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GABAB receptors: modulation of thalamocortical dynamics and synaptic plasticity.
Neuroscience ( IF 2.9 ) Pub Date : 2020-03-17 , DOI: 10.1016/j.neuroscience.2020.03.011
Maria V Sanchez-Vives 1 , Almudena Barbero-Castillo 2 , Maria Perez-Zabalza 3 , Ramon Reig 4
Affiliation  

GABAB-receptors (GABAB-Rs) are metabotropic, G protein-coupled receptors for the neurotransmitter GABA. Their activation induces slow inhibitory control of the neuronal excitability mediated by pre- and postsynaptic inhibition. Presynaptically GABAB-Rs reduce GABA and glutamate release inhibiting presynaptic Ca2+ channels in both inhibitory and excitatory synapses while postsynaptic GABAB induces robust slow hyperpolarization by the activation of K+ channels. GABAB-Rs are activated by non-synaptic or volume transmission, which requires high levels of GABA release, either by the simultaneous discharge of GABAergic interneurons or very intense discharges in the thalamus or by means of the activation of a neurogliaform interneuron in the cortex. The main receptor subunits GABABR1a, GABABR1b and GABABR2 are strongly expressed in neurons and glial cells throughout the central nervous system and GABAB-R activation is related to many neuronal processes such as the modulation of rhythmic activity in several brain regions. In the thalamus, GABAB-Rs have been found to modulate the generation of the main thalamic rhythm, spindle waves. In the cerebral cortex, GABAB-Rs also modulate the most prominent emergent oscillatory activity-slow oscillations-as well as faster oscillations like gamma frequency. Further, recent studies evaluating the complexity expressed by the cortical network, a parameter associated with consciousness levels, have found that GABAB-Rs enhance this complexity, while their blockade decreases it. This review summarizes the current results on how the activation of GABAB-Rs affects the interchange of information between brain areas by controlling rhythmicity as well as synaptic plasticity.

中文翻译:

GABA B受体:调节丘脑皮质动力学和突触可塑性。

GABAB受体(GABAB-Rs)是神经递质GABA的代谢型,G蛋白偶联受体。它们的激活诱导突触前和突触后抑制介导的神经元兴奋性的缓慢抑制控制。突触前GABA B-Rs在抑制性突触和兴奋性突触中均降低GABA和谷氨酸释放抑制突触前Ca 2+通道,而突触后GABA B通过激活K +通道诱导强大的缓慢超极化。GABAB-Rs通过非突触或体积传递而被激活,这需要高水平的GABA释放,既可以同时释放GABA能神经元,也可以在丘脑中非常强烈地放电,也可以通过皮层中神经胶质神经元的激活来实现。主要受体亚基GABABR1a,GABABR1b和GABABR2在整个中枢神经系统的神经元和神经胶质细胞中强烈表达,GABAB-R的激活与许多神经元过程有关,例如大脑多个区域的节律活动的调节。在丘脑中,已发现GABAB-R调节主要丘脑节律纺锤波的产生。在大脑皮层中,GABAB-Rs还调节最突出的紧急振荡活动-缓慢振荡-以及更快的振荡(例如伽马频率)。此外,最近评估皮质网络表达的复杂性(与意识水平相关的参数)的最新研究发现,GABAB-Rs增强了这种复杂性,而其阻滞降低了这种复杂性。
更新日期:2020-03-17
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