Cesarean plus anoxia at birth induces hyperresponsiveness to locomotor activity by dopamine D2 agonist

Ismael Juárez, Fidel De La Cruz, Sergio Zamudio, Gonzalo Flores

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Transient global anoxia after Cesarean birth in rats may produce alterations in the subcortical DA function and related behaviors. The reports only tested the behavioral changes induced by a general DA agonist, such as amphetamine or apomorphine, in adult rats. Here we investigated the role of perinatal anoxia on the locomotion induced by a specific dopamine (DA) agonist and its relation to the DA D1-like and D2-like receptors, measured by autoradiography at two different ages, prepubertal (35 days old, P35) and postpubertal (60 days old, P60). Cesarean birth with or without (C-only) an additional period of 10 min of the anoxia was done in Sprague-Dawley rats, and the effects of the DA D1-like and D2-like agonist and their receptors were studied at P35 and P60. In addition, a third group of animals born vaginally served as the control. The quantitative autoradiography study of the DA D1-like and D2-like receptors revealed an enhancement of the DA D1-like receptor levels in the nucleus accumbens (NAcc) and dorsolateral part of the caudate-putamen in the prepubertal C-only animals. The post-pubertal C-only rats showed a decrease in the levels of DA D2-like receptors in the NAcc. However, quinpirole, a DA D2 agonist (0.125 and 0.25 mg/kg, s.c.), induced a dose-dependent increase of the locomotor activity in the animals born by Cesarean with anoxia at birth at both ages. Our results suggest that Cesarean with or without anoxia at birth may mediate differently the neurodevelopmental aspects of the dopaminergic system before and after puberty. © 2005 Wiley-Liss, Inc.
Original languageAmerican English
Pages (from-to)236-242
Number of pages211
JournalSynapse
DOIs
StatePublished - 15 Dec 2005

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Dopamine Agonists
Locomotion
Parturition
Dopamine
Nucleus Accumbens
Autoradiography
Quinpirole
Dopamine D1 Receptors
Dopamine D2 Receptors
Apomorphine
Putamen
Amphetamine
Puberty
Sprague Dawley Rats
Hypoxia

Cite this

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title = "Cesarean plus anoxia at birth induces hyperresponsiveness to locomotor activity by dopamine D2 agonist",
abstract = "Transient global anoxia after Cesarean birth in rats may produce alterations in the subcortical DA function and related behaviors. The reports only tested the behavioral changes induced by a general DA agonist, such as amphetamine or apomorphine, in adult rats. Here we investigated the role of perinatal anoxia on the locomotion induced by a specific dopamine (DA) agonist and its relation to the DA D1-like and D2-like receptors, measured by autoradiography at two different ages, prepubertal (35 days old, P35) and postpubertal (60 days old, P60). Cesarean birth with or without (C-only) an additional period of 10 min of the anoxia was done in Sprague-Dawley rats, and the effects of the DA D1-like and D2-like agonist and their receptors were studied at P35 and P60. In addition, a third group of animals born vaginally served as the control. The quantitative autoradiography study of the DA D1-like and D2-like receptors revealed an enhancement of the DA D1-like receptor levels in the nucleus accumbens (NAcc) and dorsolateral part of the caudate-putamen in the prepubertal C-only animals. The post-pubertal C-only rats showed a decrease in the levels of DA D2-like receptors in the NAcc. However, quinpirole, a DA D2 agonist (0.125 and 0.25 mg/kg, s.c.), induced a dose-dependent increase of the locomotor activity in the animals born by Cesarean with anoxia at birth at both ages. Our results suggest that Cesarean with or without anoxia at birth may mediate differently the neurodevelopmental aspects of the dopaminergic system before and after puberty. {\circledC} 2005 Wiley-Liss, Inc.",
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Cesarean plus anoxia at birth induces hyperresponsiveness to locomotor activity by dopamine D2 agonist. / Juárez, Ismael; De La Cruz, Fidel; Zamudio, Sergio; Flores, Gonzalo.

In: Synapse, 15.12.2005, p. 236-242.

Research output: Contribution to journalArticle

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