Drugs online research references
J Pharmacol Exp Ther. 1989 Jan;248(1):391-9.
Pharmacological profile of moclobemide, a short-acting and reversible inhibitor of monoamine oxidase type A.
Burkard WP, Bonetti EP, Da Prada M, Martin JR, Polc P, Schaffner R, Scherschlicht R, Hefti F, Muller RK, Wyss PC, et al.
Pharmaceutical Research Department F. Hoffmann-La Roche & Co., Ltd., Basel, Switzerland.
The novel antidepressant moclobemide is a reversible inhibitor of monoamine oxidase (MAO), preferentially of type A. Moclomide was active in three animal models considered predictive for antidepressant activity: 1) it prevented dose-dependently akinesia and blepharospasm induced in mice and rats by Ro 4-1284, a short-acting amine releasing agent. Prevention of akinesia by moclobemide also depended upon the dose of Ro 4-1284. For comparison also, effects of cimoxatone, harmaline, tranylcypromine and clorgyline are presented: 2) in cats, it selectively and dose-dependently suppressed rapid eye movement sleep without disturbing the sleep-wakefulness cycle; and 3) in the behavioral despair test in mice, it decreased the immobility score to a similar degree as amitriptyline or imipramine. In addition, moclobemide potentiated 5-hydroxytryptophan-induced stereotypies in rats with a potency similar to cimoxatone and with a duration of action of less than 24 hr. Moclobemide had almost no effect on the spontaneous behavior in mice, rats, cats and monkeys. Only in higher doses, marginal sedation and slight impairment in motor performance were seen. Moclobemide did not prevent pilcarpine-induced salivation in mice, demonstrating the absence of anticholinergic activity. Blood pressure and heart rate of freely moving, spontaneously hypertensive rats were only slightly decreased for less than 3 hr. Moclobemide moderately potentiated the pressor effect of p.o. tyramine in rats. In conclusion, the reversible MAO inhibitor moclobemide is active in animal models sensitive to all major drugs used in the treatment of depression. In contrast to imipramine-like antidepressants, it lacks anticholinergic activity and it differs from classic MAO inhibitors by potentiating only weakly the pressor effect of p.o. tyramine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2913284&dopt=Abstract
Prog Neuropsychopharmacol Biol Psychiatry. 1989;13(1-2):211-5.
Chronic treatment with amitriptyline produces subsensitivity to the hypothermic effects of yohimbine.
Dilsaver SC, Davidson RK.
Department of Psychiatry, Ohio State University, Columbus.
1. Two but not one week of treatment with amitriptyline (AMI) produces subsensitivity to the hypothermic effects of the alpha 2 antagonist yohimbine. 2. Subsensitivity persisted for the three weeks during which it was measured following the discontinuation of AMI. 3. Two weeks of twice daily injections of saline did not alter the thermic response to this agent. 4. The results support other data indicating tricyclic antidepressants (TCAs) subsensitize alpha 2 mediated thermic changes and are consistent with reports that TCAs down-regulate alpha 2 receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2748861&dopt=Abstract
Eur J Pharmacol. 1990 Jan 25;176(1):69-74.
Amitriptyline-induced morphological alterations of the rat blood-brain barrier.
Sarmento A, Albino-Teixeira A, Azevedo I.
Laboratorio de Farmacologia, Faculdade de Medicina do Porto, Portugal.
Amitriptyline is known to increase the permeability of the blood-brain barrier but the morphological basis of this increase has not been studied. As catecholamines can influence pinocytosis in dog peripheral blood vessels, the effect of amitriptyline on the pinocytotic activity of blood brain microvessels was studied. Amitriptyline, 34 mg.kg-1 i.p., was injected to rats and the parietal cortex of control and treated animals was prepared for ultrastructural study. Pinocytotic vesicles in endothelial cells were quantified. Amitriptyline significantly increased the density of pinocytotic vesicles in capillary endothelial cells. No other morphological changes occurred after amitriptyline treatment. We conclude that the increase in blood-brain barrier permeability due to amitriptyline may be ascribed at least in part to an increase of pinocytotic activity in brain capillary endothelial cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2311660&dopt=Abstract
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