Table 5

Effects of DHX and PrDHX on D₂-like receptors in rat brain and pituitary

Function	Methodology	Cellular Locale	Drug
Function	Methodology	Cellular Locale	Quin	DHX	PrDHX
D₂ autoreceptors
DA release	Cerebral microdialysis; inhibition of basal DA overflow	Striatum	⁺⁺⁺	−	N.D.
DA release	In vivo voltammetry; inhibition of stimulated DA release	Striatum	⁺⁺⁺	−	−
DA cell firing	Extracellular recording; inhibition of spontaneous cell firing	Substantia nigra	⁺⁺⁺	−	N.D.
DA synthesis	Inhibition of basal tyrosine hydroxylase activity	Striatum	⁺⁺⁺	—^5-a	—^5-a
D₂ heteroreceptors
Prolactin secretion	Inhibition of 5-hydroxytryptanine-stimulated serum prolactin	Anterior pituitary	⁺⁺⁺	⁺⁺ ^5-b	⁺⁺ ^5-b
Adenylate cyclase	Inhibition of D₁ receptor-stimulated cAMP efflux	Striatum	⁺⁺⁺	⁺⁺⁺	N.D.
Adenylate cyclase	Inhibition of forskolin-stimulated AC	Striatum	⁺⁺⁺	⁺⁺⁺	⁺⁺⁺

Agonist effects of DHX and PrDHX on dopamine D₂-like receptors were measured in rodents using procedures described underExperimental Procedures. The maximal functional effects of DHX and PrDHX are depicted relative to hose elicited by the prototypical full D₂ receptor agonist quinpirole.

N.D., not determined; Quin, quinpirole; +++, full agonism indistinguishable from that of quinpirole; ++, greater than 50% inhibition relative to quinpirole, −, 20 to 50% inhibition relative to quinprole; —, less than 20% inhibition relative to quinpirole.
↵5-a Both DHX and PrDHX produce inhibition of DA synthesis but are not mediated by D₂-like receptors.
↵5-b Maximal effects on prolactin secretion could not be determined because only one dose of DHX and PrDHX were tested.