Psychopharmacology
January 1, 1991
C W Callaway, M P Johnson, L H Gold et al.
70 citations
MBDB, a derivative of amphetamine that releases little or no dopamine, caused rats to become hyperactive and suppressed their exploratory behaviors, similar to the effects of MDMA. This hyperactivity lasted over 60 minutes at higher doses. Pretreatment with fluoxetine, a serotonin reuptake inhibitor, blocked MBDB-induced hyperactivity, indicating that the behavioral effects depend on serotonin release rather than dopamine release. Fluoxetine also blocked hyperactivity from related drugs S-(+)3,4-methylenedioxyamphetamine and p-chloroamphetamine. Tissue measurements showed decreased serotonin and its metabolite 5-HIAA after MBDB or S-(+)MDMA, which was prevented by fluoxetine. S-(+)MDMA increased dopamine levels in a fluoxetine-sensitive manner, suggesting serotonin release may indirectly influence dopamine.
European journal of pharmacology
April 7, 1992
C W Callaway, M A Geyer
35 citations
Injecting S-MDMA (a form of MDMA, or ecstasy) directly into a brain region called the nucleus accumbens made rats more active, similar to the effect of amphetamine. Blocking serotonin with fluoxetine did not prevent this hyperactivity, even though it blocks the effects of systemically given S-MDMA. A drug that only releases serotonin, MBDB, did not increase activity when injected into the nucleus accumbens, though it does when given systemically. These results suggest that S-MDMA's effects in the nucleus accumbens are due to its ability to release catecholamines like dopamine, not serotonin, and differ from its systemic actions.
Pharmacology, biochemistry, and behavior
January 1, 1975
M A Geyer, J D Warbritton, D B Menkes et al.
34 citations
Rat startle responses to air puffs were measured during infusion of serotonin (5-HT), a hallucinogenic compound (5-HDMT), or saline. Serotonin reduced startle magnitude in a dose-dependent way, while the hallucinogen increased startle responses. Neither compound specifically affected sensitization or habituation. The findings suggest a central serotonin system that promotes behavioral inhibition, which indoleamine hallucinogens may oppose.
Psychopharmacology
April 1, 2000
S C Dulawa, K A Scearce-Levie, R Hen et al.
26 citations
Prepulse inhibition (PPI), a normal reduction of the startle response when a weak stimulus precedes a startling one, is reduced in several neuropsychiatric disorders. The serotonin 1B (5-HT1B) receptor's role in modulating PPI was examined using 5-HT-releasing agents in wild-type (WT) and 5-HT1B knockout (1BKO) mice. MDMA and MBDB increased PPI in 1BKO mice but did not alter PPI in WT mice. In intact mice, the 5-HT1B/1D antagonist GR 127935 (3.0 mg/kg) with MDMA also increased PPI, indicating that the lack of the 5-HT1B receptor, not developmental changes, causes the PPI increase. Activation of 5-HT1B receptors by serotonin disrupts PPI.