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

attention. Cognitive deficits, along with morphological and neurochemical
alterations illustrate that the neurological complications of diabetes are not limited
to peripheral neuropathies (Biessels et al., 1994). The central complications of
hyperglycemia include the potentiation of neuronal damage observed following
hypoglycemic events. Hypoglycemia-induced brain injury is a significant obstacle
to optimal blood glucose control in diabetic patients. As in brain injury associated
with ischemia and neurodegenerative conditions, altered neurotransmitter action
appears to play a role in hypoglycemic brain injury.
BLOOD GLUCOSE, CIRCULATING INSULIN LEVEL & BODY
WEIGHT
Several experimental models have been described which provide
information on the etiology of IDDM. Streptozotocin (STZ) is a toxic agent
selective to pancreatic β-cells that induces IDDM by causing the β-cell destruction
(Paik et al., 1980). The STZ diabetic rat serves as an excellent model to study the
molecular, cellular and morphological changes in brain induced by stress during
diabetes (Aragno et al., 2000). In the present study, STZ-induced rats were used as
an experimental model for inducing diabetes, since they provide a relevant
example of endogenous chronic oxidative stress due to the resulting
hyperglycemia (Low et al., 1997). Increased blood glucose and decreased body
weight during diabetes is similar with previous reports as a result of the marked
destruction of insulin secreting pancreatic islet β-cells by streptozotocin (Junod et
al., 1969). Hyperglycemia occurs as a result of impaired glucose transport across
membranes and almost complete suppression of the conversion of glucose into
fatty acids via acetyl-CoA. Hyperglycemic state during diabetes is due to the
increased gluconeogenic pathway, which is physiologically less sensitive to the
inhibition by insulin (Burcelin et al., 1995). Clinical and experimental studies
have revealed that altered glucose status is an important factor controlling learning
and memory processes (Messier & Gagnon, 1996).
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