Brain mast cells were studied in mice, rats, rabbits, hamsters, guinea pigs, cats, cows, monkeys, and humans with use of a variety of techniques. They were localized by staining with Astrablau or by toluidine blue-induced metachromasia and characterized by their ultrastructural appearance and by the presence of histochemically demonstrable histamine (o-phthaldiadehyde fluorescence method). The identity of the fluorophore was secured by microspectrofluorometry. Mast cells in brain usually had a perivascular localization but were also found scattered in the parenchyma. The regional variations in the number of mast cells agreed with the histamine concentration as measured fluorometrically. The variation was in the order leptomeninges greater than hypothalamus greater than cerebral cortex = mesencephalon greater than cerebellum = brain stem. In addition to histamine, murine mast cells stored serotonin, whereas bovine mast cells contained dopamine, visualized histochemically by the formaldehyde technique.

Summary. Ovulatory effects of histamine and specific antagonists were studied in isolated perfused ovaries from immature rats treated with 10 i.u. PMSG to stimulate follicular growth and maturation. Histamine alone, like LH, induced ovulation in all ovaries tested, but the number of follicular ruptures was lower after histamine (7\m=.\0 and 2\m=.\2 ruptures, respectively, per ovary). The histamine-induced ovulations could be inhibited dose-dependently by the H 1-receptor antagonist, pyrilamine, or the H2\ x=r eq-\ antagonists, cimetidine and ranitidine. At the concentrations tested, these antagonists did not, when given separately, reduce the LH-induced ovulations significantly, but pyrilamine and cimetidine in combination lowered the ovulation frequency by 65%. The prostaglandin synthesis inhibitor, indomethacin, was not able to block the histamine-induced ovulations.

Immature female rats were primed with 4 i.u. PMSG at 08:00 h of Day 26. This results in ovulation in the morning of Day 29. The number of ovulations was counted in terms of newly formed corpora lutea in the morning of Day 30. Various adrenergic drugs were delivered into the ovarian bursa bilaterally in the afternoon of Day 27 to study their effect on ovulation. A methyl cellulose gel solution was used as vehicle to minimize leakage from the bursa. Noradrenaline, terbutaline and 4-aminopyridine significantly enhanced the number of corpora lutea compared to control ovaries injected with gel vehicle alone. The effect of terbutaline was counteracted by propranolol. Phentolamine partly blocked the noradrenaline-induced enhancement and the antagonist alone significantly reduced the number of ovulations. The results indicate that stimulation of alpha-adrenergic receptors (probably via actions in the follicle wall) as well as beta-receptors (influencing steroid-producing cells) may interfere with the ovulation process.

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The immunocytochemical distribution of substance P (SP), gastrin releasing peptide (GRP), vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), and neuropeptide Y (NPY) was studied in the ovary and the Fallopian tube (oviduct) of rats, guinea-pigs, cows, pigs and humans. Generally, the nerve supply was better developed in the oviduct than in the ovary. GRP fibers were most scarce in all tissues. Nerves containing SP were particularly numerous in the oviduct of rat and guinea-pig, supplying the muscular wall and blood vessels. VIP and PHI coexisted in dense plexuses of nerves, not only around blood vessels but also in the follicular wall and the interstitial gland of the ovary, as well as within the smooth muscle layers and subepithelially in the oviduct. The general distribution of NPY was similar, but these immunoreactive nerves were even more numerous. Sequential staining for dopamine-beta-hydroxylase and NPY together with results of chemical sympathectomy with 6-hydroxydopamine suggested that NPY was stored in the noradrenergic sympathetic nerves.