Leki przeciwdepresyjne, tymoleptyki - SSRI, SNRI, iMAO, TLPD i inne
Zobacz też: Wikipedia
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Dlaczego podczas brania SSRI/SNRI tak drastycznej zmianie, ulegają takie rzeczy:

- Zmniejszenie libido lub całkowity jego brak.
- Zmiana gęstości i ilości spermy
- Zmniejszenie jąder, zmiany skórne oraz zwisająca moszna
- Problemy z utrzymaniem erekcji lub jej brak.
- Niewrażliwość skóry oraz żołądzi.

Dodatkowo po odstawieniu przez dosyc długi czas, efekty całkowitego zaniku libido, erekcji i przyjemnosci czerpanej z seksu lub masturbacji.

Jakie mechanizmy, neuroprzekaźniki za to odpowiadają?
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5-HT1A agonism (pre-synaptic) can have it's benefits, namely in reducing excess serotonin - HOWEVER, after persistent agonism - it tends to de-sensitize, which then sends a flood of disinhibited serotonin to the post-synaptic 1A receptors which then can inhibit penile erection and can reduce sexual motivation....especially regarding arousal by female pheromones or presence!

5-HT1A agonism, all in all, is far less beneficial in men, than in women - where it tends to release oxytocin more and women have different levels of serotonin receptors anyhow...

Ideally, men DO NOT want much , if hardly at all 5-HT1A/1B activation - as they both inhibit male sexual response and performance.

So for PSSD, E.D or libido issues - you're better off with an ANTAGONIST - which will have beneficial effects on all hormonal parameter's in men as well...more so when a 1A antagonist is used with a 2A antagonist...

In women, the 5-HT1A agonism releases oxytocin which helps their bonding and libido...however, in men, it kills erections at that receptor and causes testosterone to decrease in response to female presence and in general. Read all studies below thoroughly.

Psychoneuroendocrinology. 2002 Jul;27(5):609-18.
Involvement of the 5-HT(1A) and 5-HT(1B) serotonergic receptor subtypes in sexual arousal in male mice.
Popova NK1, Amstislavskaya TG.
Author information

The presence of a sexually receptive female behind a partition that prevents physical contact, but not seeing or smelling, increases blood testosterone level and induces the specific behavior in CBA male mice so that they more frequently approach the partition and spend more time near it in an attempt to make their way to the female. Treatment with the selective 5-HT(1A) serotonin receptor agonist 8-OH-DPAT (0.1, 0.25, 0.5 and 2.0 mg/kg) induced a dose-dependent decreasein the amount of time spent by the males near the partition, or "partition time", which is considered the main pattern of sexual motivation. The activating effect of female exposure on the male's pituitary-testicular system was totally blocked, as no increase in plasma testosterone level was observed. The 5-HT(1A) antagonist p-MPPI (0.1, 0.2 and 0.4 mg/kg) itself did not affect behavior or alter plasma testosterone, but attenuated the inhibiting effect of 8-OH-DPAT on behavior and totally antagonised the effect of the 5-HT(1A) agonist on testosterone response. The 5-HT(1B) agonist CGS-12066A (1.0 and 2.0 mg/kg) has no influence on the plasma testosterone increase exhibited by the male in response to female exposure. At the same time, either dose of CGS-12066A significantly reduced the partition time. The conclusion was made that the 5-HT(1A) subtype is involved in controlling both behavioral and hormonal indices of sexual arousal in male mice, while the 5-HT(1B) receptors antagonise sexual motivation, but do not modify the hypothalamic-pituitary-testicular response.
PMID: 11965359 [PubMed - indexed for MEDLINE]
Int J Neuropsychopharmacol. 2009 Sep;12(8):1045-53. DOI: 10.1017/S1461145709000406. Epub 2009 May 13.
5-HT(1A) receptor antagonism reverses and prevents fluoxetine-induced sexual dysfunction in rats.
Sukoff Rizzo SJ1, Pulicicchio C, Malberg JE, Andree TH, Stack GP, Hughes ZA, Schechter LE, Rosenzweig-Lipson S.
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Sexual dysfunction associated with antidepressant treatment continues to be a major compliance issue for antidepressant therapies. 5-HT(1A) antagonists have been suggested as beneficial adjunctive treatment in respect of antidepressant efficacy; however, the effects of 5-HT(1A) antagonism on antidepressant-induced side-effects has not been fully examined. The present study was conducted to evaluate the ability of acute or chronic treatment with 5-HT(1A) antagonists to alter chronic fluoxetine-induced impairments in sexual function. Chronic 14-d treatment with fluoxetine resulted in a marked reduction in the number of non-contact penile erections in sexually experienced male rats, relative to vehicle-treated controls. Acute administration of the 5-HT(1A) antagonist WAY-101405 resulted in a complete reversal of chronic fluoxetine-induced deficits on non-contact penile erections at doses that did not significantly alter baselines. Chronic co-administration of the 5-HT(1A) antagonists WAY-100635 or WAY-101405 with fluoxetine prevented fluoxetine-induced deficits in non-contact penile erections in sexually experienced male rats. Moreover, withdrawal of WAY-100635 from co-treatment with chonic fluoxetine, resulted in a time-dependent reinstatement of chronic fluoxetine-induced deficits in non-contact penile erections. Additionally, chronic administration of SSA-426, a molecule with dual activity as both a SSRI and 5-HT(1A) antagonist, did not produce deficits in non-contact penile erections at doses demonstrated to have antidepressant-like activity in the olfactory bulbectomy model. Taken together, these data suggest that 5-HT(1A) antagonist treatment may have utility for the management of SSRI-induced sexual dysfunction.
PMID: 19435548 [PubMed - indexed for MEDLINE]
J Androl. 2006 Sep-Oct;27(5):679-85. Epub 2006 May 25.
Doxazosin and serotonin (5-HT) receptor (1A, 2A, and 4) antagonists inhibit 5-HT-mediated human cavernosal contraction.
Lau DH1, Thompson CS, Bellringer JF, Thomas PJ, Mumtaz FH, Morgan RJ, Mikhailidis DP.
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Penile erection results from the balance between relaxation and contractile mechanisms of the corpus cavernosum. Only a few studies suggest a role for endogenous contractile agents such as 5-hydroxytryptamine (5-HT). Our aim was to confirm the possible role of 5-HT in human erection. The effect of 5-HT on human cavernosal tissues, as well as those of doxazosin (shown previously to have 5-HT inhibitory action), ketanserin (5-HT (2A) receptor antagonist), NAN-190 (5-HT (1A) receptor antagonist), and SB 203186 (5-HT (4) receptor antagonist) on 5-HT-mediated effects, were assessed using the organ bath technique, including electrical field stimulation study (EFS). Results are presented as median (mg/mg = mg contraction/mg of tissue). Consistent 5-HT-mediated (10(-3) M) contractions were demonstrated (n = 18; 63 mg/mg). These contractions were inhibited with ketanserin by 90% (n = 8), NAN-190 by 68% (n = 12), and SB 203186 by 55% (n = 12). Doxazosin showed a similar 5-HT inhibitory action in a concentration-dependent manner (10(-4) M; 94% reduction; n = 8, 10(-6) M; 68.3% reduction; n = 8). Our EFS studies indicated the presence of neuronally derived 5-HT and that a majority of the nonnoradrenogenic contraction (54%) was mediated via 5-HT(2A) receptors. These findings suggest that 5-HT may play a role in the human detumescence process via 5-HT(1A), 5-HT(2A), and 5-HT(4) receptors. Neuronally released 5-HT is probably an important contractile neurotransmitter in the erectile process. Doxazosin, ketanserin, and 5-HT(1A) and 5-HT(4) receptor antagonists may be useful as part of combination therapy used to treat erectile dysfunction.
PMID: 16728720 [PubMed - indexed for MEDLINE] Free full text
Psychopharmacology (Berl). 1992;108(1-2):47-50.
5-HT1A receptor agonists prevent in rats the yawning and penile erections induced by direct dopamine agonists.
Simon P1, Guardiola B, Bizot-Espiard J, Schiavi P, Costentin J.
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The new compound (+) S-20499, an amino chromane derivative (8[-4[N-(5-methoxychromane-3yl)N-propyl]aminobutyl] azaspiro[4-5] décane-7,9 dione), is a high affinity full 5-HT1A agonist. We have investigated its effects on dopaminergic transmission. (+) S-20499 displayed a 10(-8) M affinity for D2 dopamine (DA) receptors, 100 fold lower than for 5-HT1A receptors. The hypothermic effect of the drug was reversed by haloperidol in mice, suggesting that it behaves as a direct dopamine agonist. However, increasing doses of (+) S-20499 induced neither yawning nor penile erections, which constitute characteristic responses of direct DA agonists administered at low doses. In addition, (+) S-20499 prevented the apomorphine (100 micrograms/kg SC) induced yawning and penile erections. This inhibition appears to result from the stimulation of 5-HT1A receptors since it is an effect shared by both buspirone (from 5 mg/kg) and 8-OH-DPAT (from 0.10 mg/kg). In addition, when rats are treated with the 5-HT1A receptor antagonist tertatolol (2-5 mg/kg; SC), increasing doses of (+) S-20499 elicit the expected yawns and penile erections. It is concluded that the 5-HT1A agonist property opposes to that of D2 dopamine receptor stimulation with regard to yawning and penile erections.
PMID: 1357709 [PubMed - indexed for MEDLINE]
Eur Neuropsychopharmacol. 2004 Mar;14(2):151-5.
Hormonal and temperature responses to flesinoxan in normal volunteers: an antagonist study.
Pitchot W1, Wauthy J, Legros JJ, Ansseau M.
Author information

Flesinoxan is a highly potent and selective 5-HT1A agonist. In a recent study, in normal volunteers, flesinoxan induced a significant and dose-dependent increase in adrenocorticotropic hormone (ACTH), cortisol, prolactin (PRL), growth hormone (GH) and a decrease in body temperature.
In order to better define the role of 5-HT receptor subtypes in response to flesinoxan, we assessed the influence of 5-HT1A and 5-HT2 antagonists on hormonal and temperature responses to flesinoxan.
Hormonal and temperature responses were studied in 6 volunteers with or without pretreatment with pindolol (30 mg p.o.), a 5-HT1A antagonist, or ritanserin (10 mg p.o.), a selective 5-HT2 antagonist, using a double-blind crossover design.
Pindolol significantly antagonized ACTH, PRL, GH and temperature responses to flesinoxan and ritanserin exhibited similar activity on PRL and ACTH responses.
These results show the role of 5-HT1A mechanisms in the PRL, ACTH, GH, and temperature responses to flesinoxan, and the role of 5-HT2 mechanisms in PRL and ACTH responses. Therefore, they confirm the interest of flesinoxan as a 5-HT neuroendocrine probe.
PMID: 15013031 [PubMed - indexed for MEDLINE]

http://www.longecity.org/forum/topic/76 ... ntry714385
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Nikt nic więcej nie doda? Szkoda, bo temat jest warty rozwinięcia.
Odpłatne konsultacje na temat diet, nootropów, stymulantów, suplementów, uzależnień, zbijania tolerancji, anhedoni, depresji, porycia ponarkotykowego, harm reduction i innych.
email: hash_oil@tutanota.com
  • 288 / 19 / 0
biorę pierwszy raz paroksetyne i jakiekolwiek antydepresanty. Oczytalem sie o tym zmniejszeniu libidu a ja mam libido wieksze, ktos umie to wytlumaczyc ?
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Większość ssri podnosi poziom prolaktyny. Prolaktyna jest głównym antagonistą dopaminy, a dopamina odpowiada za libido w tym przypadku. Możliwe że to jeden z powodów
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