Topic
GABAergic
About: GABAergic is a research topic. Over the lifetime, 9595 publications have been published within this topic receiving 473568 citations.
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TL;DR: It is found that acetylcholine (ACh) is the most broadly used neurotransmitter and its usage relative to other neurotransmitters within the context of the entire connectome and within specific network motifs embedded in the connectome.
Abstract: Neurotransmitter maps are important complements to anatomical maps and represent an invaluable resource to understand nervous system function and development. We report here a comprehensive map of neurons in the C. elegans nervous system that contain the neurotransmitter GABA, revealing twice as many GABA-positive neuron classes as previously reported. We define previously unknown glia-like cells that take up GABA, as well as 'GABA uptake neurons' which do not synthesize GABA but take it up from the extracellular environment, and we map the expression of previously uncharacterized ionotropic GABA receptors. We use the map of GABA-positive neurons for a comprehensive analysis of transcriptional regulators that define the GABA phenotype. We synthesize our findings of specification of GABAergic neurons with previous reports on the specification of glutamatergic and cholinergic neurons into a nervous system-wide regulatory map which defines neurotransmitter specification mechanisms for more than half of all neuron classes in C. elegans.
301 citations
TL;DR: Striatum exerts a facilitatory influence on TSD cells by releasing these neurons from the tonic inhibitory nigral influence, discussed in the light of the current knowledge on the involvement of basal ganglia in eye/head orienting movements.
301 citations
TL;DR: Evidence for the role of γ‐aminobutyric acid (GABA) neurotransmission in cerebral ischemia‐induced neuronal death and how dysfunction of GABA neurotransmission may contribute to neuronal death are presented and how neuronal death can be prevented by GABAergic drugs are discussed.
Abstract: In this review, we present evidence for the role of gamma-aminobutyric acid (GABA) neurotransmission in cerebral ischemia-induced neuronal death. While glutamate neurotransmission has received widespread attention in this area of study, relatively few investigators have focused on the ischemia-induced alterations in inhibitory neurotransmission. We present a review of the effects of cerebral ischemia on pre and postsynaptic targets within the GABAergic synapse. Both in vitro and in vivo models of ischemia have been used to measure changes in GABA synthesis, release, reuptake, GABA(A) receptor expression and activity. Cellular events generated by ischemia that have been shown to alter GABA neurotransmission include changes in the Cl(-) gradient, reduction in ATP, increase in intracellular Ca(2+), generation of reactive oxygen species, and accumulation of arachidonic acid and eicosanoids. Neuroprotective strategies to increase GABA neurotransmission target both sides of the synapse as well, by preventing GABA reuptake and metabolism and increasing GABA(A) receptor activity with agonists and allosteric modulators. Some of these strategies are quite efficacious in animal models of cerebral ischemia, with sedation as the only unwanted side-effect. Based on promising animal data, clinical trials with GABAergic drugs are in progress for specific types of stroke. This review attempts to provide an understanding of the mechanisms by which GABA neurotransmission is sensitive to cerebral ischemia. Furthermore, we discuss how dysfunction of GABA neurotransmission may contribute to neuronal death and how neuronal death can be prevented by GABAergic drugs.
300 citations
TL;DR: This work demonstrates a novel function of GABA in regulating GABAergic innervation in the adolescent brain, when GABA is mainly known as an inhibitory transmitter and implicates GAD67-mediated GABA synthesis in activity-dependent regulation of inhibitory innervation patterns.
300 citations
TL;DR: The distribution of the high affinity gamma-aminobutyric acid (GABA) receptor labeled by [3H]muscimol, has been studied in the rat brain by light microscopic autoradiography in correlation with the known distribution of GABAergic terminals and the presence of inhibitory GABAergic mechanisms.
299 citations