División de Investigación y Estudios de Posgrado, Facultad de Psicología, Universidad Nacional Autónoma de México, 04510, Mexico.
División de Investigación y Estudios de Posgrado, Facultad de Psicología, Universidad Nacional Autónoma de México, 04510, Mexico.
Behav Brain Res. 2022 Jul 26;430:113947. doi: 10.1016/j.bbr.2022.113947. Epub 2022 May 26.
It has been shown that exposure to an enriched environment (EE) can modulate the physiological impact of aversive stimuli in animals, promoting adaptive attitudes, as well as the development of resilience to stressful situations. These changes are known to be related to increased levels of some trophic factors, such as brain-derived neurotrophic factor (BDNF), which has been considered a regulatory protein for synaptic plasticity in the adult brain. Our previous studies have demonstrated that in the insular cortex (IC), a brain region of the temporal lobe implicated in the acquisition, consolidation, and retention of conditioned taste aversion (CTA) task, BDNF can reverse the CTA memory deficit caused by a protein synthesis inhibitor. Likewise, our research group have also shown that BDNF is required for the maintenance of CTA long-term memory. Here we evaluate the effects of the exposure to an enriched environment on the CTA memory strength, using a weak and strong version of this paradigm. The exposure to an EE for 21 days was able to attenuate the strong-CTA response through the restoration of BDNF levels in the IC of adult rats. These results provide evidence that environmental enrichment is capable of reducing the strength of an aversive memory trace, restoring the BDNF levels in a neocortical region of the adult brain.
已经证明,暴露于丰富环境(EE)中可以调节动物对厌恶刺激的生理影响,促进适应性态度以及对压力情况的恢复力的发展。这些变化与一些营养因子水平的增加有关,例如脑源性神经营养因子(BDNF),它被认为是成年大脑中突触可塑性的调节蛋白。我们之前的研究表明,在脑岛皮层(IC)中,颞叶的一个与获得、巩固和保留条件味觉厌恶(CTA)任务有关的大脑区域,BDNF 可以逆转由蛋白质合成抑制剂引起的 CTA 记忆缺陷。同样,我们的研究小组还表明,BDNF 是维持 CTA 长期记忆所必需的。在这里,我们使用这种范式的弱和强版本来评估暴露于丰富环境对 CTA 记忆强度的影响。在成年大鼠的 IC 中,通过恢复 BDNF 水平,暴露于 EE 21 天能够减弱强 CTA 反应。这些结果提供了证据,证明环境丰富能够降低厌恶记忆痕迹的强度,并恢复成年大脑新皮层区域的 BDNF 水平。