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Down-Regulation of Hippocampal Genes Regulating Dopaminergic, GABAergic, and Glutamatergic Function Following Combined Neonatal Phencyclidine and Post-Weaning Social Isolation of Rats as a Neurodevelopmental Model for Schizophrenia
Author(s) -
Philip Gaskin,
Maria ToledoRodriguez,
S P H Alexander,
K.C.F. Fone
Publication year - 2016
Publication title -
the international journal of neuropsychopharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 107
eISSN - 1469-5111
pISSN - 1461-1457
DOI - 10.1093/ijnp/pyw062
Subject(s) - phencyclidine , prepulse inhibition , dopaminergic , gabaergic , dopamine , glutamatergic , hippocampal formation , neuroscience , schizophrenia (object oriented programming) , nmda receptor , psychology , glutamate receptor , endocrinology , medicine , pharmacology , biology , psychiatry , receptor , inhibitory postsynaptic potential
Dysfunction of dopaminergic, GABAergic, and glutamatergic function underlies many core symptoms of schizophrenia. Combined neonatal injection of the N-methyl-D-aspartate (NMDA) receptor antagonist, phencyclidine (PCP), and post-weaning social isolation of rats produces a behavioral syndrome with translational relevance to several core symptoms of schizophrenia. This study uses DNA microarray to characterize alterations in hippocampal neurotransmitter-related gene expression and examines the ability of the sodium channel blocker, lamotrigine, to reverse behavioral changes in this model.

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