Prenatal corticosterone treatment induces long-term changes in spontaneous and apomorphine-mediated motor activity in male and female rats.
The potential influence of glucocorticoids on fetal brain development was investigated after corticosterone administration via pellets to pregnant rats during the last trimester of gestation. We examined both spontaneous motor activity and dopamine-mediated motor responses to apomorphine, a D1, D2 and D3 receptor agonist, given at a postsynaptic dose (1 mg/kg, s.c.) to both prepubertal and adult male and female offspring. Prenatal corticosterone was found to produce the following alterations in the offspring. (1) Prepubertal stage: Male offspring: a statistically significant (P < 0.05) increase was observed in spontaneous rearing, motility and locomotion (activity measured during the first 30 min) without changes in apomorphine-induced motor responses. Female offspring: a reduction (P < 0.05) only in spontaneous rearing activity was observed during the exploratory phase (activity measured during the first 10 min) without significant changes in apomorphine-induced motor responses. (2) Adult stage: Male offspring: the exploratory activity to the novel environment was increased (P < 0.05) without significant changes in apomorphine-induced motor activity. Female offspring: an increase (P < 0.05) in spontaneous locomotion was observed during the first 30 min of testing without significant changes in exploratory activity to the novel environment. However, the apomorphine-induced motility and locomotion were reduced (P < 0.05) during the first 30 min. These observations indicate that prenatal corticosterone induces both short-term and long-term changes in spontaneous motor activity as well as long-lasting alterations in dopamine receptor response in the motor network mechanisms controlled by DA receptors. These changes are in part age and sex-dependent. The possible relationship between prenatal programming of the mesolimbic and nigrostriatal dopaminergic pathways by corticosterone and the observed changes in motor function is discussed.
Diaz
R
R
Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
Fuxe
K
K
Ogren
S O
SO
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001058:Apomorphine / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D003345:Corticosterone / Q000097:blood / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology*; D005260:Female; D008124:Locomotion / Q000187:drug effects; D008297:Male; D009043:Motor Activity / Q000187:drug effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000819:agonists / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000502:physiology; D050637:Receptors, Dopamine D3; D012737:Sex Factors; D012741:Sexual Maturation; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D018491:Dopamine Agonists; C493595:Drd3 protein, rat; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D050637:Receptors, Dopamine D3; D001058:Apomorphine; D003345:Corticosterone