Skip to content

H Y Meltzer

5 papers in the library · 141 citations · publishing 1978-1989

Papers

Altered responses to serotonergic agents in Fawn-Hooded rats.

Pharmacology, biochemistry, and behavior March 1, 1985 G A Gudelsky, J I Koenig, H Y Meltzer 54 citations

Rats of the Fawn-Hooded (FH) strain show stronger behavioral responses to certain serotonin-related drugs compared to Sprague-Dawley (SD) rats. Specifically, FH rats exhibited significantly more "wet dog" shakes when given quipazine and a greater hyperthermic response to 5MeODMT. Conversely, the hypothermic effect of 8-OH-DPAT was significantly weaker in FH rats than in SD rats. These results suggest that central nervous system serotonergic mechanisms differ markedly between the two rat strains.

Selective cross-tolerance to 5-HT1A and 5-HT2 receptor-mediated temperature and corticosterone responses.

Pharmacology, biochemistry, and behavior August 1, 1989 J F Nash, H Y Meltzer, G A Gudelsky 40 citations

Repeated administration of 5-MeODMT (3 mg/kg, twice daily for 14 days) in animals reduced the hypothermia and corticosterone secretion caused by an acute challenge with the 5-HT1A agonist 8-OH-DPAT, compared to vehicle-treated animals. Chronic 5-MeODMT did not affect hyperthermia or corticosterone secretion from the 5-HT2 agonist MK-212. Repeated administration of DOI (1 mg/kg daily for 7 days) reduced corticosterone but not body temperature increases from MK-212, and did not alter responses to 8-OH-DPAT. These results suggest that chronic 5-MeODMT selectively reduces 5-HT1A receptor-mediated responses, while chronic DOI selectively reduces 5-HT2 receptor-mediated corticosterone secretion without affecting thermoregulatory responses, supporting the independence of these receptor systems.

Stimulation of rat prolactin secretion by indolealkylamine hallucinogens.

Psychopharmacology April 11, 1978 H Y Meltzer, R G Fessler, M Simonovic et al. 24 citations

Several hallucinogenic indoleamine drugs, including N,N-dimethyltryptamine (N,N-DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine, increased levels of the hormone prolactin (PRL) in rat plasma. The effect of N,N-DMT, psilocybin, and bufotenin was blocked by methysergide, a serotonin receptor blocker. Inhibiting serotonin synthesis with parachlorophenylalanine (PCPA) made the PRL increase from N,N-DMT and psilocybin stronger. A toxin that selectively damages serotonin neurons also enhanced the PRL response to N,N-DMT. These results suggest the drugs stimulate PRL release by acting as serotonin agonists. Bufotenin, which poorly crosses the blood-brain barrier, had the strongest effect on PRL, hinting that the relevant serotonin receptors might be outside the barrier or that central receptors are especially sensitive to it.

Biphasic effect of 5-methoxy-N,N-dimethyltryptamine on rat prolactin secretion.

Brain research August 8, 1983 M Simonovic, H Y Meltzer 12 citations

5-MeODMT, a serotonin receptor agonist, has a two-phase effect on prolactin secretion in rats. It initially causes a short, dose-dependent increase in serum prolactin levels, lasting less than 30 minutes. After 30 minutes, it inhibits prolactin release stimulated by other serotonin agonists, alpha-methylparatyrosine, or low-dose haloperidol, but does not alter the effect of gamma-butyrolactone or high-dose haloperidol. The initial rise likely results from activating postsynaptic serotonin receptors, while the later inhibition appears due to increased activity of dopamine neurons. This biphasic pattern is also seen with quipazine but not with 5-MeOT, which does not cross the blood-brain barrier.

Repeated administration of 5-methoxy-N,N-dimethyltryptamine to male rats potentiates stimulation of prolactin secretion by serotonin agonists.

European journal of pharmacology October 15, 1979 M Simonovic, H Y Meltzer 11 citations

Repeated injections of the serotonin agonist 5MeODMT in rats gradually increased the prolactin-releasing effect of that drug and two other serotonin agonists, but did not change the prolactin response to anti-dopaminergic drugs. The enhanced response appears to result from sensitization of the serotonin system involved in prolactin regulation.