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The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA), ...
The ionotropic GABA A receptor protein complex is also the molecular target of the benzodiazepine class of tranquilizer drugs. Benzodiazepines do not bind to the same receptor site on the protein complex as does the endogenous ligand GABA (whose binding site is located between α- and β-subunits), but bind to distinct benzodiazepine binding sites situated at the interface between the α- and ...
GABA transporters (gamma-aminobutyric acid transporters) are a family of neurotransmitter / sodium symporters, belonging to the solute carrier 6 family. [1] [2] They are found in various regions of the brain in different cell types, such as neurons and astrocytes.
GABA is an amino acid that is the primary inhibitory neurotransmitter for the central nervous system (CNS). It reduces neuronal excitability by inhibiting nerve transmission. GABA has a multitude of different functions during development and influences the migration, proliferation, and proper morphological development of neurons.
GABA is the major inhibitory neurotransmitter in the brain, and glutamate is the major excitatory neurotransmitter. [130] Neurons link at synapses to form neural pathways , neural circuits , and large elaborate network systems such as the salience network and the default mode network , and the activity between them is driven by the process of ...
In molecular biology and physiology, something is GABAergic or GABAnergic if it pertains to or affects the neurotransmitter gamma-aminobutyric acid (GABA). For example, a synapse is GABAergic if it uses GABA as its neurotransmitter, and a GABAergic neuron produces GABA.
GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified. [6]
Gabazine treatment completely reversed the thermal hyperalgesia. The mechanism behind GABA involvement was investigated using in vitro recordings from animals treated with continuous infusions of SP or saline into the RVM. In SP-treated neurons, GABA evoked depolarization, whereas, in saline-treated neurons, it caused hyperpolarization.