Drugs online research references
Pharmacotherapy. 1998 Nov-Dec;18(6):1298-303.
Concomitant therapy with anxiolytics or hypnotics and maintenance of initial SSRI therapy.
Shields SA, Gregor KJ, Young CH, James SP.
Outcomes Research, PCS Health Systems, Inc., Scottsdale, Arizona, USA.
We conducted a retrospective analysis to evaluate the relationship between anxiolytic or hypnotic therapy and maintenance of therapy with selective serotonin reuptake inhibitors (SSRIs). Subjects were 654 patients who received anxiolytics or hypnotics early in SSRI therapy (study group ) and 15,172 patients who did not (controls). Maintenance of SSRI therapy was evaluated during the 6 months after start of therapy and included days of initial SSRI therapy and rates of discontinuation, defined as a break of more than 30 days. Rates of discontinuation in study and control groups (84% and 77%, p=0.001) and average days of initial SSRI therapy (77 and 94 days, p<0.0001) were statistically different. Thus patients receiving anxiolytic or hypnotics in the first 60 days of therapy were less likely to continue initial SSRI therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9855330&dopt=Abstract
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Neuropsychopharmacology. 2000 Apr;22(4):346-56.
Increased tonic activation of rat forebrain 5-HT(1A) receptors by lithium addition to antidepressant treatments.
Haddjeri N, Szabo ST, de Montigny C, Blier P.
Neurobiological Psychiatry Unit, McGill University, 1033 Pine Avenue West, Montreal, PQ, Canada.
The present study was undertaken to determine whether lithium addition to long-term treatment with different classes of antidepressant drugs could induce a greater effect on the serotonin (5-HT) system than the drugs given alone. Because 5-HT(1A) receptor activation hyperpolarizes and inhibits the firing activity of CA(3) pyramidal neurons in the dorsal hippocampus, the degree of disinhibition produced by the selective 5-HT(1A) receptor antagonist WAY 100635 was determined using in vivo extracellular recordings. In controls, as well as in rats receiving a lithium diet for 3 days, the administration of WAY 100635 (25-100 microg/kg, IV) did not modify the firing activity of dorsal hippocampus CA(3) pyramidal neurons. When the tricyclic antidepressant imipramine (10 mg/kg/day, SC), the monoamine oxidase inhibitor tranylcypromine (2.5 mg/kg/day, SC) and the selective 5-HT reuptake inhibitor paroxetine (10 mg/kg/day, SC) were administered alone for 21 days, a dose of 50 microg/kg of WAY 100635 was needed to increase significantly the firing activity of these neurons. On the other hand, WAY 100635, at a dose of only 25 microg/kg, increased significantly the firing rate of CA(3) pyramidal neurons in rats receiving both a long-term antidepressant treatment and a short-term lithium diet. It is concluded that the addition of lithium to antidepressant treatments produced a greater disinhibition of dorsal hippocampus CA(3) pyramidal neurons than any treatments given alone. The present results support the notion that the addition of lithium to antidepressants may produce a therapeutic response in treatment-resistant depression by enhancing 5-HT neurotransmission.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10700654&dopt=Abstract
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Biochem Pharmacol. 1999 Jan 1;57(1):111-20.
Inhibition by tetanus toxin of sodium-dependent, high-affinity [3H]5-hydroxytryptamine uptake in rat synaptosomes.
Inserte J, Najib A, Pelliccioni P, Gil C, Aguilera J.
Department de Bioquimica i de Biologia Molecular, Facultat de Medicina, Universitat Autonoma de Barcelona, Bellaterra, Spain.
Tetanus toxin (TeTx) is a powerful clostridial neurotoxin that inhibits Ca2+-dependent neurotransmitter secretion as do the botulinum neurotoxins (BoNTs). We found that TeTx (but not BoNT/A) produced a specific time- and dose-dependent inhibition of Na+-dependent [3H]5-hydroxytryptamine (serotonin, 5-HT) uptake in rat CNS synaptosomes. This effect was found in all CNS tryptaminergic areas, being maximal in the hippocampus and occipital cortex. TeTx produced the maximum reduction in [3H]5-HT uptake after 30 min of preincubation, being significant also at lower doses (10(-12) M) or shorter incubation times (10 min). Serotonin transport inhibitors such as fenfluramine (IC50, 11.0 +/- 0.9 microM), paroxetine (IC50, 33.5 +/- 0.1 microM), and imipramine (IC50, 89.9 +/- 5.7 microM) were 3 or 4 orders of magnitude less potent than TeTx (IC50, 8.7 +/- 1.0 nM). Of the two fragments of TeTx, (the C-terminal portion of the neurotoxin heavy chain, which is responsible for the binding to the nerve tissue) was consistently more effective than the L-H(N) fragment (the light neurotoxin chain disulfide linked to the N-terminal portion of the heavy chain, which is responsible for the toxic metalloprotease action) as inhibitor of [3H]5-HT uptake in synaptosomal preparations (56 +/- 5% and 95 +/- 3% with respect to control, respectively). Antagonism of the toxin-induced [3H]5-HT uptake blockade could not be reversed by zinc chelators but did have the ability to antagonize the TeTx inhibition of basal and K+-evoked [3H]5-HT release in rat synaptosomes. The reduction in serotonin accumulation induced by TeTx could be responsible for some tetanic symptoms that have been related to the serotonergic system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9920291&dopt=Abstract
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