| dc.description.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. |
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