Feeding induced by blockade of histamine H1-receptor in rat brain

Summary Histamine antagonists were infused into the third ventricle of the cerebrum in rats. All the H₁-, but none of the H₂-antagonists tested, induced initial feeding during the early portion of the light phase when histamine level was highest. No periprandial drinking was observed. Ambulation increased during feeding. The effect on feeding was attenuated when brain histamine was normally low during the early portion of the dark phase, or was decreased by -fluoromethylhistidine. Hypothalamic neuronal histamine may suppress food intake through H₁-receptors, and diurnal fluctuations of food intake may mirror neuronal histamine levels.     

Role of calcium in the histamine release induced by D-galactosamine from rat mast cells

Rat peritoneal mast cells were isolated and purified by differential centrifugation in Ficoll. Cells pooled from three to four rats were suspended at approximately 10(6) cells/ml in a buffered salt solution and incubated for 1 h at 37 degrees C in 300 microliter volumes in the absence or presence (9 X 10(-4) M) of calcium chloride. Addition of D-galactosamine hydrochloride (DGM; 2.8 X 10(-4)M) caused (in addition to basal release) a mean +/- SEM percent histamine release of 15.7 +/- 5.2 in the presence of Ca++ and 19 +/- 4.9 in the absence of Ca++ (p greater than 0.05). It is suggested that D-galactosamine does not require extracellular Ca++ for the release of histamine from the rat mast cell.     

Role of calcium in the histamine release induced by D-galactosamine from rat mast cells

Summary Rat peritoneal mast cells were isolated and purified by differential centrifugation in Ficoll. Cells pooled from three to four rats were suspended at approximately 10⁶ cells/ml in a buffered salt solution and incubated for 1 h at 37°C in 300 l volumes in the absence or presence (9×10^–4 M) of calcium chloride. Addition of D-galactosamine hydrochloride (DGM; 2.8×10^–4 M) caused (in addition to basal release) a mean ±SEM percent histamine release of 15.7±5.2 in the presence of Ca⁺⁺ and 19±4.9 in the absence of Ca⁺⁺ (p>0.05). It is suggested that D-galactosamine does not require extracellular Ca⁺⁺ for the release of histamine from the rat mast cell.A preliminary analysis of these results was presented at the International Symposium on calcium entry blockers and tissue protection, Rome, 15–16 March 1984.     

Developmental characteristics of histamine methyltransferase and phenylethanolamine-N-methyltransferase of rat brain

Summary The specific activity of histamine methyltransferase of rat brain increases rapidly from the 16th until the 25th day of gestation (7 days after birth). The specific activity of phenylethanolamine-N-methyl-transferase shows a rapid incrase during the 1st and the 2nd week after birth, the adult values being obtained by the end of the 2nd week.     

Increased vascular permeability induced in synovialis of the rat by histamine,serotonin and bradykinin

Résumé La perméabilité vasculaire de la membrane synoviale du rat est augmentée par l'histamine, la sérotonine et la bradykinine. Dans cette réaction la sérotonine est plus active que l'histamine et la bradykinine.

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L.P.B. is supported by a Medical Postgraduate Research Scholarship from the National Health and Medical Research Council of Australia.

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We are indebted to Associate ProfessorJ. Garcia-Lémé, University of São Paulo, Brazil, for advice.     

Autoradiographic localization of testosterone-3H in the female rat brain and estradiol-3H in the male rat brain

Zusammenfassung Eine halbe Stunde nach der i.v. Injektion wurde Testosterone-³H von den Nerven- und Glialzellen innerhalb des Gehirns der weiblichen Ratte und Estradiol-³H innerhalb des Gehirns der männlichen Ratte aufgenommen. Zwei Stunden nach der Injektion war die Aufnahme in hohem Masse nur noch in gewissen Teilen des hypothalamisch-limbischen Systems vorhanden.

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This investigation was supported by grants from NASA (No. NsG 496) and the John A. Hartford Foundation to Dr.H.-L. Teuber, and from the U.S. Atomic Energy Commission to Dr.J. Altman, both of the Massachusetts Institute of Technology, and the work was performed while the author was at M.I.T.     

Inter omental-cerebral vascularization induced by omental graft to the rat brain

Summary The omentum of 13 rats were removed from the abdomen and placed directly on the brain. 5–14 days later the omentum and the underlying brain were joined by numerous vascular anastomoses in 9 rats. The purpose of this work was to study the use of omentum to establish extracranial vascularization of the brain.Supported by funds from Grant RR 514 from the Jefferson Medical College General Research Fund.     

Evidence for a cholinergic mechanism inducing histamine increase in the rat brain in vivo

Résumé Pendant l'excitation du système nerveux central chez le rat, un mécanisme cholinergique augmente l'histamine cérébrale.     

Involvement of H1 receptors in the central antinociceptive effect of histamine: Pharmacological dissection by electrophysiological analysis

Intracerebroventricular (i.c.v.) administration of histamine (HA, 0.025–0.1 M/rat) to arthritic rats induces a dose-related inhibition of the neuronal thalamic firing evoked by peripheral noxious stimuli. To characterize the type(s) of HA receptors involved in this depressing activity of the amine we used electrophysiological techniques to examine the effects of i.c.v. administration of H₁ and H₂ agonists and antagonists on the spontaneous and evoked nociceptive firing of the thalamic neurons in rats rendered arthritic by Freund's adjuvant. The H₁ agonist 2-pyridylethylamine (0.4–1.0 M/rat, i.c.v) displayed a dose-dependent antinociceptive effect very similar to that of HA, while the H₂ agonist dimaprit (0.05–0.2 M/rat, i.c.v.) did not modify thalamic firing. Neither mepyramine (H₁ antagonist, 0.1 M/rat, i.c.v.) nor zolantidine (H₂ antagonist, 0.01 M/rat, i.c.v.) modified the evoked firing of rat thalamic neurons. When administered before HA (0.1 M/rat, i.c.v.) mepyramine but not zolantidine was able to inhibit the antinociceptive effect of HA. On the basis of the present electrophysiological results, we suggest that a specific interaction of histamine with H₁ receptors may be important for its antinociceptive effect on afferent peripheral inputs to the thalamus.     

Time courses and refractoriness of enhanced vascular permeability induced by histamine,serotonin and bradykinin in synovialis of the rat

Summary Enhanced vascular permeability induced in synovialis of the rat by histamine and serotonin lasts 5–15 min and that induced by bradykinin less than 5 min. Synovialis of the rat becomes refractory to the permeability effects of repeated doses of each of these substances in the hour following initial application.This work was carried out while L.P.B. was supported by a Medical Postgraduate Scholarship from the National Health and Medical Research Council of Australia.     

The role of the subependymal plate in the origin of gliomas induced by ethylnitrosourea in the rat brain

Summary The fine structure of early cell proliferations induced transplacentally by ethylnitrosourea in the rat brain reveals that the cells show features of the undifferentiated cells of the subependymal plate: high nuclear-cytoplasmic ratio, scarcity of cell organelles and dominance of free over membrane-bound ribosomes. These findings suggest that most, if not all, gliomas induced by ethylnitrosourea originate from these primitive cells.Acknowledgments. I thank D. J. Cox and G. J. Pilkington for their skilful technical assistance.     

Testosterone induced alterations in histamine metabolism in mice

Zusammenfassung Eine neuer Befund von hormonaler Beeinflussung des Histaminmetabolismus wird beschrieben und ein bisher nicht erkannter Metabolit wird chromatographisch nachgewiessen. Under dem Einfluss von Testosteron wird der Metabolit in grosser Menge in Urin der Maus ausgeschieden, während zugleich freies Histamin fast verschwindet, was dafür spricht, dass es sich um einen Histaminmetaboliten handelt, dessen chemische Struktur noch nicht festgestellt ist und von verschiedenen bekannten Histaminmetaboliten abgegrenzt werden kannte.

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This study was supported by grants from the Swedish Medical Research Council No. B70-14x-2212-04 and from the Swedish Society for Cancer Research No. 268-K70-01 X.