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

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transcription <strong>and</strong> cell metabolism (Lipton, 1999), as well as immediate effects on<br />

electrophysiological properties (Krnjevic, 2008) serve to protect neurons, thereby<br />

allowing them to recover from ischemic insults of short duration. It has been<br />

demonstrated that neuronal activity in many systems is required to provide trophic<br />

factors essential for neuronal survival (Thoenen, 1995). Any sustained decrease in<br />

neuronal activity resulting from stress could therefore lead to a decreased supply<br />

of essential trophic factors, which would likely be detrimental to hippocampal<br />

neurons (Johnson & Deckwerth, 1993). Recent investigations have shown that the<br />

hypoglycemic condition, even in the absence of isoelectricity, induce discrete<br />

neuronal damage in vulnerable regions, such as hippocampus, when it is sustained<br />

for prolonged periods of time (Tkacs et al., 2005; Ennis et al., 2008; Haces et al.,<br />

2010). Furthermore, increased lipoperoxidation has been observed in the<br />

hippocampus of hypoglycemic animals not subjected to a coma period (Patockova<br />

et al., 2003; Haces et al., 2010). The impairment in cognitive abilities is associated<br />

with insulin induced hypoglycemic neuronal damage (Roghani et al., 2006).<br />

Present study suggests that cognitive <strong>and</strong> memory deficits associated with<br />

hypoglycemia is attributed to the altered cholinergic expression <strong>and</strong> thereby<br />

function mediated through muscarinic receptors in the hippocampus. Stress<br />

condition due to hypoglycemia result in deficits in several neurotransmitter<br />

systems, including cholinergic transmission (Ghajar et al., 1985) which support<br />

the present findings that stress during glucose deprivations affects acetylcholine<br />

metabolism <strong>and</strong> cholinergic neurotransmission in the hippocampus.<br />

MUSCARINIC RECEPTOR ALTERATIONS IN THE PANCREAS<br />

Diabetes mellitus, characterized by uncontrolled hyperglycemia <strong>and</strong><br />

maintenance of blood glucose within the physiological range is critical for the<br />

prevention of diabetes-related complications. Insulin secretion from pancreatic<br />

islet β-cells is a tightly regulated process, under the close control of blood glucose<br />

concentrations <strong>and</strong> several hormones <strong>and</strong> neurotransmitters. However, tight<br />

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