title: Neonatal lesions of the left entorhinal cortex affect dopamine metabolism in the rat brain.
abstract: The present study was performed to determine the effects of neonatal excitotoxic lesions of the left entorhinal cortex on dopamine (DA) metabolism and release in limbic regions of the rat brain. Quinolinic acid or phosphate buffered saline was infused into the left entorhinal cortex of rat pups on postnatal day 7 (PD7). Concentrations of DA,3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the lateral amygdala, nucleus accumbens, caudate-putamen, and medial prefrontal cortex were determined in the postmortem brains of lesioned and sham-operated rats on PD35 and PD56. On PD35, concentrations of DA in the bilateral lateral amygdala and HVA in the left lateral amygdala were significantly increased in lesioned rats compared with sham-operated animals, while no significant change was observed in the other three brain areas. On PD56, in addition to the increased concentration of DA in the left lateral amygdala, those of DA, DOPAC and HVA in the caudate-putamen, and DA in the nucleus accumbens were found to be increased, but DA concentrations in the right medial prefrontal cortex were decreased. The DOPAC/DA concentration ratio was, however, decreased in the amygdala and nucleus accumbens of the lesioned rats. In an in vivo microdialysis study, methamphetamine (MAP: 2 mg/kg, i.p.)-induced DA release in the amygdala of lesioned rats was significantly enhanced compared with sham-operated rats on both PD35 and PD56. There were no significant differences in MAP-induced DA release in the caudate-putamen between the sham-operated and lesioned rats at any time point. These findings provide evidence that neonatally induced structural abnormalities in the entorhinal cortex affect DA transmission in the limbic regions at the adolescent stage.
authors.affiliation: Department of Neuropsychiatry, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630, Sugitani, Toyama, Japan. uehara@ms.toyama-mpu.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Uehara
authors.forename: Y
authors.initials: Y
authors.lastname: Tanii
authors.forename: T
authors.initials: T
authors.lastname: Sumiyoshi
authors.forename: M
authors.initials: M
authors.lastname: Kurachi
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000679:Amygdala / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000378:metabolism*; D002421:Caudate Nucleus / Q000378:metabolism; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D018728:Entorhinal Cortex / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006719:Homovanillic Acid / Q000378:metabolism; D008694:Methamphetamine / Q000494:pharmacology; D017551:Microdialysis; D009498:Neurotoxins / Q000633:toxicity*; D009714:Nucleus Accumbens / Q000378:metabolism; D017397:Prefrontal Cortex / Q000378:metabolism; D017378:Quinolinic Acid / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D012559:Schizophrenia / Q000473:pathology; D013702:Temporal Lobe / Q000473:pathology
chemical_list: D018491:Dopamine Agonists; D009498:Neurotoxins; D015102:3,4-Dihydroxyphenylacetic Acid; D008694:Methamphetamine; D017378:Quinolinic Acid; D004298:Dopamine; D006719:Homovanillic Acid