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

varying inhibitory potential. Our results showed that changes in the GABAergic
activity, motor learning and memory deficit are induced by the occurrence of
hyperexcitability and seizures during hypoglycemia during intensive insulin
therapy. The receptor analysis and gene expression studies implicated a role for
GABA receptors in the modulation of neuronal network excitability and cerebellar
motor learning.
Brain stem
GABA is one of the most important, identified neurotransmitters and
generally have an inhibitory action (Cherubini et al., 1998) and because GABA is
unable to act without its receptors. GABA, inhibitory neurotransmitter in the
Inferior colliculus neurons in the brainstem is known to be critical to audiogenic
seizures (Faingold, 1999). IC in lower brainstem plays major roles in the
processing of afferent and efferent information in the auditory system (Oliver &
Huerta, 1992). GABA increases the production of α-brain waves (a state often
achieved by meditation, characterized by being relaxed with greater mental focus
and mental alertness) and reduces β- waves (associated with nervousness,
scattered thoughts, and hyperactivity). GABA regulates proper function and
neurotransmission.
Biosynthetic enzyme, GAD showed significant downregulation in
hypoglycemic rats compared to diabetic and control. Expression GABAAα1
receptor showed upregulation and GABAB significantly down regulated in
hypoglycemic rats. The increase in GABAA receptor density may represent a
compensatory to reduced inhibitory input from local GABAergic interneurons.
The reduction in GABA release would presumably evoke an up-regulation of
GABA receptors on the postsynaptic neuron (Luo et al., 2007). GABA receptor
binding decreased in brain stem of hypoglycemic rats. Progressive decrease of
neuronal malfunction results from decreased utilization of energy during
hypoglycemic deprivation of glucose (Bendtson, 1993). An appropriate balance
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