ArticlePharmacology, biochemistry, and behavior2008
Atypical anti-schizophrenic drugs prevent changes in cortical N-methyl-D-aspartate receptors and behavior following sub-chronic phencyclidine administration in developing rat pups.
Article in Pharmacology, biochemistry, and behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Risperidone accelerates bone loss in mice models of schizophrenia by inhibiting osteoblast autophagy.Heliyon · 2024Article
- Neonatal phencyclidine as a model of sex-biased schizophrenia symptomatology in adolescent mice.Psychopharmacology · 2023Article
- Modified climbing fiber/Purkinje cell synaptic connectivity in the cerebellum of the neonatal phencyclidine model of schizophrenia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neonatal phencyclidine and social isolation in the rat: effects of clozapine on locomotor activity, social recognition, prepulse inhibition, and executive functions deficits.Psychopharmacology · 2021Article
- Olanzapine Prevents the PCP-induced Reduction in the Neurite Outgrowth of Prefrontal Cortical Neurons via NRG1.Scientific reports · 2016Article
- Local inactivation of Gpr88 in the nucleus accumbens attenuates behavioral deficits elicited by the neonatal administration of phencyclidine in rats.Molecular psychiatry · 2015Article
- Neonatal phencyclidine administration and post-weaning social isolation as a dual-hit model of 'schizophrenia-like' behaviour in the rat.Psychopharmacology · 2014Article
- Chronic nicotine attenuates phencyclidine-induced impulsivity in a mouse serial reaction time task.Behavioural brain research · 2014Article
- Animal models of schizophrenia.British journal of pharmacology · 2011Review
- Brain-derived neurotrophic factor prevents phencyclidine-induced apoptosis in developing brain by parallel activation of both the ERK and PI-3K/Akt pathways.Neuropharmacology · 2010Article
- Differential role of N-methyl-D-aspartate receptor subunits 2A and 2B in mediating phencyclidine-induced perinatal neuronal apoptosis and behavioral deficits.Neuroscience · 2009Article
- Long-term effects of neonatal MK-801 treatment on prepulse inhibition in young adult rats.Psychopharmacology · 2009Article
- Deficits in adult prefrontal cortex neurons and behavior following early post-natal NMDA antagonist treatment.Pharmacology, biochemistry, and behavior · 2009Article
- Activation of dopamine D1 receptors blocks phencyclidine-induced neurotoxicity by enhancing N-methyl-D-aspartate receptor-mediated synaptic strength.Journal of neurochemistry · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We sought to determine the relationship between phencyclidine (PCP)-induced alterations in behavior and NMDAR expression in the cortex by examining the effect of anti-schizophrenic drug treatment on both. Sprague-Dawley rat pups were pretreated with risperidone or olanzapine prior to treatment with PCP on postnatal day 7 (PN7) or sub-chronically on PN7, 9, and 11. Pre-pulse inhibition (PPI) of acoustic startle was measured on PN24-26 and following a challenge dose of 4 mg/kg PCP, locomotor activity was measured on PN28-35. PCP treatment on PN7 did not cause a deficit in PPI, but did cause locomotor sensitization. This was prevented by both antipsychotics. PCP treatment on PN7 caused an up-regulation of NR1 and NR2B, which was not affected by either anti-schizophrenic drug. PCP treatment on PN7, 9, and 11 caused a deficit in PPI and a sensitized locomotor response to PCP challenge as well as an up-regulation of NR1 and NR2A, all of which were prevented by both atypical anti-schizophrenic drugs. These data support the hypothesis that sub-chronic, but not single injection PCP treatment in developing rats results in behavioral alterations that are sensitive to antipsychotic drugs and these behavioral changes observed could be related to up-regulation of cortical NR1/NR2A receptors.
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