Deutsch Stephen I, Rosse Richard B, Schwartz Barbara L, Mastropaolo John, Burket Jessica A, Weizman Abraham
Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, Virginia 23507-1912, USA.
Isr J Psychiatry Relat Sci. 2010;47(1):17-26.
GABA, the major inhibitory neurotransmitter in the brain, is synthesized from L-glutamate and packaged within a family of highly differentiated inhibitory interneurons. Individual GABA inhibitory interneurons in the frontal cortex can make terminal synaptic connections with more than 200 distinct pyramidal neurons, the principal output neuron. Moreover, the sites of these synaptic connections include shafts of dendritic spines, soma, dendritic branches, and initial axon segments. The phasic activity of GABAergic neurons regulate intermittent oscillations of assemblies of pyramidal cell neurons, which are critical for many higher cortical functions such as working memory. Potentially, there are several viable pharmacotherapeutic strategies for facilitating GABAergic neurotransmission. A major research question is whether tonically-administered, selective GABAergic therapeutic interventions can mimic and correct disruptions of the intermittent oscillatory activity of assemblies of cortical pyramidal cell neurons.
γ-氨基丁酸（GABA）是大脑中主要的抑制性神经递质，由L-谷氨酸合成，并包裹在一类高度分化的抑制性中间神经元中。额叶皮质中的单个GABA抑制性中间神经元可与200多个不同的锥体神经元（主要的输出神经元）建立终末突触连接。此外，这些突触连接的部位包括树突棘的轴、胞体、树突分支和轴突起始段。GABA能神经元的相位活动调节锥体细胞神经元集合的间歇性振荡，这对许多高级皮质功能（如工作记忆）至关重要。潜在地，有几种可行的药物治疗策略可促进GABA能神经传递。一个主要的研究问题是，持续给予的选择性GABA能治疗干预是否能模拟并纠正皮质锥体细胞神经元集合间歇性振荡活动的破坏。
