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

impairments in cognitive function and hippocampal synaptic plasticity was
reversed by insulin replacement (Magarinos et al., 2001) supporting a role for
insulin in cognitive function. Insulin receptors are present in particularly high
concentrations in neurons, and in lower levels in glia. The messenger RNA of
insulin receptors is abundantly localized in neuronal somata, and receptor protein
is found in both cell bodies and synapses (Zhao & Alkon, 2001). The major
molecular structure and most of the properties of brain insulin receptors are
identical to peripheral insulin receptors (Wozniak et al., 1993).
Our study on insulin receptor expression in brain regions showed down
regulation in cerebral cortex and up regulated expression in cerebellum, brain
stem, corpus striatum and hippocampus of hypoglycemic and diabetic rats when
compared to control. This indicates impairment in insulin metabolism in the brain
during hypoglycemia. Insulin-associated modulation of neuroendocrine counter
regulation, hypoglycemia perception and cerebral function occur in insulindependent
diabetes mellitus, which indicates an intrinsic effect of insulin on the
human brain (Lingenfelser et al., 1996). Our results are consistent with the
hypothesis that acute increases in insulin cross the blood-brain barrier and
augment counter regulation via acute interactions with CNS insulin receptors as
shown by increased insulin receptors in brain regions. Insulin injection can reduce
blood glucose and lead to hypoglycemia which is associated with impaired
memory (Kopf & Baratti, 1996). Given the importance of insulin signalling in
neurons; altered expression of insulin receptors in brain regions in the present
study during hypoglycemic condition is suggestive of cognitive impairments. In
this study, intensive insulin treatment during diabetes treatment, proved to be
detrimental to insulin signaling. Altered insulin receptor expression in the brain
regions of hypoglycemic and diabetic rats elicits cognitive deficits.
Under conditions of hypoglycemia, when the autonomic nervous system is
activated, elevated insulin levels have been shown to inhibit (Diamond et al.,
1991) the sympathoadrenal response. Thus impaired expression of insulin
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