(Q28590145)

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Amphetamine-induced Fos is reduced in limbic cortical regions but not in the caudate or accumbens in a genetic model of NMDA receptor hypofunction

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scholarly article

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PubMed publication ID

31 January 2017

Amphetamine-induced Fos is reduced in limbic cortical regions but not in the caudate or accumbens in a genetic model of NMDA receptor hypofunction (English)

1 reference

PubMed publication ID

31 January 2017

Glutamate receptor, ionotropic, NMDA1 (zeta 1)

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GOA release 2020-03-11

Jeffrey Lieberman

5

object named as

Jeffrey A. Lieberman

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PubMed publication ID

31 January 2017

author name string

Seiya Miyamoto

1

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PubMed publication ID

31 January 2017

John N. Snouwaert

2

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PubMed publication ID

31 January 2017

Beverly H. Koller

3

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PubMed publication ID

31 January 2017

Sheryl S. Moy

4

1 reference

PubMed publication ID

31 January 2017

Gary E. Duncan

6

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PubMed publication ID

31 January 2017

language of work or name

0 references

publication date

1 December 2004

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PubMed publication ID

31 January 2017

Neuropsychopharmacology

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PubMed publication ID

31 January 2017

29

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PubMed publication ID

31 January 2017

12

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PubMed publication ID

31 January 2017

2180–2188

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PubMed publication ID

31 January 2017

Alterations of benzodiazepine receptors in type II alcoholic subjects measured with SPECT and [123I]iomazenil.

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Phencyclidine-induced dysregulation of dopamine response to amphetamine in prefrontal cortex and striatum

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Subchronic continuous phencyclidine administration potentiates amphetamine-induced frontal cortex dopamine release

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Association of ketamine-induced psychosis with focal activation of the prefrontal cortex in healthy volunteers

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Schizophrenia is associated with elevated amphetamine-induced synaptic dopamine concentrations: evidence from a novel positron emission tomography method

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Amphetamine, cocaine, phencyclidine and nomifensine increase extracellular dopamine concentrations preferentially in the nucleus accumbens of freely moving rats.

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Neurotransmitter interactions in schizophrenia--therapeutic implications

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The glutamatergic dysfunction hypothesis for schizophrenia

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MK801 induces c-fos protein in thalamic and neocortical neurons of rat brain.

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Neuroanatomical characterization of Fos induction in rat behavioral models of anxiety.

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Alterations in regional brain metabolism in genetic and pharmacological models of reduced NMDA receptor function

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Metabolic mapping of the rat brain after subanesthetic doses of ketamine: potential relevance to schizophrenia.

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Deficits in sensorimotor gating and tests of social behavior in a genetic model of reduced NMDA receptor function

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Differential patterns of regional c-Fos induction in the rat brain by amphetamine and the novel wakefulness-promoting agent modafinil

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Targeted disruption of NMDA receptor 1 gene abolishes NMDA response and results in neonatal death

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Provocation of Schizophrenic Symptoms by Intravenous Administration of Methylphenidate

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Recent advances in the phencyclidine model of schizophrenia

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

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Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses

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Increased dopamine transmission in schizophrenia: relationship to illness phases

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Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects

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Whisker-related neuronal patterns fail to develop in the trigeminal brainstem nuclei of NMDAR1 knockout mice

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Is schizophrenia a neurodegenerative disorder? A clinical and neurobiological perspective

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Provocative tests with psychostimulant drugs in schizophrenia

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Neurochemical sensitization in the pathophysiology of schizophrenia: deficits and dysfunction in neuronal regulation and plasticity

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Ketamine-induced exacerbation of psychotic symptoms and cognitive impairment in neuroleptic-free schizophrenics.

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NMDA receptor function and human cognition: the effects of ketamine in healthy volunteers.

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AMPA-receptor involvement in c-fos expression in the medial prefrontal cortex and amygdala dissociates neural substrates of conditioned activity and conditioned reward.

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Recent advances in the neurobiology of schizophrenia

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Effects of ketamine, MK-801, and amphetamine on regional brain 2-deoxyglucose uptake in freely moving mice.

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Blunted brain metabolic response to ketamine in mice lacking D(1A) dopamine receptors

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Reversal of phencyclidine effects by a group II metabotropic glutamate receptor agonist in rats

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Mice with reduced NMDA receptor expression display behaviors related to schizophrenia

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Heteromeric NMDA receptors: molecular and functional distinction of subtypes

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Interaction between the noradrenergic and serotonergic systems in locomotor hyperactivity and striatal expression of Fos induced by amphetamine in rats

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Molecular diversity of glutamate receptors and implications for brain function

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Ketamine-induced NMDA receptor hypofunction as a model of memory impairment and psychosis.

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Glutamate receptor dysfunction and schizophrenia

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Differential interactions of desipramine with amphetamine and methamphetamine: evidence that amphetamine releases dopamine from noradrenergic neurons in the medial prefrontal cortex

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Striatal c-fos induction by drugs and stress in neonatally dopamine-depleted rats given nigral transplants: importance of NMDA activation and relevance to sensitization phenomena.

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The effects of phencyclidine pretreatment on amphetamine-induced behavior and c-Fos expression in the rat.

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The delayed effects of phencyclidine enhance amphetamine-induced behavior and striatal C-Fos expression in the rat.

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NMDA receptors mediate amphetamine-induced upregulation of zif/268 and preprodynorphin mRNA expression in rat striatum

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Amphetamine and dopamine-induced immediate early gene expression in striatal neurons depends on postsynaptic NMDA receptors and calcium.

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Identifiers

10.1038/SJ.NPP.1300548

1 reference

PubMed publication ID

31 January 2017

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0 references

PubMed publication ID

1 reference

PubMed publication ID

31 January 2017

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