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

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Discussion
metabolic cycles are reviewed (Martin & Tobin, 2000; Bak et al., 2006). However,
there is an increasing recognition that regulating neurotransmitter metabolism
provides another avenue for neuromodulation. In terms of the GABAergic system,
the anticonvulsant vigabatrin enhances the GABA content of neurons and glia by
blocking its degradation, thereby increasing vesicular concentrations (French,
1993) while the expression of the synthetic enzyme, GAD, is enhanced following
a seizure (Esclapez & Houser, 1999). Moreover, both experimental and modeling
studies have shown that modulating the intracellular content determines the degree
of vesicular GABA release (Wu et al., 2001; Engel et al., 2001; Axmacher et al.,
2004).
The present study on GABA receptor subtypes; GABAAα1, GABAB and
GAD in brain regions showed significant alterations in expression pattern which
throws light on the fact that GABAergic neurotransmission is impaired during
hypoglycemia and this contributes to hypoglycemic seizure and the subsequent
neurological deficits.
Cerebral cortex
GABA neurons constitute 20–30% of all neurons in the cerebral cortex
and perform critical roles in modulating cortical functional output (Cherubini &
Conti, 2001; Krimer & Goldman-Rakic, 2001). GABA, the principal inhibitory
neurotransmitter in the cerebral cortex, maintains the inhibitory tones that counter
balances neuronal excitation. When this balance is perturbed, seizures ensue
(Gregory & Mathews, 2007). GABA is formed within GABAergic axon terminals
and released into the synapse, where it acts at one of two types of receptor
GABAA and GABAB (Labrakakis et al., 1997). GABAA receptor binding
influences the early portion of the GABA mediated inhibitory postsynaptic
potential, whereas GABAB binding influences the late portion. GABAA receptor
activation in neurons induced a complex physiological response, namely the
activation of a Cl - conductance in concert with a blockade of the resting K +