Department of Physiology and Pharmacology, SUNY Downstate Medical Center Brooklyn, NY 11203, USA.
Front Neural Circuits. 2013 Sep 3;7:135. doi: 10.3389/fncir.2013.00135. eCollection 2013.
The onset of puberty is associated with alterations in mood as well as changes in cognitive function, which can be more pronounced in females. Puberty onset in female mice is associated with increased expression of α4βδ γ-amino-butyric acid-A (GABAA) receptors (GABARs) in CA1 hippocampus. These receptors, which normally have low expression in this central nervous system (CNS) site, emerge along the apical dendrites as well as on the dendritic spines of pyramidal neurons, adjacent to excitatory synapses where they underlie a tonic inhibition that shunts excitatory current and impairs activation of N-methyl-D-aspartate (NMDA) receptors, the trigger for synaptic plasticity. As would be expected, α4βδ expression at puberty also prevents long-term potentiation (LTP), an in vitro model of learning which is a function of network activity, induced by theta burst stimulation of the Schaffer collaterals to the CA1 hippocampus. The expression of these receptors also impairs spatial learning in a hippocampal-dependent task. These impairments are not seen in δ knock-out (-/-) mice, implicating α4βδ GABARs. α4βδ GABARs are also a sensitive target for steroids such as THP ([allo]pregnanolone or 3α-OH-5α[β]-pregnan-20-one), which are dependent upon the polarity of GABAergic current. It is well-known that THP can increase depolarizing current gated by α4βδ GABARs, but more recent data suggest that THP can reduce hyperpolarizing current by accelerating receptor desensitization. At puberty, THP reduces the hyperpolarizing GABAergic current, which removes the shunting inhibition that impairs synaptic plasticity and learning at this time. However, THP, a stress steroid, also increases anxiety, via its action at α4βδ GABARs because it is not seen in δ(-/-) mice. These findings will be discussed as well as their relevance to changes in mood and cognition at puberty, which can be a critical period for certain types of learning and when anxiety disorders and mood swings can emerge.
青春期的开始与情绪变化以及认知功能的改变有关,而女性的这些变化更为明显。在雌性小鼠中,青春期的开始与 CA1 海马体中 α4βδγ-氨基丁酸-A(GABAA)受体(GABARs)的表达增加有关。这些受体在中枢神经系统(CNS)的这个部位通常表达水平较低,它们出现在锥体细胞的树突顶端以及树突棘上,与兴奋性突触相邻,在那里它们构成了一种紧张性抑制,使兴奋性电流转移,并损害 N-甲基-D-天冬氨酸(NMDA)受体的激活,后者是突触可塑性的触发因素。正如预期的那样,青春期时 α4βδ 的表达也阻止了长时程增强(LTP),这是一种体外学习模型,是网络活动的功能,由 Schaffer 侧支到 CA1 海马体的θ爆发刺激诱导。这些受体的表达也会损害依赖海马体的空间学习任务中的学习能力。在 δ 敲除(-/-)小鼠中没有观察到这些损伤,这暗示了 α4βδ GABARs 的作用。α4βδ GABARs 也是类固醇如 THP([allo] 孕烷醇酮或 3α-OH-5α[β]-孕烷-20-酮)的敏感靶点,这些类固醇依赖 GABA 能电流的极性。众所周知,THP 可以增加由 α4βδ GABARs 门控的去极化电流,但最近的数据表明,THP 可以通过加速受体脱敏来减少超极化电流。在青春期,THP 减少超极化 GABA 能电流,从而消除了此时损害突触可塑性和学习的转移抑制。然而,THP 是一种应激类固醇,通过其在 α4βδ GABARs 上的作用也会增加焦虑,因为在 δ(-/-) 小鼠中没有观察到这种作用。这些发现将与青春期时情绪和认知的变化有关,青春期是某些类型的学习的关键时期,也是焦虑症和情绪波动可能出现的时期。