Thesis (Ph. D.)--Princeton University, 1925.

Thesis (Ph. D.)--Princeton University, 1926.

Thesis (Ph. D.)--University of Illinois, 1921. / Vita.

Thesis (Ph. D.)--University of Wisconsin, 1965. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin, 1966. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

Antagonistic inotropic actions of barbiturates and adrenergic amines have, been demonstrated in dog hearts. The present work was undertaken to ascertain whether a similar antagonism occurred in other tissues, and if so, how specific and potent it is. The tissues selected for studying these phenomena were rabbit kidney cortex slices, uterine horns of previously estrogenized rabbits and guinea pig terminal ileum. The tone and contractility of the isolated smooth muscle preparation and the active transport of sodium para-aminohippuric acid (PAH) by the kidney cortex slices, were the processes monitored. No antagonism of the barbiturate induced depression of the active uptake of PAH by kidney cortex slices on the part of adrenergic amines was observed. Only a weak antagonism between these two groups of drugs was evident under suitable conditions in the guinea pig ileum. However, in contrast to these observations, a potent antagonism similar to that demonstrated in the dog hearts, was evident in the rabbit uterine horns. The experimental data indicated that adrenergic amines and barbiturates are antagonistic only in those tissues where barbiturates depress and adrenergic amines stimulate the energy utilizing process studied. The antagonism when evident is not specific and may be classified as independent or physiological. / Medicine, Faculty of / Anesthesiology, Pharmacology and Therapeutics, Department of / Graduate

The roles of the noradrenergic and serotonergic innervations of the hippocampus were investigated with respect to their involvement in the intracranial self-stimulation of this structure. In the first study, 6-hydroxydopamine-induced lesions of the dorsal tegmental noradrenergic bundle ascending to the forebrain had no effect on hippocampal self-stimulation in rats. In the second study, intragastric administration of para-chlorophenylalanine decreased hippocampal self-stimulation, suggesting the importance of a serotonin input in maintaining this behavior. Identical para-chlorophenylalanine treatments resulted in temporary depletions of brain serotonin which paralleled the changes in hippocampal self-stimulation. The maximal decreases in both the biochemical and behavioral measures occurred at 4 days' post-drug. Interpretations of this deficit in hippocampal self-stimulation in terms of gross sensory and/or motor changes were ruled out, as animals with lateral hypothalamic electrodes showed increases in self-stimulation paralleling the post-drug serotonin changes. An intrasessional analysis of the para-chlorophenylalanine-induced behavioral changes revealed that lateral hypothalamic self-stimulation was facilitated mainly during the first hr of the 2 hr test sessions, whereas the depression in hippocampal self-stimulation occurred primarily in the last hour of the sessions. The differential effects of para-chlorophenylalanine on lateral hypothalamic and hippocampal self-stimulation provide evidence against simple monoamine theories of reinforcement. / Arts, Faculty of / Psychology, Department of / Graduate

The selectivity observed with 2,4,7-triamino-6-methylsulfonyl-pteridine when reacted with "hard" aliphatic amines and "soft" aryl-thiols resulting in amine exchange at the 2-, 4-, and 7-positions and displacement of the 6-methylsulfonyl moiety, respectively, was further investigated in other ring systems. The substrates tested were disubstituted with amino- and methylsulfonyl- moieties, and included the benzene, pyridine, pyrazine, quinoxaline, quinazoline and pteridine ring systems. The methylsulfonyl moiety is preferentially displaced by both thiols and amines with quinoxaline and quinazoline substrates, and is more reactive towards displacement by thiol than amine nucleophiles. Amine exchange occurs with the quinoxaline substrate subsequent to displacement of the methylsulfonyl moiety and apparently takes place by an AE mechanism. The nucleophilic aromatic substitution patterns generally observed with benzenes pyridine, pyrazines, quinoxalines, quinazolines, and pteridines are reviewed.

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