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Ögren SO.
“The effects of chronic treatment with nomifensine and zimelidine on 3H-d-LSD binding in the rat cerebral cortex”.
12th Congress of the Collegium Internationale Neuro-Pharmacologicum (CINP), Göteborg (S), Jun 22-26 1980. 1980;p268.
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Abstract
Groups of male rats (each n=8) were administered orally with saline, the MA and DA uptake inhibitor nomifensine and the 5-HT uptake inhibitor zimelidine twice daily (10 umol/kg per dose) for a period of 14 days. The rats were decapitated 24 hours after the last administration. The effect of this treatment on specific 3H-5-HT and 3H-d-LSD -binding in the dorsal cerebral cortex was examined according to the procedure of Bennett & Snyder (Molec. Pharmac. 12, 373-389, 1976) and modified by Nelson et al (Molec. Pharmac.,14, 983-995, 1978). In the saline group evidence was obtained for only one type of binding site for 3H-5-HT (KD= 1.2 nM, Bmax=7.8 pmol/g) and for M-d-LSD (KD=3.8 nM, Bmax=38.5 pmol/g) Long term treatment with nomifensine induced a low affinity site for Both 3H-5-HT and 3H-d-LSD. The K, values and B of the low affinity site for 3H-5-HT were: Kd=7.7 nM, Bmax=5.6 pmol/g. Corresponding values for the high affinity site: KD= 2.4 nM, Bmax = 2.5 pmol/g. The RD values of the low affinity site for 3H-LSD binding were: KD=12.6 nM, Bmax= 33.5 pmol/g and for the high affinity site: KD = 2.3 nM, Bmax=13.7 nmol/g. Long term treatment with zimelidine produced in accordance with previous results (Fuxe et al, Neurosc.Lett. 13, 307-312, 1979) a low affinity site for 3H-5-HT. This treatment induced also a low affinity site for 3H-d-LSD binding. The values for the low-affinity site were: KD=23.5 nM, Bmax =70.5 pmol/g and for the high affinity site: KD=3.0 nM, Bmax=15.0 pmol/g. These results suggest that chronic treatment with antidepressant drugs may produce adaptive changes at postsynaptic 5-HT receptor sites.
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| Notes # : Abstr. No. 496
(Progress in Neuro-Psychopharmacology 1980, Suppl. 1) |
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