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

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Discussion
hypoglycemic seizure to different part of the brain which leads to seizure
generation. Evidence has accumulated that GABA is involved in the regulation of
cholinergic (Ferkany & Enna, 1980; Scatton & Bartholini, 1982) neurons.
Hippocampus
Coulter (2001) reported that repeated seizures caused an attenuation of
GABA mediated inhibition of the granule cells and in the pyramidal cells of the
hippocampus. This change cannot be explained by a selective loss of GABAergic
inhibitory interneuron, since the GABA immunoreactive neurons were shown to
be more resistant to seizure-induced injury than other hippocampal neurons
(Sloviter et al., 1987).
Analysis of GAD expression was used as a marker of over all GABAergic
activity and was found to be lower in hypoglycemic rats. GAD plays a very
important role in maintaining excitatory inhibitory balance of the central nervous
system (Quan et al., 2003). GABA receptor binding significantly decreased along
with decreased expression of its subtypes; GABAAα1 and GABAB.. The decreased
expression was confirmed by results from immunohistochemistry studies.
Dysfunction of GABAergic neurotransmitter systems is implicated in the
generation of seizure, since an imbalance between excitation and inhibition
produced by a decrease in GABAergic and/or an increase in glutamatergic
transmission has been associated with the generation of this pathological
condition, both in animal models and in humans (Bradford, 1995). Failure of
GABAergic inhibition or enhancement of excitatory neurotransmission
contributed to seizure initiation, especially at or near the site of seizure initiation
(Balters & Francesco, 2002). Thus it is clear that the decreased GABA receptors
along with decreased GAD gene expression in the hippocampus have an important
role in hypoglycemic seizure and thereby neurological deficit. Research into
seizures has gravitated to mechanisms associated with synaptic transmission
because of its critical role in maintaining the balance between excitation and