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• W193944754 abstract "The principal inhibitory neurotransmitter in the central nervous system (CNS) is γ -aminobutyric acid (GABA). The majority of fast neuronal inhibition is mediated through the GABA A receptor. The GABA A receptor is a member of the ligand-gated ion channel superfamily of neurotransmitter receptors. In general, the activation of the receptor by GABA induces a neuronal influx of chloride ions through the GABA A receptor-regulated ion channel, thereby leading to hyperpolarization of the neuron. GABA A receptor function is modulated by ligands that recognize different binding sites within the receptor complex. Some of these are clinically important compounds—for example, the 1,4-benzodiazepines and the barbiturates, which exert their action by potentiating GABA A receptor function. Agonism of the action of GABA at the GABA A receptor leads to anxiolysis, sedation, muscle relaxation, and anticonvulsion, whereas antagonism generally has the opposite effects. Increased knowledge of the contribution of individual GABA A receptor subunits to the properties of GABA A receptor complexes and to GABA-ergic neurotransmission may lead to improved understanding of the physiological roles of different GABA A receptor subtypes. Antisense technology represents a rational approach to address this important issue." @default.
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• W193944754 date "2000-01-01" @default.
• W193944754 modified "2023-09-27" @default.
• W193944754 title "[2] Targeting brain GABAA receptors with antisense oligonucleotides: Implications for epilepsy" @default.
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• W193944754 doi "https://doi.org/10.1016/s0076-6879(99)14092-8" @default.
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