Jackson,James; Paulose,C S(Department of Biotechnology, November 19, 1998)
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Abstract:
5-Hydroxytryptamine2A (5-HT2A) receptor kinetics was studied in cerebral cortex and brain stem of streptozotocin (STZ) induced
diabetic rats. Scatchard analysis with [3H] (±) 2,3dimethoxyphenyl-l-[2-(4-piperidine)-methanol] ([3H]MDL100907) in cerebral
cortex showed no significant change in maximal binding (Bmax) in diabetic rats compared to controls. Dissociation constant
(K) of diabetic rats showed a significant decrease (p < 0.05) in cerebral cortex, which was reversed to normal by insulin treatment.
Competition studies of [3H]MDL100907 binding in cerebral cortex with ketanserin showed the appearance of an additional
low affinity site for 5-HT2A receptors in diabetic state, which was reversed to control pattern by insulin treatment. In brain stem,
scatchard analysis showed a significant increase (p < 0.05) in Bmax accompanied by a significant increase (p < 0.05) in Kd.
Competition analysis in brain stem also showed a shift in affinity towards a low affinity State for 5-HT2A receptors. All these
parameters were reversed to control level by insulin treatment. These results show that in cerebral cortex there is an increase
in affinity of 5-HT2A receptors without any change in its number and in the case of brain stem there is an increase in number of
5HT2A receptors accompanied by a decrease in its affinity during diabetes. Thus, from the results we suggest that the increase
in affinity of 5-HT2A receptors in cerebral cortex and upregulation of 5-HT2A receptors in brain stem may lead to altered neuronal
function in diabetes.
Sherin, Antony; Dr. Paulose, C S(Cochin University of Science & Technology, May , 2010)
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Abstract:
In the present study, a detailed investigation on the alterations of
muscarinic M1, M3, α7 nicotinic acetylcholine receptor (α7 nAchR), GABA
receptors and its subtypes; GABAAα1 and GABAB in the brain regions of
streptozotocin induced diabetic and insulin induced hypoglycemic rats were
carried out. Gene expression of acetylcholine esterase (AChE), choline
acetyltransferase (ChAT), GAD, GLUT3, Insulin receptor, superoxide dismutase
(SOD), Bax protein, Phospholipase C and CREB in hypoglycemic and
hyperglycemic rat brain were studied. Muscarinic M1, M3 receptors, AChE,
ChAT, GABAAα1, GABAB, GAD, Insulin receptor, SOD, Bax protein and
Phospholipase C expression in pancreas was also carried out. The molecular
studies on the CNS and PNS damage will elucidate the therapeutic role in the
corrective measures of the damage to the brain during hypoglycemia and
hyperglycemia.
Description:
Department of Biotechnology,Cochin University of Science and Technology