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Mirtazapine's Pharmacologic Profile

  1. Adrenoceptors and Serotonin Receptor function
    J Clin Psychiatry 1996;57 Suppl 4:4-8

  2. Mirtazapine's pharmacologic profile
    J Clin Psychiatry 1996;57 Suppl 4:19-25

  3. Mirtazapine's pharmacology in relation to adverse effects
    Acta Psychiatr Scand Suppl 1997;391:31-7




#1

Adrenoceptors & Serotonin Receptor Function:
Relevance To AntiDepressant Action

Potter, WZ
J Clin Psychiatry 1996;57 Suppl 4:4-8
National Institute of Mental Health, Section on Clinical Pharmacology, Bethesda, Md. 20892, USA
PMID# 8636064; UI# 96237826
Abstract

Hypotheses of AntiDepressant action which argue that even NorEpinephrine (NE) uptake inhibitors ultimately work through potentiation of Serotonergic function are critically reviewed.

Preclinical ElectroPhysiologic data can be interpreted as evidence for enhanced Serotonin (5-HT) throughput as a common mechanism of action of all AntiDepressants.

Biochemical data in rats (e.g., microdialysis) and humans (e.g., opposite effects of ECT on 5-HIAA in CerebroSpinal Fluid), however, suggest that more is involved than simply enhanced 5-HT function when NE uptake inhibition is combined with 5-HT uptake inhibition.

The case, however, for NorAdrenergic effects on 5-HT function is quite strong either with regard to stimulation of alpha 1 Receptors on 5-HT cell bodies or alpha 2 Heteroreceptors on 5-HT nerve endings.

Even the reported ability of Pindolol to potentiate the AntiDepressant effects of 5-HT uptake inhibitors may prove to involve NorAdrenergic effects and not simply antagonism of 5-HT1A receptors as currently hypothesized.

The biochemically specific drugs needed to directly test these concepts are not yet available.

On the other hand, compounds which combine NorAdrenergic and Serotonergic effects (e.g., alpha 2 Antagonism and 5-HT2 Antagonism) that go beyond those of the classic uptake inhibitors are emerging as agents to test the clinical potential of selective manipulation of these interacting NeuroTransmitter systems.



#2

Mirtazapine's Pharmacologic Profile

de Boer, T
J Clin Psychiatry 1996;57 Suppl 4:19-25
Scientific Development Group, Neuropharmacology Dept, N.V. Organon, The Netherlands
PMID# 8636062; UI# 96237829
Abstract

Mirtazapine (Org 3770) is a new AntiDepressant with prominent alpha 2-Adrenergic Auto- and Heteroreceptor Antagonistic properties and no effect on Monoamine Reuptake.

Mirtazapine increases NorAdrenergic and Serotonergic transmission, as measured by on-line microdialysis and by enhancement of NorAdrenergic Locus Ceruleus and Serotonergic Raphe Nucleus Cell firing.

Mirtazapine has a low affinity for 5-HT1A receptors but shows 5-HT1A-agonistic-like effects in a conditioned taste aversion test and by causing lower lip retraction in rats.

Mirtazapine therefore causes enhancement of 5-HT1-mediated transmission. Other studies show that both 5-HT2 and 5-HT3 receptors are specifically blocked.

The enhancement of both NorAdrenergic and Serotonergic transmission probably underlies the therapeutic activity of Mirtazapine.

Blockade of 5-HT2 and 5-HT3 receptors possibly prevents side effects associated with nonselective 5-HT activation and may also contribute to the Anxiolytic and sleep-improving properties of Mirtazapine.



#3

Mirtazapine's Pharmacology
In Relation To Adverse Effects

Nutt, D
Acta Psychiatr Scand Suppl 1997;391:31-7
Univ of Bristol, School of Medical Sciences, United Kingdom
PMID# 9265949; UI# 97410900
Abstract

Mirtazapine is a new AntiDepressant that falls into the general class of Receptor-Blocking drugs rather than being an Uptake or Enzyme Inhibitor.

It can be described as a NorAdrenergic and Specific Serotonergic AntiDepressant (NaSSA). The unique pharmacology of Mirtazapine means that it has a very different side effect profile from the TriCyclic AntiDepressants.

Mirtazapine produces less alpha 1 Adrenergic and Muscarinic blockade, than the Selective Serotonin Reuptake Inhibitors (SSRIs) and the Serotonin-NorAdrenaline Reuptake Inhibitors (SNRIs), causing much less Nausea and Sexual Dysfunction by virtue of its blockade of 5-HT2 and 5-HT3 receptors.



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