Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

changes in ambient GABA can alter tonic inhibition and thus the overall synaptic
tone of a brain region (Farrant & Nusser, 2005). There is an extensive literature
showing that seizures can be provoked by blocking GABA synthesis with 3mercaptoproprionic
acid (MPA) in vivo (Mares et al., 1993). These studies were
demonstrating the involvement of GABA in the prevention of the overstimulation
of neuronal networks.
GABA Receptors
GABA mediates its actions via three distinct receptors: the ionotropic
GABAA and GABAC receptors and the metabotropic GABAB receptors (Bormann,
2000). In addition to its CNS functions, the GABAergic system is also present in
peripheral tissues, including the gastrointestinal tract (Gilon et al., 1990, 1991;
Harty et al., 1991; Krantis et al., 1994). Ionotropic GABA receptors are the most
important Cl− channels in the central nervous system CNS and their expression
has also been found in peripheral organs. These receptors mediate a fast inhibitory
neurotransmission in the CNS (Akinci & Schofield, 1999). Ionotropic GABA
receptors can be categorized into GABAA and GABAC receptors based on their
subunit compositions and pharmacological properties (Bormann, 2000).
GABAB receptors mediate slow prolonged inhibition in the brain by
activating postsynaptic G protein-coupled inwardly rectifying K+ channels
(GIRKs) and inactivating presynaptic voltage-gated Ca2+ channels. GABAB
receptors also inhibit adenylate cyclase, leading to diminished activity of PKA
signaling pathways (Bowery, 2006). Structurally GABAB receptors are members
of the class C family of G-protein coupled receptors (GPCR) and are encoded in
vertebrates by two genes - GABAB receptor-1 (GABABR1) and GABABR2
respectively (Couve et al., 2002; Bettler et al., 2004).
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