title: Effects of estrogen on the basal ganglia.
abstract: Recent research suggests that estrogen regulates the activity of dopamine-containing fibers originating in the midbrain and terminating in the basal ganglia, and/or dopamine-sensitive cells in the basal ganglia. The mechanism by which estrogen acts is not clear, since cells in neither of these regions concentrate estrogens. Nevertheless, estrogens clearly affect behaviors mediated by the basal ganglia, as illustrated in human patients suffering from extrapyramidal disorders. Both biochemical and behavioral research in animals has confirmed that estrogen modulates basal ganglia function, but there has not been agreement concerning either the locus, the direction, or the mechanism of its action. These topics are the focus of this review. The effects of estrogen on behaviors mediated by DA in the basal ganglia depend on the dose of estrogen administered, the time interval between estrogen treatment and testing, the behavior measured, and the part of the basal ganglia from which the behavior is elicited. A high dose of estrogen results in an initial suppression and later enhancement of DA-related behaviors elicited from the striatum. However, no later enhancement of these behaviors occurs if a low dose of estrogen is given. Even after low doses of estrogen, the latency to behavioral suppression varies depending upon the behavior measured. These varying latencies suggest that more than one mechanism is involved in the effects of estrogen on basal ganglia output. In addition, estrogen may also act on some regions in the mesolimbic DA system. While estrogen may act indirectly via the catechol estrogens and prolactin, it has been demonstrated that estrogen can act directly on the striatum. These findings are related to the effects of estrogen on human extrapyramidal disorders.
authors.forename: C
authors.initials: C
authors.lastname: Van Hartesveldt
authors.forename: J N
authors.initials: JN
authors.lastname: Joyce
mesh_terms: D000109:Acetylcholine / Q000032:analysis; D000818:Animals; D014150:Antipsychotic Agents / Q000009:adverse effects; D001479:Basal Ganglia / Q000502:physiology*; D001480:Basal Ganglia Diseases; D002375:Catalepsy / Q000139:chemically induced; D002819:Chorea / Q000503:physiopathology; D004298:Dopamine / Q000502:physiology*; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology*; D005260:Female; D000882:Haplorhini; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D008297:Male; D008636:Mesencephalon / Q000502:physiology; D009043:Motor Activity / Q000187:drug effects; D009434:Neural Pathways / Q000502:physiology; D010052:Ovariectomy; D011187:Posture; D011388:Prolactin / Q000378:metabolism; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects; D012399:Rotation; D013239:Stereotyped Behavior / Q000187:drug effects; D013997:Time Factors
chemical_list: D014150:Antipsychotic Agents; D004967:Estrogens; D011954:Receptors, Dopamine; D011388:Prolactin; D000109:Acetylcholine; D004298:Dopamine