Literature DB >> 15765522

Comparative behavioral changes in postpubertal rats after neonatal excitotoxic lesions of the ventral hippocampus and the prefrontal cortex.

Gonzalo Flores1, Adriana B Silva-Gómez, Osvaldo Ibáñez, Remi Quirion, Lalit K Srivastava.   

Abstract

The neonatal ventral hippocampal (nVH) and the neonatal prefrontal cortex (nPFC) lesions in rats have been used as models to test the hypothesis that early neurodevelopmental abnormalities lead to behavioral changes putatively linked to schizophrenia. We investigated the role of the nVH and the nPFC lesions on behavioral characteristics related to locomotor behaviors, social interaction, and grooming. Bilateral ibotenic acid lesions of the VH, the PFC, or both were made in neonatal Sprague-Dawley rats (postnatal day 7, P7) and their behaviors studied at P35 and P60. No significant differences in any of the behaviors were observed between sham animals and rats with ibotenic acid lesions at P35. Postpubertally (at P60), the spontaneous locomotor activity of nVH-lesioned rats was significantly enhanced compared to the sham controls; however, this hyperactivity was reversed by nVH and nPFC double lesions. Neonatal PFC lesion alone did not alter spontaneous activity, although a trend of increased activity was observed. The duration of grooming was significantly decreased in rats with neonatal lesions of the VH. Similar to the data on locomotion, nVH plus nPFC lesion normalized the grooming behavior. Lesion of the PFC alone was without any significant effect on grooming behavior. Neonatal VH-lesioned animals spent less time in active social interaction, and this effect persisted even in nVH plus nPFC-lesioned animals. By itself, nPFC lesion did not alter social behavior. These data suggest that subtle developmental aberrations within PFC caused by nVH lesions, rather than the lesion of PFC itself, may contribute to some of the behavioral changes seen in the nVH-lesioned rats.

Entities:  

Mesh:

Substances:

Year:  2005        PMID: 15765522     DOI: 10.1002/syn.20140

Source DB:  PubMed          Journal:  Synapse        ISSN: 0887-4476            Impact factor:   2.562


  15 in total

1.  Chronic administration of the neurotrophic agent cerebrolysin ameliorates the behavioral and morphological changes induced by neonatal ventral hippocampus lesion in a rat model of schizophrenia.

Authors:  Rubén Antonio Vázquez-Roque; Brenda Ramos; Carolina Tecuatl; Ismael Juárez; Anthony Adame; Fidel de la Cruz; Sergio Zamudio; Raúl Mena; Edward Rockenstein; Eliezer Masliah; Gonzalo Flores
Journal:  J Neurosci Res       Date:  2011-09-19       Impact factor: 4.164

2.  Chronic tolerance to the social consequences of ethanol in adolescent and adult Sprague-Dawley rats.

Authors:  Elena I Varlinskaya; Linda P Spear
Journal:  Neurotoxicol Teratol       Date:  2006-09-09       Impact factor: 3.763

3.  Chronic intermittent ethanol exposure during adolescence: effects on social behavior and ethanol sensitivity in adulthood.

Authors:  Elena I Varlinskaya; Eric Truxell; Linda P Spear
Journal:  Alcohol       Date:  2014-05-15       Impact factor: 2.405

Review 4.  Epigenetics and biomarkers in the staging of neuropsychiatric disorders.

Authors:  Trevor Archer; Richard J Beninger; Tomas Palomo; Richard M Kostrzewa
Journal:  Neurotox Res       Date:  2010-03-17       Impact factor: 3.911

Review 5.  Models of neurodevelopmental abnormalities in schizophrenia.

Authors:  Susan B Powell
Journal:  Curr Top Behav Neurosci       Date:  2010

6.  Affiliative behavior requires juvenile, but not adult neurogenesis.

Authors:  Lan Wei; Michael J Meaney; Ronald S Duman; Arie Kaffman
Journal:  J Neurosci       Date:  2011-10-05       Impact factor: 6.167

Review 7.  Using the MATRICS to guide development of a preclinical cognitive test battery for research in schizophrenia.

Authors:  Jared W Young; Susan B Powell; Victoria Risbrough; Hugh M Marston; Mark A Geyer
Journal:  Pharmacol Ther       Date:  2009-03-06       Impact factor: 12.310

8.  Folate deficiency induces neurodegeneration and brain dysfunction in mice lacking uracil DNA glycosylase.

Authors:  Golo Kronenberg; Christoph Harms; Robert W Sobol; Fernando Cardozo-Pelaez; Heinz Linhart; Benjamin Winter; Mustafa Balkaya; Karen Gertz; Shanna B Gay; David Cox; Sarah Eckart; Michael Ahmadi; Georg Juckel; Gerd Kempermann; Rainer Hellweg; Reinhard Sohr; Heide Hörtnagl; Samuel H Wilson; Rudolf Jaenisch; Matthias Endres
Journal:  J Neurosci       Date:  2008-07-09       Impact factor: 6.167

Review 9.  The neonatal ventral hippocampal lesion as a heuristic neurodevelopmental model of schizophrenia.

Authors:  Kuei Y Tseng; R Andrew Chambers; Barbara K Lipska
Journal:  Behav Brain Res       Date:  2008-12-03       Impact factor: 3.332

10.  Developmental etiology for neuroanatomical and cognitive deficits in mice overexpressing Galphas, a G-protein subunit genetically linked to schizophrenia.

Authors:  M P Kelly; J M Stein; C G Vecsey; C Favilla; X Yang; S F Bizily; M F Esposito; G Wand; S J Kanes; T Abel
Journal:  Mol Psychiatry       Date:  2008-11-25       Impact factor: 15.992

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.