Drugs online research references









Eur J Pharmacol. 1993 Aug 24;240(2-3):319-23.
Modification of the N-methyl-D-aspartate response by antidepressant sigma receptor ligands.

Bergeron R, Debonnel G, De Montigny C.

Department of Psychiatry, McGill University, Montreal, Quebec, Canada.

Sertraline, a selective serotonin reuptake inhibitor, and clorgyline, a monoamine oxidase inhibitor, both of which have high affinity for sigma receptors, were assessed in an electrophysiological model. In keeping with previous data obtained with other sigma receptor ligands, low doses of sertraline and of clorgyline potentiated selectively with a bell-shaped dose-response curve the effect of N-methyl-D-aspartate (NMDA) on pyramidal neurons in the CA3 region of the rat dorsal hippocampus. This potentiation was reversed by the sigma receptor ligands haloperidol and BMY-14802. The selective serotonin reuptake inhibitor paroxetine and the monoamine oxidase inhibitor tranylcypromine, both devoid of affinity for sigma receptors, had no effects on the NMDA response. These data suggest that the effects of sertraline and clorgyline on the NMDA response are due to their affinity for sigma receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8243549&dopt=Abstract

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Acta Psychiatr Scand. 1993 Oct;88(4):300-1.
Lithium augmentation in sertraline-resistant depression: a preliminary dose-response study.

Dinan TG.

Department of Psychological Medicine, St Bartholomew's Hospital, London, United Kingdom.

Eleven patients with DSM-III-R major depression who were treatment-resistant to sertraline were allocated for lithium augmentation therapy. In conjunction with their sertraline, 6 received lithium carbonate 400 mg at night and 5 received 800 mg at night. A total of 7 patients responded within 1 week. The degree of response was not related to the serum lithium level. Patients with lithium levels as low as 0.3 mEq/l responded. No significant side effects were reported.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8256650&dopt=Abstract

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Neuroscience. 1993 Jun;54(3):561-5.
Indirect serotonergic agonists attenuate neuronal opiate withdrawal.

Akaoka H, Aston-Jones G.

Department of Mental Health Sciences, Hahnemann University, Philadelphia, PA 19102.

Withdrawal from opiates in dependent subjects produces strongly aversive psychological and autonomic responses which contribute to the chronic ingestion of opiates and the high incidence of relapse after withdrawal. A variety of evidence indicates that hyperactivity of noradrenergic locus coeruleus (LC) neurons is an important brain substrate of opiate withdrawal. In particular, only a few agents have been found to be clinically useful in alleviating these symptoms and treating opiate dependence, all of which potently attenuate the activation of noradrenergic neurons in the LC evoked by opiate withdrawal. However, current pharmacotherapies, especially methadone and clonidine, have serious side effects, including hypotension, sedation and their own withdrawal reactions. Our goal was to find an alternative pharmacological treatment to reduce the magnitude of LC hyperactivity during opiate withdrawal. Previous studies indicated that brain serotonin (5-HT) systems may be involved in opiate withdrawal. Two results from our laboratory led us to study the effect of enhanced serotonergic neurotransmission on withdrawal-induced LC hyperactivity: (i) a substantial part of such LC hyperactivity is mediated by an excitatory amino acid input to the locus coeruleus, and (ii) 5-HT selectively attenuates excitation of LC neurons mediated by excitatory amino acids. Here, we report that agents which increase serotonergic neurotransmission attenuate the hyperactivity of LC neurons induced by naloxone-precipitated withdrawal from chronic morphine exposure in rats. The 5-HT releaser/uptake blocker, d-fenfluramine, as well as the 5-HT reuptake blockers fluoxetine or sertraline, significantly attenuated the withdrawal-induced hyperactivity of LC neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8332249&dopt=Abstract

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