Drugs online research references
Behav Brain Res. 1997 Feb;83(1-2):209-12.
Protective effect of citalopram against the attenuation of the alpha 1-potentiation of cAMP formation in Fischer 344 strain rats.
Izumi J, Washizuka M, Hayashi-Kuwabara Y, Yoshinaga K, Tanaka Y, Ikeda Y, Kiuchi Y, Oguchi K.
Central Research Laboratories, Zeria Pharmaceutical Co. Ltd., Saitama, Japan.
We investigated the effects of citalopram, a selective serotonin reuptake inhibitor (SSRI), using an animal model for a depressive state. In Fischer 344 rats, known as emotional animals, repeated stress by twice-daily intraperitoneal (i.p.) saline injections for 14 days elicited a depressive state characterized by a decreased open-field activity and a prolonged immobility during the tail-suspension test. Concomitantly, suppression of norepinephrine (NE)-induced cAMP formation was found in the cerebral cortical slices of the stress-exposed rats without changes in adrenergic alpha 1- or beta-receptors. The difference in cAMP formation between the intact and the stress groups was totally abolished under the blockade of the alpha 1-receptor system or by the stimulation with isoproterenol or forskolin, whereas the suppressed response in the stress group was also observed in combination with isoproterenol and phenylephrine. From these results, we confirmed that the potentiation of the beta-receptor-stimulated cAMP formation by the alpha 1-receptor is attenuated following repeated stress. Chronic i.p. administration of citalopram dissolved in saline improved both the suppressed open-field activity and the prolonged immobility in the tail-suspension test. The animals treated with citalopram exhibited a comparable alpha 1-potentiation effect as observed in the intact rats. However, another SSRI, paroxetine, was less effective on the attenuation of the alpha 1-potentiation in spite of its behavioral improvement in the depressive state. These findings suggest that citalopram has a protective effect against the repeated stress-induced depressive state by mechanisms besides the serotonin reuptake inhibition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9062686&dopt=Abstract
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Vet Hum Toxicol. 1997 Apr;39(2):86-8.
Paroxetine (Paxil) overdose: a pediatric focus.
Myers LB, Krenzelok EP.
Pittsburgh Poison Center, Children's Hospital of Pittsburg, PA 15213, USA.
The antidepressant paroxetine (PAXIL) was approved for use in 1993. Thus far, this selective serotonin reuptake inhibitor (SSRI) has shown a high threshold for the development of toxic manifestations in adult overdoses. However, the toxic threshold doses and profile of toxic manifestations for pediatric exposures has not been well-established. All pediatric paroxetine exposures reported at a certified regional poison information center over a 24-mo period were reviewed. The parameters evaluated included age, amount, co-ingestants, symptoms, treatment and outcome. Thirty-five pediatric paroxetine exposures were documented. Ages ranged from 10.5 mo to 17 y. Paroxetine alone accounted for 28 cases and 7 were with concomitant medications. Of the paroxetine-alone ingestants, 16 cases were in children < or = 5 y (mean age 2.4 y) with ingestant amounts ranging from 10-120 mg. All patients remained asymptomatic with or without gastrointestinal decontamination. The remainder of sole ingestant cases included 12 patients > or = 12 y (mean age 17.2 y) who ingested 100-800 mg (mean 292 mg). Most remained asymptomatic. There were 7 patients in the co-ingestant group > or = 13 y. Only 2 remained asymptomatic, but the symptoms reported were also consistent with the co-ingestants taken. Paroxetine is less sedating and has fewer cardiovascular effects than the tricyclic antidepressants, even in the pediatric population. The high therapeutic index is consistent with other SSRI's. In contrast to more toxic antidepressants in the pediatric group, paroxetine overdose patients are less likely to develop toxic manifestations. Ingestions of 120 mg or less in children < or = 5 y led to favorable outcomes following gastrointestinal decontamination and minimal supportive care. However, continued evaluation of paroxetine is essential to determine more specific toxic thresholds.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9080633&dopt=Abstract
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Psychopharmacology (Berl). 1997 Feb;129(3):197-205.
Behavioral profiles of SSRIs in animal models of depression, anxiety and aggression. Are they all alike?
Sanchez C, Meier E.
H. Lundbeck A/S, Copenhagen-Valby, Denmark.
The behavioral profiles of five clinically used selective serotonin reuptake inhibitors (SSRIs) citalopram, paroxetine, sertraline, fluvoxamine and fluoxetine, have been compared in animal models of antidepressant (mouse forced swim test), anxiolytic (exploration of black and white test box and foot-shock-induced ultrasonic vocalization in the rat) and antiaggressive (isolation-induced aggressive behavior in the mouse) activity. the results are discussed in relation to receptor binding data from the literature. Furthermore, affinities for the sigma 1 and sigma 2 binding sites are presented. Citalopram reversed the immobility induced by forced swimming with a potency similar to that of imipramine. Paroxetine, fluvoxamine and fluoxetine reversed swim-induced immobility less potently and with a maximum of 40-50% reversal. Citalopram produced a mixed anxiogenic-/anxiolytic-like response in rats tested in the two-compartment black and white box. Paroxetine induced an anxiogenic-like response at low doses and the other SSRIs were without major effects. Citalopram and paroxetine inhibited footshock-induced ultrasonic vocalization with high potencies. The dose-response curve was biphasic for citalopram with a maximum of 64% inhibition. Sertraline and fluvoxamine inhibited the vocalization less potently, and fluoxetine induced a weak inhibitory effect corresponding to a maximum of 32%. Sertraline, fluvoxamine and fluoxetine inhibited isolation-induced aggressive behavior, whereas citalopram and paroxetine were inactive. Both 5-HT1 and 5-HT2 receptors are involved, and there was a functional interaction between 5-HT1A and 5-HT2A or 5-HT2C receptors, as ritanserin potentiated the antiaggressive effect of 1,5-HTP as well as that of 8-OH-DPAT.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9084057&dopt=Abstract
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