Elsevier

Developmental Brain Research

Volume 70, Issue 2, 18 November 1992, Pages 191-195
Developmental Brain Research

Research report
Plasticity and ontogeny of the central 5-HT transporter: effect of neonatal 5,7-dihydroxytryptamine lesions in the rat

https://doi.org/10.1016/0165-3806(92)90197-5Get rights and content

Abstract

5,7-Dihyroxytrptamine (5,7-DHT) is unique as a serotonin (5-HT) neurotoxin in that i.p. injection of neonatal rats increases concentrations of 5-HT in brainstem while depleting 5-HT in cortex, hippocampus and spinal cord. To study the mechanism of this effect we measured the 5-HT transporter or uptake site, a presynaptic marker, using [3H]paroxetine binding. There were significant regional differences in Bmax of vehicle-injected rats: biencephalon > striatum, cortex, spinal cord > hippocampus, cerebellum. There were also regional differences in the ontogeny of bindings: at postnatal day 7,[3H]paroxetine sites were 39% of adult levels in cortex compared to 63% in brainstem. Thirty days after 100 mg/kg 5,7-DHT i.p., Bmax of [3H]paroxetine binding was significantly increased in brainstem (+67%) and diencephalon (+136%), whereas it decreaed in cortex (-59%), hippocampus (-94%) and spinal cord (-99%), striatum (-41%) and cerebellum (-37%). KD remained unaltered. In dose-response studies (0–200 mg/kg),was the threshold dose for Bmax effects and 200 mg/kg was letha In weekly time-course studies, changes were apparent 1 week after 5,7-DHT lesions. Binding site increases in diencephalon and brainstem were not maximal until 3 weeks after injection, whereas percent decreases in cortical sites remained unchanged at eeek studied. Lesion effects on theontogeny of [3H]paroxetine binding sites were region-dependent: cortical sites continued to increased with age but spinal sites did not. There was no significant recovery in spinal cord. These data show significant regional, dose- and time-dependent effects of neonatal 5,7-DHT lesions made by i.p. injection on [3H]paroxetine binding sites. They are evidence for brainstem 5-HT hyperinnervation (sprouting) as a cause of increased 5-HT concentrations rather than other mechanisms following neonatal i.p. 5,7-DHT injections.

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