Reference

Induction of the platelet release reaction by 1,3-dimethyl-5-aminoadamantane, a new adamantane derivative

Induction of the platelet release reaction by 1,3-dimethyl-5-aminoadamantane, a new adamantane derivative. Haacke, Uta; Wesemann, Wolfgang (Inst. Physiol. Chem.In this study， 50-67-9 and 58-64-0 are also used. II, Philipps-Univ., Marburg, Ger.). Thromb. Haemostasis, 37(1), 62-72 (English) 1977. CODEN: THHADQ. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) The amantadine deriv. D 145 (I) [19982-08-2] induced in high concns. of 2-10 mM the blood platelet release reaction. Adenine nucleotides and hydroxytryptamine (5-HT) [50-67-9] were liberated to the same extent and in the same ratio as found after thrombin-induced release. The time course of release was very slow; max. release was reached in 15-20 min. The process was temp.-dependent and dependent on energy derived from glycolysis and oxidative phosphorylation. Extracellular Ca++ did not promote the release process. I inhibited 5-HT uptake non-competitively, KI = 0.15 mM. In concns. of 0.1-1 mM I triggered only the liberation of 5-HT, adenine nucleotides were not liberated. The ADP [58-64-0] induced platelet aggregation was completely inhibited after preincubation with a 1 mM soln. of I. .

Evidence for presynaptic antagonism by amantadine of indirectly acting central stimulants

Evidence for presynaptic antagonism by amantadine of indirectly acting central stimulants. Menon, M. K.; Vivonia, Charlotte A.; Haddox, Victor G. (Psychopharmacol. Res. Lab., Veterans Adm. Med. Cent., Sepulveda, CA 91343, USA). Psychopharmacology (Berlin), 82(1-2), 89-92 (English) 1984. CODEN: PSCHDL. ISSN: 0033-3158. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) In mice, amantadine [768-94-5] pretreatment (150 mg/kg, but not 10 mg/kg, 2 h prior to testing) markedly inhibited the locomotor stimulation produced by submaximal doses of d-amphetamine [51-64-9], amfonelic acid [15180-02-6], methylphenidate [113-45-1], caffeine [58-08-2], memantine [19982-08-2], phencyclidine [77-10-1], and cocaine [50-36-2]. A 50-mg/kg dose was ineffective in blocking the effects of caffeine and memantin, but blocked the responses to the other 5 stimulants. Amantadine did not modify the locomotor stimulant effect of apomorphine [58-00-4] in reserpinized mice. These results indicate that amantadine acts as a presynaptic antagonist to the above 7 stimulants. 768-94-5 and 50-36-2 which are cas registry numbers of chemicals are mentioned. Even the highest dose of amantadine did not modify the hyperactivity induced in mice by morphine [57-27-2] and levorphanol [77-07-6]. This result is consistent with evidence, showing opiate actions at postsynaptic striatal neurons, sites where presumably amantadine is unable to exert an antagonist effect. Amantadine did not modify the central depressant effects of ethyl alc. [64-17-5] and pentobarbital [76-74-4]. Amantadine could be of value as a pharmacol. tool in understanding the mode of action of central stimulants, and in the management of stimulant abuse. The present data do not support the currently held view that the antiparkinsonism effect of amantadine results from its ability to potentiate the central effects of dopamine [51-61-6]. .