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J. David Jentsch

Researcher at Binghamton University

Publications -  96
Citations -  7667

J. David Jentsch is an academic researcher from Binghamton University. The author has contributed to research in topics: Dopamine & Impulsivity. The author has an hindex of 42, co-authored 89 publications receiving 7156 citations. Previous affiliations of J. David Jentsch include University of Pittsburgh & Semel Institute for Neuroscience and Human Behavior.

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The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia.

TL;DR: To support the contention that NMDA receptor antagonist administration represents a viable model of schizophrenia, the behavioral and neurobiological effects of these drugs are discussed, especially with regard to differing profiles following single-dose and long-term exposure.
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Enduring Cognitive Deficits and Cortical Dopamine Dysfunction in Monkeys After Long-Term Administration of Phencyclidine

TL;DR: The data suggest that repeated administration of phencyclidine in monkeys may be useful for studying psychiatric disorders associated with cognitive dysfunction and dopamine hypofunction in the prefrontal cortex, particularly schizophrenia.
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The HMG-CoA Reductase Inhibitor Lovastatin Reverses the Learning and Attention Deficits in a Mouse Model of Neurofibromatosis Type 1

TL;DR: Lovastatin decreased the enhanced brain p21Ras-MAPK activity of the nf1+/- mice, rescued their LTP deficits, and reversed their spatial learning and attention impairments, demonstrating that lovastatin may prove useful in the treatment of Neurofibromatosis Type 1.
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A Neurobehavioral Systems Analysis of Adult Rats Exposed to Methylazoxymethanol Acetate on E17: Implications for the Neuropathology of Schizophrenia

TL;DR: The "MAM-E17" rodent models key aspects of neuropathology in circuits that are highly relevant to schizophrenia are examined, including cognitive inflexibility, orofacial dyskinesias, sensorimotor gating deficits and a post-pubertal-emerging hyper-responsiveness to amphetamine.
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Impairments of reversal learning and response perseveration after repeated, intermittent cocaine administrations to monkeys.

TL;DR: The results indicate that repeated cocaine administrations produce enduring impairments of object discrimination learning when the inhibition of a previously conditioned response is required and suggest that long-term cocaine administration may disrupt orbitofrontal efferents to the striatum, resulting in impaired inhibition of established conditioned responses.