Prenatal methylazoxymethanol acetate alters behavior and brain NGF levels in young rats: a possible correlation with the development of schizophrenia-like deficits - PubMed (original) (raw)

Comparative Study

Prenatal methylazoxymethanol acetate alters behavior and brain NGF levels in young rats: a possible correlation with the development of schizophrenia-like deficits

M Fiore et al. Neuropharmacology. 1999 Jun.

Abstract

It has been hypothesized that a deleterious key contribution to schizophrenia (SZ) development is a failure of migration and setting of young neurons into their appropriate cortical target sites, particularly in the entorhinal cortex (EC). To test this hypothesis in an animal model, we injected, in pregnant rats, on gestational day (GD) 9, or 10, or 11, or 12, the antimitotic compound methylazoxymethanolacetate (MAM) known to cause EC neuronal loss. We investigated whether or not EC disruption during prenatal development is able to affect behavior, including memory and learning, and brain nerve growth factor (NGF). Prenatally MAM treated young rats didn't display gross behavioral changes in social interaction, open-field and novel object investigation tests. By contrast, GD11 and GD12 MAM treated rats had a retardation in passive avoidance acquisition, while, in GD12 animals, pain sensitivity was reduced. GD12 animals also showed increased NGF in the EC and remaining cortex. MAM treated animals showed no changes in paw NGF or substance P levels suggesting that the altered nociceptive response is not related to local downregulation of these two molecules. The possibility that these behavioral and biochemical alterations might be associated with the onset of SZ is discussed.

PubMed Disclaimer

Cited by

Schizophrenia-relevant behavioral testing in rodent models: a uniquely human disorder?
Powell CM, Miyakawa T. Powell CM, et al. Biol Psychiatry. 2006 Jun 15;59(12):1198-207. doi: 10.1016/j.biopsych.2006.05.008. Biol Psychiatry. 2006. PMID: 16797265 Free PMC article. Review.
A volumetric screening procedure for the Göttingen minipig brain.
Jelsing J, Olsen AK, Cumming P, Gjedde A, Hansen AK, Arnfred S, Hemmingsen R, Pakkenberg B. Jelsing J, et al. Exp Brain Res. 2005 May;162(4):428-35. doi: 10.1007/s00221-004-2026-7. Epub 2005 Jan 25. Exp Brain Res. 2005. PMID: 15668795
Altered prepulse inhibition in rats treated prenatally with the antimitotic Ara-C: an animal model for sensorimotor gating deficits in schizophrenia.
Elmer GI, Sydnor J, Guard H, Hercher E, Vogel MW. Elmer GI, et al. Psychopharmacology (Berl). 2004 Jul;174(2):177-89. doi: 10.1007/s00213-003-1757-7. Psychopharmacology (Berl). 2004. PMID: 14985933
Disruption of cortical-limbic interaction as a substrate for comorbidity.
Grace AA. Grace AA. Neurotox Res. 2006 Oct;10(2):93-101. doi: 10.1007/BF03033238. Neurotox Res. 2006. PMID: 17062371 Review.
A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia.
Moore H, Jentsch JD, Ghajarnia M, Geyer MA, Grace AA. Moore H, et al. Biol Psychiatry. 2006 Aug 1;60(3):253-64. doi: 10.1016/j.biopsych.2006.01.003. Epub 2006 Apr 11. Biol Psychiatry. 2006. PMID: 16581031 Free PMC article.

Prenatal methylazoxymethanol acetate alters behavior and brain NGF levels in young rats: a possible correlation with the development of schizophrenia-like deficits - PubMed (original) (raw)