PMID- 9138441 OWN - NLM STAT- MEDLINE DCOM- 19970508 LR - 20150311 IS - 0893-133X (Print) IS - 0893-133X (Linking) VI - 16 IP - 3 DP - 1997 Mar TI - Characterization of the disruptions of prepulse inhibition and habituation of startle induced by alpha-ethyltryptamine. PG - 246-55 AB - Alpha-ethyltryptamine (AET), a monoamine oxidase inhibitor and potent monoamine releasing agent, has been sold illicitly as a substitute for the entactogen 3,4-methylenedioxy-N-methylamphetamine (MDMA), and is the first example of an indolealkylamine analog demonstrated to substitute in MDMA-trained animals. Previous studies have demonstrated that MDMA and AET have similar effects on unconditioned motor behavior in rats. Furthermore, the locomotor-activating effects of both MDMA and AET are blocked by pretreatment with fluoxetine, a selective serotonin (5-HT) uptake inhibitor, suggesting that the two compounds may share a presynaptic mechanism of action. This study examined the effects of AET using measures of startle plasticity, specifically prepulse inhibition (PPI), and habituation. PPI, a measure of sensorimotor gating, is reduced in rats treated with hallucinogens, 5-HT releasers, and dopamine agonists. In contrast, startle habituation is reduced in rats treated with hallucinogens and 5-HT releasers. AET (1.25, 2.5, 5, and 10 mg/kg) decreased PPI of acoustic startle and reduced the habituation of tactile startle. To determine whether AET produces these effects via pre- or postsynaptic actions, fluoxetine (10 mg/kg) was used as a pretreatment. By itself, fluoxetine did not disrupt PPI, but did reduce startle habituation. Fluoxetine pretreatment prevented the AET-induced disruption of PPI and reduced the AET-induced disruption of startle habituation. Combined with previous findings, these results confirm that AET produces behavioral effects that mimic those of other indirect 5-HT agonists and that the effects of AET on startle plasticity are due to the release of presynaptic 5-HT. FAU - Martinez, D L AU - Martinez DL AD - Department of Neuroscience, University of California, San Diego, La Jolla 92093-0804, USA. FAU - Geyer, M A AU - Geyer MA LA - eng GR - K05MH01228/MH/NIMH NIH HHS/United States GR - R02DA02925/DA/NIDA NIH HHS/United States GR - R37MH42228/MH/NIMH NIH HHS/United States GR - etc. PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - Neuropsychopharmacology JT - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JID - 8904907 RN - 0 (Serotonin Receptor Agonists) RN - 0 (Tryptamines) RN - 01K63SUP8D (Fluoxetine) RN - GR181O3R32 (etryptamine) SB - IM MH - Animals MH - Dose-Response Relationship, Drug MH - Fluoxetine/pharmacology MH - Male MH - Rats MH - Rats, Sprague-Dawley MH - Reflex, Startle/*drug effects MH - Serotonin Receptor Agonists/*pharmacology MH - Tryptamines/antagonists & inhibitors/*pharmacology EDAT- 1997/03/01 00:00 MHDA- 1997/03/01 00:01 CRDT- 1997/03/01 00:00 PHST- 1997/03/01 00:00 [pubmed] PHST- 1997/03/01 00:01 [medline] PHST- 1997/03/01 00:00 [entrez] AID - S0893133X96002400 [pii] AID - 10.1016/S0893-133X(96)00240-0 [doi] PST - ppublish SO - Neuropsychopharmacology. 1997 Mar;16(3):246-55. doi: 10.1016/S0893-133X(96)00240-0.