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Vol. 286, Issue 1, 272-281, July 1998
Experimental Therapeutics Branch, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, Maryland
Many studies have used the D1 agonist SKF 38393 to
characterize D1 receptor influences on firing rates in
basal ganglia nuclei in vivo. However, SKF 38393 is a
partial agonist and so may not be ideal for delineating D1
receptor effects. This study characterizes the effects of four full
D1 agonists, SKF 82958 (chloro-APB), SKF 81297 (6-chloro-PB), dihydrexidine and A-77636, on the firing rates of
midbrain dopamine and globus pallidus neurons. Recordings were done in
fully anesthetized or paralyzed, locally anesthetized rats, and drugs
were given systemically intravenously. Dihydrexidine, SKF 81297 and
A-77636 were free of rate effects on midbrain dopamine neurons (up to
10.2 mg/kg) and also did not antagonize the inhibitory effects of
quinpirole. In contrast, SKF 82958 strongly inhibited dopamine
cells through activation of D2 autoreceptors
(ED50 = 0.70 mg/kg). Of these drugs, SKF 82958 also was the only one to increase pallidal unit firing rates when given
alone (at 5.0 but not 1.0 mg/kg); the other compounds appeared to be
selective for postsynaptic D1 receptors. The results
suggest that SKF 82958 may be more properly classified as a mixed
D1/D2 agonist. In addition, all four agonists
strongly potentiated the pallidal response to quinpirole, demonstrating
a D1 receptor potentiation of D2 receptor effects. The results support the role of D1 receptors in
the midbrain and globus pallidus as previously characterized with SKF
38393. The similar actions of partial and full D1 agonists
in these systems support evidence for a D1 receptor reserve
and possibly an effector system other than adenylate cyclase.
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