The zona incerta (ZI) is a site of dopamine nerve terminals and part of the incertohypothalamic tract (I-H). Previous findings indicate that dopamine in the ZI has a stimulatory control on the release of luteinizing hormone (LH) and occurrence of ovulation. The effect of acute administration into anaesthetised rats of selective D₁ and D₂ dopamine agonists and antagonists injected into the ZI on plasma luteinizing hormone (LH) and on the occurrence of ovulation has now been investigated. It was found that bilateral injections on the day of pro-oestrus of a selective D₁ antagonist, Sch 23390, inhibited ovulation at 10 µg/side/rat. Unilateral injections of a selective D₁ agonist, SKF 38393, at 10 µg/rat stimulated a significant rise in plasma LH concentration in ovariectomised oestrogen-primed rats, and this was partially reversed by systemic pre-treatment with Sch 23390. The selective D₂ agonist, LY 171555, and D₂ antagonists, sulpiride and domperidone, had no effect on plasma LH levels or ovulation. This indicates that D₁ receptors (but not D₂ receptors) in the ZI are involved in the control of gonadotrophin release and may have a physiological function in reproductive processes.

Intraventricular infusions of adrenaline and various pharmacological agents acting on beta-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 microliter) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed beta 1- and beta 2-agonist), fenoterol (a beta 2-agonist) and atenolol (a beta 1-antagonist). In contrast, prenalterol (a beta 1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)++ +butan-2-ol (ICI 118,551) (a selective beta 2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective beta 2-agonist), propranolol (a mixed beta-antagonist) and metoprolol (a beta 1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118,551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118,551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a beta 2-stimulatory component and the suppression of a beta 1-inhibitory component.