Kathleen L. Hauser

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NKP608 is a non-peptidic derivative of 4-aminopiperidine which acts as a selective, specific and potent antagonist at the neurokinin-1 (NK-1) receptor both in vitro and in vivo. In vitro, the binding of NKP608 to bovine retina was characterized by an IC50 of 2.6+/-0.4 nM, whereas the compound's affinity to other receptor binding sites, including NK-2 and(More)
Raloxifene,[2-(4-hydroxyphenyl)-6-hydroxybenzo[b]thien-3-yl] [4-[2-(1-piperidinyl)ethoxy]phenyl]methanone hydrochloride (2), is representative of a class of compounds known as selective estrogen receptor modulators (SERMs) that possess estrogen agonist-like actions on bone tissues and serum lipids while displaying potent estrogen antagonist properties in(More)
A peripheral injection of DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine] produced a marked, selective, and lasting depletion of norepinephrine in certain regions of the rat central nervous system. This depletion at 10 days after injection was associated with regional alterations in some, but not all, adrenergic binding sites (receptors) as determined(More)
Subchronic, peripheral infusion of clenbuterol, a beta-adrenergic agonist, markedly reduced beta receptor density and isoproterenol-sensitive adenylate cyclase activity in the cerebellum of the rat. In contrast, infusion of salbutamol, isoproterenol or desipramine did not alter the beta receptor. The result of clenbuterol administration demonstrates, for(More)
Trimipramine is a tricyclic antidepressant which has only weak effects on noradrenergic systems. Its mechanism of action is not understood, but its clinical effectiveness has been proven over a period of 20 years. In the present investigation, trimipramine was shown to have no effect on noradrenaline (NA)-stimulated adenylate cyclase activity after either(More)
Ifoxetine (CGP 15210 G; (+/-)-bis-[cis-3-hydroxy-4-(2,3-dimethyl-phenoxy)]-piperidine sulfate) prevented the depletion of serotonin (5-HT) induced by H 75/12 and p-chloromethamphetamine in the rat brain, and that caused by endogenously released dopamine after the combined administration of haloperidol and amfonelic acid in the rat striatum. These effects(More)
GABA level and the activity of L-glutamate-1-decarboxylase (GAD) (EC were studied in brains of mice treated with beta-vinyllactic acid, a new, selective and pyridoxal phosphate-independent GAD inhibitor. Valproate and diazepam protected mice against convulsions caused by beta-vinyllactic acid although both anti-epileptic drugs antagonized neither(More)