Dakshinamurti,K; Paulose,C S(Department of Biotechnology, May , 1983)
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Abstract:
The concentrations of serotonin in various brain areas were significantly decreased in
the pyridoxine-deficient young rat.
2. There was no change in the concentration of dopamine.
3. Both Bmax and Kid of [3H]serotonin binding to membrane preparations from cerebral cortex
were increased in deficiency and were restored to normal upon pyridoxine supplementation.
4. There was no change in [3H]spiroperidol binding to corpus striatal membrane preparations
in pyridoxine-deficient rats.
Paulose,C S; Dakshinamurti,K(Department of Biotechnology, December 19, 1984)
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Abstract:
The high-affinity bindings of [3H]-5-hydroxytryptamine to serotonin S-1 receptors,
[3H]-ketanserin to serotonin S-2 receptors in the cerebral cortex, [3H]-
fluphenazine to dopamine D-1 receptors, and [3H]-spiroperidol to dopamine D-2
receptors in the corpus striatum were studied in pyridoxine-deficient rats and
compared to pyridoxine-supplemented controls. There was a significant increase
in the maximal binding (Bmax) of serotonin S-1 and S-2 receptors with a significant
decrease in their binding affinities (Kd). However, there were no significant
changes either in the maximal binding or binding affinity of striatal dopamine D-
1 and D-2 receptors. Receptor sensitivity seems to correlate negatively with the
corresponding neurotransmitter concentrations in the pyridoxine-deficient rats.
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.