This review examines possible neural mechanisms involved in the expression of parental behavior in the ring dove, Streptopelia risoria. This avian species has proved an excellent animal model for studies concerning endocrine-behavior interactions for many years. Studies were performed to localize the expression of central androgen and progesterone receptor in both sexes. Expression of androgen receptor (androgen receptor immunoreactivity, AR-ir) was widespread but increased, similarly in both sexes, with increasing day-length. Progesterone receptor-immunoreactivity (PR-ir) was more localized in several discrete areas of the hypothalamus. Similarly, no sex differences were observed in PR-ir, and expression increased in birds maintained on long days. AR-ir demonstrated dramatic changes over the breeding cycle, being greatest in courting birds and almost undetectable in parenting birds of both sexes brooding their young. PR-ir showed a differential expression over the breeding cycle relative to its hypothalamic localization. PR-ir decreased in the tuberal hypothalamic area in brooding birds of both sexes; whereas in the preoptic area, PR-ir was maintained. Significant increases in dopaminergic activity during the parenting phase of the breeding cycle occurred in specific neural regions including the PVM and DMA. Studies demonstrated the ability of the diencephalon of both sexes of the ring dove brain to synthesize progesterone, with indications that in the male brooding dove, synthesis is increased. Finally, a model is presented that proposes a mechanism whereby these central systems may interact to result in the expression of full parental behavior in both sexes of the ring dove.

At 1 h after a single subcutaneous injection of haloperidol into early proestrous rats, there was an 11-fold elevation in serum prolactin. Pituitary prolactin concentration 4 h after administration of 50 µg haloperidol/100 g BW was significantly decreased (52% of control values). In male rats, a single subcutaneous injection of 50 µg haloperidol produced an approximately 4-fold increase in serum prolactin at the end of 1 h, and a significant reduction in pituitary prolactin concentration at the end of 4 h. Hypothalamic PIF activity in male rats was reduced significantly by haloperidol whenever serum prolactin levels were elevated. These results suggest that the increased release of pituitary prolactin by haloperidol is mediated by a decrease in hypothalamic PIF activity.

Following the discovery that 3-(dimethylamino)-1,1-diphenyl-2-propanol hydrobromide (1) possesses potent reserpine-prevention activity in mice, a series of analogues of 1 was synthesized and evaluated as potential antidepressant agents. Several routes to analogues of 1 were evaluated, the most generally applicable of which was the regiospecific ring opening of a suitably functionalized 1,1-diaryl-2,3-epoxypropane (obtained in three stages from the corresponding benzophenone) with the appropriate amine. The more interesting compounds of the series were evaluated for their propensity to cause undesirable peripheral anticholinergic effects, all compounds tested being markedly less active than imipramine on this parameter. On the basis of its good activity in biochemical and pharmacological animal models of depression, together with its relative lack of anticholinergic side effects, 1-(3-chlorophenyl)-3-(dimethylamino)-1-phenyl-2-propanol hydrochloride (20, BRL 14342) was chosen for further evaluation.

Rats maintained on a tryptophan deficient diet had reduced brain and serum tryptophan and brain 5-hydroxyindolacetic acid levels compared to controls. 5-Hydroxytryptophan and L-tryptophan administered to these deficient rats in a combination (5:95) produced a greater elevation of indolamines and tryptophan in the brain than either amino acid alone. In rats maintained on a normal diet the urinary output of 3-hydroxykynurenine was considerably reduced by treatment with the combination of amino acids as compared to tryptophan treatment. 5-Hydroxytryptophan reduced the induction of kynurenine synthesis in the liver produced by tryptophan, implying that it is capable of inhibiting the enzyme tryptophan pyrrolase in vivo. It is suggested that the possession by 5-hydroxytryptophan of tryptophan pyrrolase inhibitory properties may make the administration of the combination a better treatment of depressed patients exhibiting an indolamine deficit than either amino acid alone.

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