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Mirtazapine also blocks the effect of histamine. The antinociceptive effect of mirtazapine in mice is mediated through serotonergic, noradrenergic and opioid mechanisms. In this particular case, the cause of death was ibogaine-induced cardiac arrest, which led to cerebral edema and brain death. Because most individuals won’t like the idea of [potentially] sacrificing their brain cells and/or brain structures to attain sobriety, ibogaine may be perceived as a suboptimal intervention. Neurotoxicity is thought to result from excessive excitatory transmission in which brain cells die from overstimulation. For reference, delta-opioid receptors are densest within the basal ganglia and neocortical areas of the brain and are thought to influence arousal, mood, nociception, and regulate aspects of drug reward. Moreover, it is known that delta-opioid receptors are implicated in the assignment of hedonic values to addictive drugs, which may influence drug-seeking behavior.

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Still, ibogaine’s more prominent actions at other receptor sites may be augmented by delta-opioid receptor agonism. To be clear, alterations in brain energy metabolism that are observed post-ibogaine administration are likely a secondary or downstream effect stemming from its primary interactions with neurotransmitter systems. 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. The enhancement of both noradrenergic and serotonergic transmission probably underlies the therapeutic activity of mirtazapine. Subjectively, mirtazapine induced an improvement of sleep.

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The aim of the locomotor activity test was to select a dose which had no influence on the motility of the animals and, at the same time, was active at least in one behavioral test. In the maze test, mirtazapine shortened the food finding time (it improved memory) and counteracted memory loss induced by scopolamine. Moreover, citalopram still inhibited, and mirtazapine still failed to influence, dorsal raphe serotonergic neurons. In rats chronically treated with imipramine or mirtazapine this effect was completely antagonized. These results demonstrate that long-term treatment with either imipramine or mirtazapine reduces the sensitivity of cortical cholinergic neurons to stress or to an anxiogenic drug with an efficacy similar to that of acute administration of benzodiazepines. Because dopaminergic transmission in the prefrontal cortex is sensitive to anxiogenic or stressful stimuli, the effects of two antidepressant drugs with different mechanisms of action, imipramine and mirtazapine, on the response of rat cortical dopaminergic neurons to stress were investigated. Long-term administration of imipramine or mirtazapine had no marked effect on the stress-induced increases in the brain or plasma concentrations of neuroactive steroids or corticosterone.

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In depressed patients, mirtazapine produces a significant shortening of sleep-onset latency, increases a total sleep time, and leads to a marked improvement in sleep efficiency. Mirtazepine is a potential alternative anti-depressant with multiple additional benefits. It is becoming increasingly clear that differences exist between antidepressants with respect to this property, both within and between pharmacologic classes. The positive predictive value of an early improvement was significantly higher during mirtazapine treatment compared with paroxetine.

Mirtazapine was consistently superior to placebo, and equivalent in efficacy to the tricyclic antidepressants amitriptyline, doxepin and clomipramine, but with an improved tolerability profile. In addition, mirtazapine does not appear to be associated with sexual dysfunction. Mirtazapine in fixed and ascending nocturnal dosing regimens was found to facilitate sleep, but it does not generally reduce daytime alertness. Mirtazapine did not significantly alter rapid eye movement sleep parameters. The available data show that mirtazapine is superior to placebo in depressed patients with high baseline anxiety and/or agitation. Mirtazapine provides early and effective relief of both depressive and anxiety symptoms, reducing the need for polypharmacy.

The evaluation of the safety was based on data from all patients who took at least one dose of study medication during studies comparing mirtazapine with placebo, amitriptyline or other active comparators. These complaints were typically mild and transient in nature, and decreased over time despite increased doses of mirtazapine. The low seizure-inducing potential combined with a lack of cardiotoxic properties allows safety in an overdose of mirtazapine, even in elderly patients. Weight gain is the most commonly reported side-effect of mirtazapine, although there is evidence to suggest that this is not a significant problem during long-term treatment.