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Gamma-Aminobutyric acid (γ-Aminobutyric acid, GABA) is the predominating inhibitory neurotransmitter in the mammalian CNS. As exogenous GABA cannot penetrate the blood-brain barrier, it is synthesized in the GABAergic neurons in the CNS, converted from glutamate, the principal excitatory neurotransmitter, using the enzyme glutamic acid decarboxylase (GAD) and pyridoxal phosphate as a cofactor.
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GABAergic Synapse Pathway A maintained balance between excitatory and inhibitory synaptic transmission plays a crucial role in normal function and long-term homeostasis of the neuronal circuits. While glutamatergic synaptic transmission acts as the primary mode of excitatory neurotransmission mediating fast neuronal communication in central nervous system (CNS), inhibitory synapses are thought to provide a brake to neural firing and are important for a number of purposes which include, but are not limited to, preventing postsynaptic neurons from reaching threshold, modulating the pattern of action potential firing, and modifying synaptic strength. Inhibitory strength is not constant but must adapt to dynamically changing patterns and degrees of network activity. GABA Synthesis, Uptake and Release Gamma-Aminobutyric acid (γ-Aminobutyric acid, GABA) is the predominating inhibitory neurotransmitter in the mammalian CNS. As exogenous GABA cannot penetrate the blood-brain barrier, it is synthesized in the GABAergic neurons in the CNS, converted from glutamate, the principal excitatory neurotransmitter, using the enzyme glutamic acid decarboxylase (GAD) and pyridoxal phosphate as a cofactor. GAD appears to be expressed only in cells that use GABA as a neurotransmitter. Once synthesized, GABA is packaged into vesicles by vesicle GABA transporters (VGAT), releases to the synaptic cleft when the presynaptic neuron is depolarized, and diffuses across the cleft to the target receptors distributed on the postsynaptic surface. Find more: https://www.creative-diagnostics.com/gabaergic-synapse-pathway.htm