Nootropic Candidates Inhibit Head-Twitches Induced by Mescaline in Mice.

Abstract

ABSTRACT-The effects of various nootropic candidates on mescaline-induced head-twitches were stud ied in mice. The number of head-twitches induced by mescaline (100 mg/kg, s.c.) was significantly re duced by idebenone (32 and 100 mg/kg, i.p.), minaprine (0.32-10 mg/kg, p.o.) and nebracetam (100 mg/kg, p.o.). Cholinesterase inhibitors such as tetrahydroaminoacridine (1 and 10 mg/kg, p.o.), NIK 247 (10 and 18 mg/kg, p.o.) and physostigmine (0.32 mg/kg, i.p.) also suppressed the head-twitch re sponse to mescaline. These results suggest that the direct or indirect cholinergic-activating effects of these drugs may be involved in inhibiting mescaline-induced head-twitches.

Aniracetam attenuates the 5-HT2 receptor-mediated head-twitch response in rodents as a hallucination model

“…However, the cooperative effect with other metabolites (i.e., N-anisoyl-GABA) or the action of aniracetam itself could not be ruled out. With respect to other nootropics, tacrine and idebenone significantly inhibited HTR induced by 5-HTP, consistent with previous results with another 5-HT 2 agonist, mescaline [Yamamoto et al, 1992]. Tacrine acts as a cholinesterase inhibitor, and idebenone has some cholinergic activating action [Yamazaki et al, 1985].…”

“…Matsuno et al [1993] found that p-chloroamphetamine dose-dependently decreased the step-down latencies in the retention test of the passive avoidance task in mice, and physostigmine, tacrine, and 5-HT 2 antagonists attenuated p-chloroamphetamine-induced amnesia. In addition, the direct or indirect cholinergic activating effects of nootropics played an important role in inhibiting mescaline-induced HTR in mice [Yamamoto et al, 1992]. On the contrary, the removal of cholinergic input by a chemical lesion led to a profound and widespread increase in serotonergic activity [Hörtnagl et al, 1987].…”

“…Quattrochi et al [1993] have shown that the rapid eye movement sleep and ponto-geniculo-occipital (PGO) activity were suppressed by the administration of 5-HT 1 agonist, suggesting that the cholinergic/PGO burst cell network was sensitive to serotonergic inhibitory control. In addition, cholinergic activators have been demonstrated to inhibit mescaline-induced head-twitch response (HTR) as a hallucination model [Yamamoto et al, 1992]. Moreover, the intracerebroventricular injection of cholinotoxin in rats decreased acetylcholine (ACh) level and increased serotonin (5-HT) turnover in the hippocampus, indicating that the central cholinergic system exerted an inhibitory control over the serotonergic neurons [Hörtnagl et al, 1987].…”

Effects of hallucinogenic agents mescaline and phencyclidine on zebrafish behavior and physiology

“…The clinical effects of mescaline, similar to the psychedelic action of lysergic acid diethylamide (LSD) and 3,4-methylenedioxymethamphetamine (MDMA), include euphoria, hallucinations, depersonalization and psychoses (Gouzoulis-Mayfrank et al, 1998; Hermle et al, 1992; Schwarz et al, 1956; Wolbach et al, 1962). In rodent models, mescaline modulates locomotion, exploration, cognitive function (Geyer et al, 1979; Koupilova et al, 1999; Palenicek et al, 2008; Sykes, 1986), aggression, startle (Palenicek et al, 2008; Sbordone and Carder, 1974; Sbordone et al, 1979) and motor responses (Canal et al, 2010; Silva and Calil, 1975; Yamamoto et al, 1992). …”

Urine Mescaline Screening With a Biochip Array Immunoassay and Quantification by Gas Chromatography–Mass Spectrometry

“…16,[20][21][22] In rodent models, mescaline modulates locomotion, exploration, cognitive function, 19,[23][24][25] aggression, and startle 19,26,27 and motor responses. [28][29][30] Mescaline is reported to undergo O-demethylation, N-acetylation, and amine oxidation 31,32 ; however, all metabolites are believed to be inactive. 18 There are multiple published analytical methods for mescaline quantification in plasma, 33,34 urine, 35 hair, 36 and postmortem tissues, 37 or as part of a sympathomimetic amine screening assay.…”