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Herein, we demonstrate that selective overexpression of the stress protein heme oxygenase-1 (HO-1) in astrocytes of novel GFAP.HMOX1 transgenic mice results in subcortical oxidative stress and mitochondrial damage\/autophagy; diminished neuronal reelin content (males); induction of Nurr1 and Pitx3 with attendant suppression of their targeting miRNAs, 145 and 133b; increased tyrosine hydroxylase and \u03b1-synuclein expression with downregulation of the targeting miR-7b of the latter; augmented dopamine and serotonin levels in basal ganglia; reduced D\n                    <jats:sub>1<\/jats:sub>\n                    receptor binding in nucleus accumbens; axodendritic pathology and altered hippocampal cytoarchitectonics; impaired neurovascular coupling; attenuated prepulse inhibition (males); and hyperkinetic behavior. The GFAP.HMOX1 neurophenotype bears resemblances to human schizophrenia and other neurodevelopmental conditions and implicates glial HO-1 as a prime transducer of inimical (endogenous and environmental) influences on the development of monoaminergic circuitry. Containment of the glial HO-1 response to noxious stimuli at strategic points of the life cycle may afford novel opportunities for the effective management of human neurodevelopmental and neurodegenerative conditions.\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.6469-11.2012","type":"journal-article","created":{"date-parts":[[2012,8,8]],"date-time":"2012-08-08T12:54:11Z","timestamp":1344430451000},"page":"10841-10853","source":"Crossref","is-referenced-by-count":60,"title":["Schizophrenia-Like Features in Transgenic Mice Overexpressing Human HO-1 in the Astrocytic 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