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

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Discussion
CHOLINERGIC ENZYME ALTERATIONS IN BRAIN AND PANCREAS
OF EXPERIMENTAL RATS.
Central cholinergic activity was studied in experimental rats using ChAT
and AChE as markers. ChAT is the rate-limiting enzyme of Ach production,
which is synthesized in cholinergic neuronal cell bodies and is often used in the
studies of tissue localization and functional activity. Acetylcholine is the primary
neurotransmitter of the cholinergic system and its activity is regulated by AChE.
The termination of nerve impulse transmission is accomplished through the
degradation of acetylcholine into choline and acetyl CoA by AChE (Weihua Xie
et al., 2000). It is suggested that the changes in the plasma glucose or insulin
levels be the stimuli that influence the activity of cholinergic neurons. Our results
showed an increased expression of AChE in cerebral cortex, cerebellum,
brainstem and hippocampus of hypoglycemic and diabetic rats when compared to
control rats. In corpus striatum there was a decrease in the expression of AChE in
both hypoglycemic and diabetic groups. The decrease in AChE activity has a
negative correlation with the blood glucose level, suggested to be due to impaired
glucose oxidation and glucose transport. These results are in accordance with
Kuhad et al (2007), where a significant elevation in AChE activity was observed
in cerebral cortex from STZ-induced diabetic rats. AChE activation leads to a fast
ACh degradation and a subsequent down regulation of ACh receptors causing
undesirable effects on cognitive functions (Appleyard et al., 1990).
ChAT shows a decreased expression in cerebral cortex, cerebellum, brain
stem, corpus striatum and hippocampus in hypoglycemic rats compared to diabetic
rats. It is suggested that the increase in AChE activity caused by recurrent
hypoglycemia during diabetes leading to a reduction in the efficiency of
cholinergic neurotransmission due to a decrease in acetylcholine levels in the
synaptic cleft, thus contributing to the progressive cognitive impairment and other
neurological dysfunctions seen in diabetic patients (Biessels et al., 1994). STZ