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

2004; Suh et al., 2007), although its temporality and regional distribution in brain
have not been explored in detail. Metabolism of glucose during stress such as
hyperglycemia, lead to excess free-radical generation and oxidative stress.
Oxidative stress has been suggested as a mechanism contributing to neuronal
death induced by hypoglycemia, and an early production of reactive species (RS)
during the hypoglycemic episode has been observed.
Our results showed a decreased expression of SOD in hypoglycemic and
diabetic rats compared to control in cerebral cortex, cerebellum, corpus striatum
and hippocampus and an increased expression in brain stem and pancreas.
Regional difference in expression of antioxidant enzymes showed how the specific
brain regions respond to changes in glucose homeostasis. The decreased SOD
activity suggests that the accumulation of superoxide anion radical is responsible
for increased lipid peroxidation. The inactivity of the antioxidant enzymes, SOD
in the diabetes-induced groups was attributed to peroxidative damage to the tissues
caused by administering STZ (Kwag, 2001). Chang et al (2007) reported that
hypoglycemia down-modulate the activity of oxygen free radical scavengers and
potentiate the excitotocity of brain cell. In line with this, our results showed that
cerebral cortex, cerebellum, corpus striatum and hippocampus are more vulnerable
to oxidative stress during impaired glucose metabolism during hypoglycemia and
diabetes induced hyperglycemia. During prolonged periods of stress, exhaustion of
neuronal defense mechanisms, such as anti-oxidant enzymes, reported to increase
neuronal vulnerability to the point where neuronal adaptation shifts from neuronal
plasticity towards neuronal damage (Reagan et al., 2000).
Severe hypoglycemia has been shown in adult rats and those with
experimentally-induced diabetes to produce increases in markers of oxidative
stress (Singh et al., 2004). Recent investigations have shown that the
hypoglycemic condition, even in the absence of isoelectricity, induce discrete
neuronal damage in vulnerable regions, such as the cerebral cortex, when it is
sustained for prolonged periods of time (Tkacs et al., 2005; Ennis et al., 2008;
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