Department of Biological and Environmental Sciences, Longwood University, 201 High Street, Farmville, VA 23909, USA.
Brain Res. 2012 May 15;1454:80-9. doi: 10.1016/j.brainres.2012.03.028. Epub 2012 Mar 19.
The hormones of pregnancy and lactation (e.g., estrogen, progesterone, and oxytocin) have been shown to modulate learning, memory, and the restructuring of brain areas not traditionally associated with maternal behavior. Given the impact of reproductive experience on plasticity of brain areas such as the hippocampus, kainic acid (KA) was used in the current study to induce hippocampal-specific neurotoxic insult in adult multiparous and virgin Long-Evans rats. In Experiment I, Fluoro-Jade B, an indicant of degenerating cells, revealed significant neuronal damage in KA-treated hippocampi at 16 h post-injection in both maternal and virgin rats. In Experiment II, maternal and virgin rats were assessed in spatial and novel object preference tasks to determine the effects of KA on subsequent behavioral and cognitive responses. Twenty-four hours post injection, saline maternal animals exhibited superior memory in a spatial task. Further, maternal saline-injected rats were more similar to maternal KA-injected rats than both the virgin groups. Forty-eight hours following the KA or saline injection, compared to virgins, maternal animals demonstrated enhanced memory in the novel object memory test, regardless of type of injection. Further, neurobiological assessments in Experiment II indicated that virgin KA exposed rats had significantly more glial fibrillary acidic protein (GFAP)-immunoreactivity in the hippocampus, suggesting that they were in an earlier stage of neural recovery compared to maternal animals or, alternatively, may have exhibited more trauma than maternal animals. Together, these data suggest that the previously reported plasticity of the maternal brain may facilitate neural and behavioral recovery from neural insults.
妊娠和哺乳期间的激素(例如雌激素、孕酮和催产素)已被证明可以调节学习、记忆和大脑区域的重构,这些区域通常与母性行为无关。鉴于生殖经验对海马等大脑区域可塑性的影响,本研究在成年多产和处女长耳大鼠中使用海人酸(KA)诱导海马特异性神经毒性损伤。在实验 I 中,荧光黄 B(一种指示退化细胞的指示剂)在 KA 处理后的海马体中在注射后 16 小时在母鼠和处女鼠中均显示出明显的神经元损伤。在实验 II 中,对母鼠和处女鼠进行空间和新物体偏好任务评估,以确定 KA 对随后的行为和认知反应的影响。注射后 24 小时,盐水母鼠在空间任务中表现出更好的记忆。此外,与生理盐水注射的母鼠相比,生理盐水注射的母鼠与 KA 注射的母鼠更相似,而与处女组相比则不然。在 KA 或生理盐水注射后 48 小时,与处女相比,母鼠在新物体记忆测试中表现出增强的记忆,无论注射类型如何。此外,实验 II 中的神经生物学评估表明,KA 暴露的处女鼠在海马体中具有明显更多的神经胶质纤维酸性蛋白(GFAP)免疫反应性,这表明它们处于神经恢复的早期阶段与母鼠相比,或者可能比母鼠表现出更多的创伤。总的来说,这些数据表明,先前报道的母体大脑的可塑性可能促进了神经和行为从神经损伤中的恢复。