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Changes in paroxetine binding in the cerebral cortex of polydipsic rats
1Department of Biological Research, Hoechst-Roussel Pharmaceuticals Inc., Somerville, NJ 08876, USA.
European Journal of Pharmacology
|May 4, 1995
Summary
Schedule-induced polydipsia in rats involves changes in the serotonin reuptake carrier. Fluoxetine treatment reversed these alterations, suggesting a link between serotonin transporter function and this behavior.
Area of Science:
- Neuroscience
- Behavioral Pharmacology
Background:
- Schedule-induced polydipsia is a behavior observed in food-deprived rats under fixed-time feeding schedules.
- Chronic fluoxetine administration is known to reduce this behavior over several weeks.
Purpose of the Study:
- To investigate alterations in the serotonin reuptake carrier following the development of schedule-induced polydipsia.
- To determine if fluoxetine reverses these changes in the serotonin reuptake carrier.
Main Methods:
- Rats were subjected to a fixed-time feeding schedule to induce polydipsia.
- [3H]paroxetine binding assays were used to measure serotonin reuptake carrier parameters (Kd and Bmax).
- Effects of food deprivation alone and fluoxetine treatment were assessed.
Main Results:
- Schedule-induced polydipsia was associated with a 40% increase in Kd and a 50% decrease in Bmax of the serotonin reuptake carrier.
- These changes were reversed by chronic fluoxetine administration.
- Food deprivation alone did not alter these binding parameters.
Conclusions:
- Changes in the serotonin reuptake carrier (serotonin transporter) are correlated with the development of schedule-induced polydipsia.
- Fluoxetine's therapeutic effect on this behavior involves the reversal of these serotonin transporter alterations.