和腹侧海马体。已知产前酒精暴露（PAE）会破坏社会行为发展，导致终身社会功能受损。有PAE的个体经历早期生活逆境（ELA）的风险增加，而ELA会独立影响社会行为发展；然而，关于PAE和ELA对社会行为的联合影响知之甚少。
我们之前证明PAE和ELA会在整个青春期影响社会识别记忆；在此，我们结合PAE和ELA的动物模型，以深入了解这些损伤对青春期早期和晚期雄性和雌性大鼠社会行为网络神经活动的独立和交互作用。在进行社会识别记忆测试后，我们测量了整个网络的神经活动（c-fos mRNA表达）。
我们的研究结果表明，PAE和ELA均与支持社会识别记忆的区域神经活动改变有关，特别是OB、PCX、mPFC、杏仁核和PVN。这些影响的方向和受影响的特定区域因评估时的性别和年龄而异。重要的是，不同脑区对每种类型的损伤表现出不同的敏感性，PAE通常导致杏仁核活动减退，而ELA会改变mPFC活动。
这些数据有助于形成一个更完整的社会神经行为概况，同时考虑PAE和ELA，以支持早期诊断和干预。
