Serotonin involvement in aversive conditioning: reversal of the fear retention deficit by long-term p-chloroamphetamine but not p-chlorophenylalanine.
Neuroscience Letters December 23, 1982 DOI: 10.1016/0304-3940(82)90095-7 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | 5-MeO-DMT fenfluramine p-chloroamphetamine p-chlorophenylalanine |
| Dose | 2 × 10 mg/kg long-term PCA; 2.5 mg/kg acute PCA; 5 mg/kg fenfluramine; 4 mg/kg 5-MeO-DMT; 200, 100, 100 mg/kg PCPA |
| Topics | Serotonin |
| Citations | 24 |
| Key findings | Depletion of central serotonin neurons after long-term PCA treatment completely blocked the fear retention impairment caused by acute PCA and fenfluramine, and partially blocked that from 5-MeO-DMT, while PCPA-induced depletion did not, indicating involvement of different serotonin stores. |
Abstract
5-Methoxy-N,N-dimethyltryptamine (5-MeO-DMT), a serotonin (5-HT) agonist, fenfluramine and p-chloroamphetamine (PCA), which are 5-HT releasers, produce deficits in fear retention as indicated by a notable lack of the immobility resulting from inescapable shocks. Depletion of central 5-HT neurones after long-term PCA treatment (2 X 10 mg/kg) completely blocked the retention impairment resulting from acute PCA (2.5 mg/kg) and fenfluramine (5 mg/kg), and partially blocked the deficit produced by 5-MeO-DMT (4 mg/kg). 5-HT depletion after p-chlorophenylalanine (PCPA) treatment (200, 100, 100 mg/kg, 72, 48 and 24 h before) did not do so; this is in agreement with other findings which suggest the involvement of different 5-HT stores in the action of PCA and PCPA. These data further underline the importance of the ascending 5-HT pathway in aversive conditioning in the rat.