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

inhibition. As more research have identified the molecular mechanisms of synaptic
transmission, the defects in almost every step can lead to seizures (Babb & Brown,
1987; Sutula et al., 1989). Glutamatergic and GABAergic transmission, as the
major excitatory and inhibitory transmitters of the nervous system respectively,
have a direct relationship to seizures.
The depression of synaptic transmission is one of the earliest events
observed during glucose withdrawal and it has been observed in all brain regions
in which it has been studied (Martin et al., 1994) and the mechanism which
mediates this include reduction in the release of neurotransmitters from the
synaptic terminals. GABA receptor hypofunction during hypoglycemia in the
present study is in accordance with these reports.
GABA RECEPTOR ALTERATIONS IN PANCREAS OF
EXPERIMENTAL RATS
Neurotransmitters have been shown to be present in the nerves innervating
the pancreas (Adeghate & Donath, 1990; 1991). This indicates that
neurotransmitters, therefore, have a functional role in the regulation of pancreatic
function. The presence of high concentrations of GABA and its metabolic
enzymes in the pancreas has been known for nearly two decades (Taniguchi et al.,
1982; Sorenson et al., 1991). The recent discovery of an association between GAD
and insulin-dependent diabetes mellitus (IDDM) has generated increased interest
in the physiologic role of GABA in the pancreas and the regulation of its
metabolic enzymes. GABA acts on GABAA and GABAB, receptors. GABAA
receptors are ligand-gated chloride channels modulated by a variety of drugs.
GABAB receptors are essentially presynaptic, usually coupled to potassium or
calcium channels and they function via a GTP binding protein. The presence of
GABA and functional GABA-A and GABA-B receptors in pancreatic endocrine
cells and their ability to modulate secretion of insulin and glucagons (Brice et al.,
2002).
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