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

parasympathetic nervous system and also could be corrected with carbachol (Patel,
1984).
In the present study, hypoglycemic group showed significantly increased
AChE expression and decreased ChAT expression. Our findings showed the affect
of hypoglycemia on cholinergic enzymes and cholinergic hypofunction in the
pancreas during recurrent hypoglycemia. This is suggested to inhibit glucagon
response to hypoglycemia and blunts the counter regulatory mechanism which
exacerbates the neuronal damage induced by diabetes. Acute hypoglycemia is
associated with stimulation of the pancreatic α-cells and a concurrent, prolonged
suppression of insulin secretion by the β-cells. The islets receive a rich autonomic
innervation and therefore are subjected to control by adrenergic and cholinergic
mechanisms (Roger et al., 1981). Recurrent hypoglycemia also leads to insulin
insensitivity. Previous studies reported impaired glucagon secretion in diabetes
(Unger & Orci, 1975) and insulin-induced hypoglycemia (Ishida et al., 1993).
CENTRAL MUSCARINIC RECEPTOR ALTERATIONS
Muscarinic receptors are a family of G protein-coupled receptors that have
a primary role in central cholinergic neurotransmission. Specific agonists, which
activate postsynaptic muscarinic receptors, stimulate cholinergic signalling
(Valentin et al., 2006). It is known that different parts of the brain, particularly the
hypothalamus and the brainstem are important centers involved in the monitoring
of glucose status. The effect of the cholinergic receptors blocked by the
muscarinic antagonist atropine showed the involvement of muscarinic receptors in
the central cholinergic glucose homeostasis. The muscarinic M1, M2 and M4
subtypes of mAChRs are the predominant receptors in the CNS. These receptors
activate a multitude of signaling pathways important for modulating neuronal
excitability, synaptic plasticity and feedback regulation of ACh release (Volpicelli
et al., 2004). It is now widely accepted that processes such as sustained attention
and working memory are regulated by central cholinergic systems (Sarter et al.,
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