Neuropsychopharmacology
November 2001
Carl L. Hart, W Van Gorp, Margaret Haney et al.
Although the ability to perform complex cognitive operations is assumed to be impaired following acute marijuana smoking, complex cognitive performance after acute marijuana use has not been adequately assessed under experimental conditions. In the present study, we used a within-participant double-blind design to evaluate the effects acute marijuana smoking on complex cognitive performance in...
Neuropsychopharmacology
October 1, 2001
Adrienne C. Lahti, M A Weiler, B A Tamara Michaelidis et al.
This study evaluates the effects of ketamine on healthy and schizophrenic volunteers (SVs) in an effort to define the detailed behavioral effects of the drug in a psychosis model. We compared the effects of ketamine on normal and SVs to establish the comparability of their responses and the extent to which normal subjects might be used experimentally as a model. Eighteen normal volunteers (NVs)...
Neuropsychopharmacology
July 1, 2001
E J Duncan, S H Madonick, A Parwani et al.
The clinical similarities between PCP psychosis and schizophrenia have contributed importantly to the development of the glutamate hypothesis of schizophrenia. Sensory gating, as measured by prepulse inhibition of the acoustic startle reflex (PPI), is impaired in patients with schizophrenia. In animals, the noncompetitive NMDA antagonists PCP and ketamine disrupt PPI in a way that resembles the...
Neuropsychopharmacology
March 1, 2001
S V Kyosseva, S M Owens, A D Elbein et al.
We have previously demonstrated elevation of the extracellular signal-regulated kinase (ERK) pathway in the cerebellum from patients with schizophrenia, an illness that may involve dysfunction of the N-methyl-D-aspartate (NMDA) receptor. Since the NMDA antagonist, phencyclidine (PCP), produces schizophrenic-like symptoms in humans, and abnormal behavior in animals, we examined the effects of...
Neuropsychopharmacology
June 2000
W B West, A Lou, K Pechersky et al.
Drugs such as PCP and MK-801 can cause psychotic reactions in humans by antagonizing NMDA receptors. This action is ultimately toxic to certain cortical neurons and may be one mechanism underlying neurodegenerative diseases, including schizophrenia. It has been reported that hallucinogens such as LSD, DOM, and DOI can block the neurotoxic effects of NMDA antagonists, possibly by activating...
Neuropsychopharmacology
May 1, 2000
Matthias E. Liechti, Christine Baumann, Alex Gamma et al.
3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”) is a recreational drug that has been shown to release serotonin (5-HT) and dopamine (DA) in animals. The effect of MDMA on 5-HT release can be blocked by 5-HT uptake inhibitors such as citalopram, suggesting that MDMA interacts with the 5-HT uptake site. It is unknown whether this mechanism is also responsible for the psychological effects of...
Neuropsychopharmacology
August 1, 1999
J Backstrom
55 citations
For more than 40 years the hallucinogen lysergic acid diethylamide (LSD) has been known to modify serotonin neurotransmission. With the advent of molecular and cellular techniques, we are beginning to understand the complexity of LSD's actions at the serotonin 5-HT2 family of receptors. Here, we discuss evidence that signaling of LSD at 5-HT2C receptors differs from the endogenous agonist...
Neuropsychopharmacology
August 1999
George K. Aghajanian, Gerard J. Marek
This brief review traces the serotonin (5-HT) hypothesis of the action of hallucinogenic drugs from the early 1950s to the present day. There is now converging evidence from biochemical, electrophysiological, and behavioral studies that the two major classes of psychedelic hallucinogens, the indoleamines (e.g., LSD) and the phenethylamines (e.g., mescaline), have a common site of action as...
Neuropsychopharmacology
July 1, 1999
C Zubaran, M Shoaib, I P Stolerman et al.
31 citations
The discriminative stimulus effects of ibogaine and noribogaine in rats have been examined in relation to their concentrations in blood plasma and brain regions and to receptor systems through which they have been proposed to act. Rats were trained to discriminate ibogaine (10 mg/kg i.p.), the NMDA antagonist dizocilpine (0.08 mg/kg i.p.) or the kappa-opioid agonist U50,488 (5 mg/kg i.p.) from...
Neuropsychopharmacology
July 1, 1999
Z A Martinez, G D Ellison, Mark A. Geyer et al.
Phencyclidine (PCP), a non-competitive NMDA antagonist with actions at multiple other central nervous system receptors, can cause both acute and lasting psychoses in humans, and has also been used in cross-species models of psychosis. Acute exposure to PCP in rats produces behavioral changes, including a loss of prepulse inhibition (PPI) of the startle reflex, which parallels the loss of PPI...
Neuropsychopharmacology
July 1, 1999
J Väisänen, A M Lindén, M Lakso et al.
We have characterized excitatory effects of non-competitive NMDA receptor antagonists MK-801, PCP, and ketamine in the rat entorhinal cortex and in cultured primary entorhinal cortical neurons using expression of immediate early gene c-fos as an indicator. NMDA receptor antagonists produced a strong and dose-dependent increase in c-fos mRNA and protein expression confined to neurons in the...
Neuropsychopharmacology
June 1, 1999
Euphrosyne Gouzoulis‐mayfrank
224 citations
The neurometabolic effects of the hallucinogen psilocybin (PSI; 0.2 mg/kg), the entactogen 3,4-methylenedioxyethylamphetamine (MDE; 2 mg/kg) and the stimulant d-methamphetamine (METH; 0.2-0.4 mg/kg) and the drugs' interactions with a prefrontal activation task were investigated in a double-blind, placebo-controlled human [F-18]fluorodeoxyglucoseFDG-positron emission tomographicPET study (each...
Neuropsychopharmacology
May 1999
Franz X. Vollenweider, P Vontobel, Daniel Hell et al.
The modulating effects of serotonin on dopamine neurotransmission are not well understood, particularly in acute psychotic states. Positron emission tomography was used to examine the effect of psilocybin on the in vivo binding of [11C]raclopride to D2-dopamine receptors in the striatum in healthy volunteers after placebo and a psychotomimetic dose of psilocybin (n = 7). Psilocybin is a potent...
Neuropsychopharmacology
July 1, 1998
F Sams-Dodd
D-amphetamine (AMPH) and phencyclidine (PCP) can induce a model psychosis that mimic the positive symptoms of schizophrenia, but only PCP also mimics the negative symptoms. Recent studies in the rat social interaction test have shown that PCP, and not AMPH, induce social withdrawal following single and repeated injections, and this effect may, therefore, be used to model negative symptoms....
Neuropsychopharmacology
September 1997
H K Kramer, Jose C Poblete, Efrain C. Azmitia
This report further characterizes the intermediate metabolic effects of the psychotropic amphetamine derivative, 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy"), on the activity of second messenger-dependent kinases. Previous work has demonstrated that two injections of MDMA (20 mg/kg) elicits a prolonged translocation of the calcium and phospholipid-dependent enzyme, protein kinase C...
Neuropsychopharmacology
June 1997
J D Jentsch, E Andrusiak, A Tran et al.
The present study examined delta 9-tetrahydrocannabinol (THC)-induced alterations in monoamine transmission in the rat forebrain as well as the effects of the enantiomers of 3-amino-1-hydroxypyrrolid-2-one (HA966) on the monoamine response to THC. Activation of dopamine (DA) and norepinephrine (NE) but not serotonin (5-HT) turnover in the prefrontal cortex (PFC) was observed after THC (5 mg/kg...
Neuropsychopharmacology
May 1997
Franz X. Vollenweider, K L Leenders, C Scharfetter et al.
The effects of the indolehallucinogen psilocybin, a mixed 5-HT2 and 5-HT1 agonist, on regional cerebral glucose metabolism were investigated in 10 healthy volunteers with PET and [F-18]-fluorodeoxyglucose (FDG) prior to and following a 15- or 20-mg dose of psilocybin. Psychotomimetic doses of psilocybin were found to produce a global increase in cerebral metabolic rate of glucose (CMRglu) with...
Neuropsychopharmacology
August 1996
J H Kehne, H J Ketteler, T C McCloskey et al.
(+/-)3,4-Methylenedioxymethamphetamine (MDMA) releases dopamine and serotonin in vivo and stimulates locomotor activity. Previous work demonstrated that MDMA-stimulated dopamine release could be reduced by the selective 5-HT2A receptor antagonist [R-(+)-a- (2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinem ethanol] (MDL 100,907). In the present study MDL 100,907 significantly...
Neuropsychopharmacology
June 1996
K R Bonson, J W Buckholtz, D L Murphy
This study investigates the possible interactions of antidepressant agents and hallucinogens in humans through structured interviews using a standardized questionnaire. Volunteer subjects recruited through announcements placed on the Internet or other sources were asked to describe the somatic, hallucinatory, and psychological effects of self-administered LSD prior to and during chronic...
Neuropsychopharmacology
May 1996
A K Malhotra, D A Pinals, H Weingartner et al.
A rapidly growing body of preclinical data has implicated the glutamatergic N-methyl-d-aspartate (NMDA) receptor in memory and other cognitive processes. There is comparatively less information about this receptor system in human cognition. We examined the effects of subanesthetic doses of ketamine, a noncompetitive NMDA receptor antagonist, on two forms of memory, free recall and recognition,...
Neuropsychopharmacology
April 1, 1996
H D Abraham, A M Aldridge, P Gogia
155 citations
Hallucinogenic drugs have been inhaled, ingested, worshipped, and reviled since prehistory. With the purification and synthesis of bontanical preparations and the ensuing discovery of chemically unique agents, hope was raised regarding their therapeutic potential, but this hope has been clouded by an epidemic of abuse and an inventory of adverse effects. This review examines aspects of that...
Neuropsychopharmacology
August 1, 1995
Adrienne C. Lahti, B Koffel, D LaPorte et al.
We administered ketamine to schizophrenic individuals in a double-blind, placebo-controlled design using a range of subanesthetic doses (0.1, 0.3, and 0.5 mg/kg) to evaluate the nature, dose characteristics, time course, and neuroleptic modulation of N-methyl-D-aspartate (NMDA) antagonist action on mental status in schizophrenia. Ketamine induced a dose-related, short (< 30 minutes) worsening...
Neuropsychopharmacology
July 1994
E T Leonardi, Efrain C. Azmitia
3,4-Methylenedioxymethamphetamine (MDMA), a serotonin (5-HT) neurotoxin, has been shown to promote the release of serotonin (5-HT) and block its reuptake. The increased buildup of extracellular 5-HT should normally be degraded by monoamine oxidase (MAO). The effects of both enantiomers of MDMA were examined on MAO-A and monoamine oxidase-B (MAO-B) activity in rat brain homogenates. Both...
Neuropsychopharmacology
April 1994
U D McCann, A Ridenour, Y Shaham et al.
(+/-)3,4-Methylenedioxymethamphetamine (MDMA; "Ecstasy"), an increasingly popular recreational drug, is known to damage brain serotonin 5-hydroxytryptamine (5-HT) neurons in experimental animals. Whether MDMA is neurotoxic in humans has not been established. Thirty MDMA users and 28 controls were admitted to a controlled inpatient setting for measurement of biologic and behavioral indexes of...
Neuropsychopharmacology
May 1993
E Gouzoulis, U Von Bardeleben, A Rupp et al.
The drug 3,4-methylenedioxyethamphetamine ([MDE] also known as "Eve") is a less toxic analog of 3,4-methylenedioxymethamphetamine (also known as "Ecstasy") with similar psychotropic effects in humans. In a double-blind placebo-controlled, cross-over study we administered 140 mg of MDE or placebo orally to eight healthy male volunteers at 1:30 P.M. Serum cortisol, prolactin (PRL), and growth...