Rats given dopamine-depleting brain lesions as neonates are subsensitive to dopaminergic antagonists as adults.
Extensive damage to central dopamine (DA)-containing neurons are known to produce akinesia and sensory neglect when the lesions are made in adult rats. Similar behavioral impairments occur when dopaminergic function is disrupted temporarily by DA receptor blocking agents, and brain-damaged rats are particularly sensitive to the effects of those drugs. The present experiments offer a striking contrast to these well-accepted findings that central DA-containing neurons are critical to the initiation of voluntary movement. After near-total destruction of the dopaminergic neurons in 3-day-old rats, there were no conspicuous behavioral dysfunctions at any time during the subsequent 5-8 months, even when the animals were given large doses of DA receptor blocking agents. These findings suggest that some other neuronal system had replaced the absent dopaminergic neurons in the central control of movement.
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D005476:Fluphenazine / Q000494:pharmacology; D006220:Haloperidol / Q000494:pharmacology; D006892:Hydroxydopamines / Q000494:pharmacology; D008297:Male; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains
D006892:Hydroxydopamines; D016627:Oxidopamine; D006220:Haloperidol; D005476:Fluphenazine; D004298:Dopamine