Abstract：
:Male rats were treated with 10 mg/kg D-fenfluramine (DF) i.p., twice a day for 4 days. Five days later there was a strong reduction (70-100%) in the Bmax of [3H]citalopram binding and the Vmax of [3H]5-HT uptake in cortical and hippocampal synaptosomes; 2 months after the treatment these parameters were reduced by 40-70%. The effect of treatment was also evaluated in synaptosomes preloaded with [3H]5-HT, superfused and exposed for 3 min to a releasing stimulus (15 mM K+ or 0.5 microM DF). In our experimental conditions, the stimulated [3H]5-HT release is Ca(2+)-dependent and takes place only from 5-HT nerve endings. The K(+)-stimulated release was not consistently altered by the DF treatment whereas DF-stimulated [3H]5-HT release was markedly reduced, either 5 days and 2 months after the treatment. The effect of chronic DF was different from the effect of i.c.v. 5,7-DHT, a specific 5-HT neurotoxin which completely abolished the K(+)-induced release. Since the decrease of synaptosomal [3H]5-HT uptake induced by 5,7-DHT (82%) was similar to that found after chronic DF (70-80%), these data suggest that the decrease of 5-HT uptake sites induced by chronic DF is not (only) due to neurodegeneration. That chronic DF could induce a functional down-regulation of 5-HT uptake sites (i.e. decreased density per intact nerve ending) was suggested by the decrease of DF-induced release, since the releasing activity of DF is dependent on functional 5-HT uptake sites. However, due to the characteristics of our model, our results are compatible with either the absence or the presence of a concomitant, partial neurodegeneration of 5-HT nerve endings in DF-treated rats. In summary, our data indicate that after treatment with high doses of DF, the 5-HT uptake carriers undergo a long-lasting down-regulation, thus totally or partly explaining the lower [3H]citalopram binding and the lower synaptosomal [3H]5-HT uptake.
journal_name
Brain Resjournal_title
Brain researchauthors
Gobbi M,Mancini L,Presti ML,Mennini Tdoi
10.1016/0006-8993(96)00435-0subject
Has Abstractpub_date
1996-08-19 00:00:00pages
165-72issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(96)00435-0journal_volume
730pub_type
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