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

GLUT3 EXPRESSION IN BRAIN OF EXPERIMENTAL RATS
The brain requires a constant glucose supply which does not vary with the
blood glucose concentration. This is brought about primarily by glucose
metabolism itself being the rate-limiting step. Transport does have influence and is
thought to be rate limiting at very low glucose concentrations (Robinson &
Rapaport, 1986). Glucose transport into the brain is critical for the maintenance of
brain metabolism. Although under basal conditions the rate of glucose transport is
not the rate-limiting step for glycolysis in the central nervous system,
hypoglycemia or hyperglycemia is known to change the glucose transport system
in the brain (Devivo et al., 1991), suggesting that there is glucose-regulatable
mechanisms associated with the transport of glucose. The expression, regulation
and activity of glucose transporters play an essential role in neuronal homeostasis,
because glucose represents the primary energy source for the brain (Pardridge,
1983). GLUT-3 mRNA is widely expressed in the brain, including the pyramidal
neurons of the hippocampus and the granule neurons of the dentate gyrus
(Nagamatsu et al., 1993) and immunohistochemical analysis has demonstrated
that GLUT-3 protein expression also exhibits a widespread distribution in the
brain (Zeller et al., 1995). Under normal physiological conditions, cerebral
glucose metabolism is limited by the rate of glucose phosphorylation, but during
hypoglycemia glucose transport can become rate limiting. Since glucose transport
is facilitated by transport proteins for glucose, the global or local expression of
such transport proteins are altered during hypoglycemia.
Severe hypoglycemia is a factor that can damage neurons. The gradient
for glucose from capillaries to neurons has been reported by Gjedde, (1983).
During hypoglycemia, the glucose concentrations in the brain tissue are decreased
which could result in critical levels of glucose concentrations around neurons. Our
study on GLUT3 expression in brain regions showed an upregulation of GLUT3
in cerebral cortex, cerebellum, brain stem, corpus striatum and hippocampus in
hypoglycemic and diabetic hyperglycemic rats. The results showed that both
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