Neuropharmacology
March 2012
John D Elsworth, Stephanie M Groman, J David Jentsch et al.
Repeated, intermittent administration of the psychotropic NMDA antagonist phencyclidine (PCP) to laboratory animals causes impairment in cognitive and executive functions, modeling important sequelae of schizophrenia; these effects are thought to be due to a dysregulation of neurotransmission within the prefrontal cortex. Atypical antipsychotic drugs have been reported to have measurable, if...
The International Journal of Neuropsychopharmacology
November 2011
John D Elsworth, Tibor Hajszan, Csaba Leranth et al.
Schizophrenia patients, long-term abusers of phencyclidine (PCP), and monkeys treated with PCP all exhibit enduring cognitive deficits. Evidence indicates that loss of prefrontal cortex spine synapses results in cognitive dysfunction, suggesting the presence of synaptic pathology in the monkey PCP model; however, there is no direct evidence of such changes. In this study we use the monkey PCP...
Neuropsychopharmacology
September 2011
John D Elsworth, Bret A Morrow, Tibor Hajszan et al.
Enduring cognitive deficits exist in schizophrenic patients, long-term abusers of phencyclidine (PCP), as well as in animal PCP models of schizophrenia. It has been suggested that cognitive performance and memory processes are coupled with remodeling of pyramidal dendritic spine synapses in prefrontal cortex (PFC), and that reduced spine density and number of spine synapses in the medial PFC of...
Psychopharmacology
June 2007
Bret A Morrow, John D Elsworth, Robert H Roth
Repeated exposure to the N-methyl-D-aspartate antagonist, phencyclidine, has been shown to result in biochemical and cognitive changes similar to aspects of schizophrenia. Recently, emerging evidence indicated that the symptoms of schizophrenia might result at least in part from dysfunction of local circuit neurons containing parvalbumin, including a loss of their axo-axonic projections to...
Neuropsychopharmacology
March 2004
Christopher D. Verrico, J David Jentsch, Robert H Roth et al.
The residual neuropsychological effects of marijuana abuse in man indicate a dysfunction of the attentional/executive systems. Moreover, experimental investigations suggest that repeated, intermittent (subchronic) Delta(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient of marijuana, alters neurotransmission in the frontal cortex of rats and humans, a key neural site mediating...
Synapse
July 2003
Christopher D. Verrico, J David Jentsch, Robert H Roth
Long-term abuse of delta-9-tetrahydrocannabinol (THC), the major psychoactive constituent of marijuana, produces behavioral and metabolic signs of frontal cortical dysfunction in humans; these effects persist even after short-term abstinence. Based on a preliminary finding that repeated administration of THC to rats reduces basal frontal cortical dopamine turnover (Jentsch et al. [1998]...