Det är jättesvårt att sluta med Remeron.
Man måste sänka extremt sakta.
Trots man gör det är det ett helvete.
Man måste göra det på ett rätt sätt som kan vara krångligt med.
Det finns en effekt med Remeron (neurotransmitter termostaten rubbas)
Det kan förklara en stor del i svårigheterna och att Remeron verkar på massa signalsystem. "Antagonist/inverse agonist effekten".
Själv slutade jag med Remeron efter 2 månaders bruk, tvärt. Hade svåra biverkningar i 10 månader men blev ganska återställd. Var uppe i 30-60 mg.
http://en.wikipedia.org/wiki/Mirtazapin ... codynamics
Mirtazapine is an antagonist/inverse agonist at the following receptors:[71][72]
* 5-HT2A receptor (Ki = 69 nM)
* 5-HT2B receptor (Ki = ? (~20-fold lower than for 5-HT2A/2C))[73]
* 5-HT2C receptor (Ki = 39 nM)
* 5-HT3 receptor (Ki = ? (similar to 5-HT2A/2C))[74]
* 5-HT7 receptor (Ki = 265 nM)
* α1-adrenergic receptor (Ki = 608 nM)
* α2A-adrenergic receptor (Ki = 20 nM)
* α2C-adrenergic receptor (Ki = 18 nM)
* H1 receptor (Ki = 1.6 nM)
* mACh receptors (Ki = 794 nM)
As well as an inhibitor of the following transporters:
* Norepinephrine transporter (Ki = 1,640 nM)
All affinities listed were assayed using human materials except those for α1-adrenergic, mACh, and NET which are for rat tissues, due to human values being unavailable.[71][72] Though not known to have ever been screened, mirtazapine may act on the 5-HT6 and α2B-adrenergic receptors as well. Notably, mianserin (which is 6-desazamirtazapine) has been shown to have high affinity for 5-HT6 and does not produce cAMP accumulation (indicating it is an antagonist).[75]
Antagonization of the α2-adrenergic receptors which function largely as autoreceptors and heteroreceptors enhances adrenergic and serotonergic neurotransmission, notably central 5-HT1A receptor-mediated transmission.[3][76][77][78][79] Because of this, mirtazapine has been said to be a functional "indirect agonist" of the 5-HT1A receptor.[78] Increased activation of the central 5-HT1A receptor is thought to be the primary mediator of efficacy of most antidepressant drugs.[80] Unlike most conventional antidepressants, however, mirtazapine is not a reuptake inhibitor and has no appreciable affinity for the serotonin, norepinephrine, or dopamine transporters, nor is it an MAOI or have any efficacy at inhibiting/inducing any other enzyme for that matter.
More recent findings suggest that mirtazapine also possesses a second antidepressant property, which is likely to be just as important as it's actions at the α2-adrenergic receptor in mitigating depression, mirtazapine's secondary antidepressant properties are likely to be mediated by its blockade of serotonin receptors, notably 5-HT2C.[81][82][83][83] The 5-HT2C receptor normally works to inhibit the release of the neurotransmitters dopamine and norepinephrine in various parts of the brain, notably in the pleasure centers such as the ventral tegmental area (VTA).[84][85] By blocking it, mirtazapine disinhibits dopamine and norepinephrine activity in these areas, causing a pronounced antidepressant and anxiolytic response.[86] Indeed, the novel antidepressant agomelatine acts primarily as a 5-HT2C receptor antagonist and has antidepressant efficacy at least comparable to that of the SSRIs and SNRIs.[87][88]
Antagonism of the 5-HT2A and 5-HT2C receptors has beneficial effects on anxiety, sleep and appetite, as well as sexual function regarding the latter.[76][89] Additionally, antagonism of the 5-HT3 receptor, the mechanism of action of antiemetic ondansetron, significantly improves pre-existing symptoms of nausea, vomiting, diarrhea, and general irritable bowel syndrome in afflicted individuals.[90] Mirtazapine may be used as an inexpensive and possibly even superior antiemetic alternative to ondansetron.[30] Blockade of the 5-HT3 receptors has also shown to improve anxiety and to be effective in the treatment of drug addiction in several studies.[91] Mirtazapine appears to be nootropic via enhancing memory functioning as well.[92] In contrast to mirtazapine, the SSRIs, SNRIs, TCAs, and MAOIs all increase the general activity of the 5-HT2A, 5-HT2C, and 5-HT3 receptors, leading to a host of negative changes and side effects, the most prominent of which include anorexia, insomnia, sexual dysfunction (impaired libido and anorgasmia), nausea, and diarrhea, among others. As a result, mirtazapine is often used in conjunction with these drugs to reduce their side effect profile and to produce a stronger antidepressant effect.[89][93][94][95][96][97]
Mirtazapine is a very strong H1 receptor antagonist and as a result, it can cause powerful sedative and hypnotic effects.[83] After a short period of chronic treatment, however, the H1 receptor tends to sensitize and the antihistamine effects become more tolerable. Many patients may also dose at night to avoid the effects and this appears to be an effective strategy for combating them. Blockade of the H1 receptor may improve pre-existing allergies, pruritus, nausea, and insomnia in afflicted individuals; hence, this may actually be a positive thing for some. It may also contribute to weight gain, however. Mirtazapine has very low affinity for the muscarinic acetylcholine receptors and therefore lacks significant anticholinergic properties at clinically used doses.