Originariamente inviata da Tocris.com

A drug that attenuates the effect of an agonist. Can be competitive or non-competitive, each of which can be reversible or irreversible. A competitive antagonist binds to the same site as the agonist but does not activate it, thus blocks the agonist’s action. A non-competitive antagonist binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor. A reversible antagonist binds non-covalently to the receptor, therefore can be “washed out”. An irreversible antagonist binds covalently to the receptor and cannot be displaced by either competing ligands or washing.

Originariamente inviata da Tocris.com

A drug that binds to and activates a receptor. Can be full, partial or inverse. A full agonist has high efficacy, producing a full response while occupying a relatively low proportion of receptors. A partial agonist has lower efficacy than a full agonist. It produces sub-maximal activation even when occupying the total receptor population, therefore cannot produce the maximal response, irrespective of the concentration applied. An inverse agonist produces an effect opposite to that of an agonist, yet binds to the same receptor binding-site as an agonist.

Originariamente inviata da Life (Messaggio 2154825)

Non funziona, almeno con me

Originariamente inviata da Crystal (Messaggio 2154953)

Nel mio ha caso funzionato bene vs la dep...l'unico che migliorava l'umore in maniera discreta. Gli altri che ho provato erano pressoché acqua tiepida.

Nel leggere la farmaco dinamica di alcuni farmaci, mi vien da ridere quando trovi scritto: non si comprende ancora bene in che modo funzioni...ma sembra che... :mannaggia:
Namobbene...:mrgreen:

Originariamente inviata da Noriko (Messaggio 2154952)

Sverso sei un genio! :)

Accipicchia questi del forum …. :bene:

.. gli antidepressivi calmano quindi si calmano anche i pensieri cupi.
L'antipsicotico calma i pensieri deliranti e mette a tacere le voci.
A basse dose va bene anche per i depressi perché comunque è un sedativo a suo modo come l'antidepressivo, anche se non è specifico e mirato.

Scusate la banalità :miodio:

Originariamente inviata da Svers0 (Messaggio 2154957)

Il fatto è che per fermare le voci e i pensieri deliranti bisogna bloccare la dopamina, questo farmaco invece tende a bloccare più alcuni recettori serotoninergici mentre quelli dopaminergici li stimola, a quanto ho capito si sostiuisce alla dopamina ed è lui che stimola i recettori dopaminergici evitando che la dopamina sia troppa e quindi delirio o troppo poca e quindi avolizione, anedonia e così via, almeno questo mi pare di aver capito.

Se fossi un vero genio sarei già a lavorare in qualche casa farmaceutica. :mrgreen:

Originariamente inviata da Badblues (Messaggio 2154960)

Ma fa ingrassare?

Originariamente inviata da Badblues (Messaggio 2154960)

Ma fa ingrassare?

Originariamente inviata da Life (Messaggio 2154955)

Quando sei migliorato prendevi solo abilify? Io lo prendo a 10mg ma è come acqua

Originariamente inviata da zucchina (Messaggio 2155498)

che ne pensate del sapore dell'abilify?:mrgreen: uno schifo , misto amaro e dolce!

Originariamente inviata da Badblues (Messaggio 2157005)

Voglio provare qualcosa oltre alla parox

Originariamente inviata da Badblues (Messaggio 2157008)

Devo trovare uno psichiatra decente non un vecchio smidollato

Originariamente inviata da Svers0 (Messaggio 2157012)

Si, non arrenderti, ci sono un sacco di farmaci e ho notato che gli psichiatri tendono ad essere molto prudenti prima di smollarti qualcosa che funziona veramente anche perché i farmaci più forti hanno anche effetti collaterali più forti.

Originariamente inviata da Badblues (Messaggio 2157057)

Che poi pure il mio medico di base si mette di traverso nelle prescrizioni

Originariamente inviata da Life (Messaggio 2157063)

Cioè?

Originariamente inviata da Wikipedia

5-HT1A receptor agonists are involved in neuromodulation. They decrease blood pressure and heart rate via a central mechanism, by inducing peripheral vasodilation, and by stimulating the vagus nerve.[10] These effects are the result of activation of 5-HT1A receptors within the rostral ventrolateral medulla.[10] The sympatholytic antihypertensive drug urapidil is an α1-adrenergic receptor antagonist and 5-HT1A receptor agonist, and it has been demonstrated that the latter property contributes to its overall therapeutic effects.[11][12] Vasodilation of the blood vessels in the skin via central 5-HT1A activation increases heat dissipation from the organism out into the environment, causing a decrease in body temperature.[13][14]

Activation of central 5-HT1A receptors triggers the release or inhibition of norepinephrine depending on species, presumably from the locus coeruleus, which then reduces or increases neuronal tone to the iris sphincter muscle by modulation of postsynaptic α2-adrenergic receptors within the Edinger-Westphal nucleus, resulting in pupil dilation in rodents, and pupil constriction in primates including humans.[15][16][17]

5-HT1A receptor agonists like buspirone[18] and flesinoxan[19] show efficacy in relieving anxiety[20] and depression,[21] and buspirone and tandospirone are currently approved for these indications in various parts of the world. Others such as gepirone,[22] flesinoxan,[19] flibanserin,[23] and naluzotan[24] have also been investigated, though none have been fully developed and approved yet. Some of the atypical antipsychotics like lurasidone[25] and aripiprazole[26] are also partial agonists at the 5-HT1A receptor and are sometimes used in low doses as augmentations to standard antidepressants like the selective serotonin reuptake inhibitors (SSRIs).[27]

5-HT1A autoreceptor desensitization and increased 5-HT1A receptor postsynaptic activation via general increases in serotonin levels by serotonin precursor supplementation, serotonin reuptake inhibition, or monoamine oxidase inhibition has been shown to be a major mediator in the therapeutic benefits of most mainstream antidepressant supplements and pharmaceuticals, including serotonin precursors like L-tryptophan and 5-HTP, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), tetracyclic antidepressants (TeCAs), and monoamine oxidase inhibitors (MAOIs).[28] 5-HT1A receptor activation likely plays a significant role in the positive effects of serotonin releasing agents (SRAs) like MDMA ("Ecstasy") as well.[29][30]

5-HT1A receptors in the dorsal raphe nucleus are co-localized with neurokinin 1 (NK1) receptors and have been shown to inhibit the release of substance P, their endogenous ligand.[31][32] In addition to being antidepressant and anxiolytic in effect, 5-HT1A receptor activation has also been demonstrated to be antiemetic[33][34] and analgesic,[35][36] and all of these properties may be mediated in part or full, depending on the property in question, by NK1 receptor inhibition. Consequently, novel NK1 receptor antagonists are now in use for the treatment of nausea and emesis, and are also being investigated for the treatment of anxiety and depression.[37]

5-HT1A receptor activation has been shown to increase dopamine release in the medial prefrontal cortex, striatum, and hippocampus, and may be useful for improving the symptoms of schizophrenia and Parkinson's disease.[38][39] As mentioned above, some of the atypical antipsychotics are 5-HT1A receptor partial agonists, and this property has been shown to enhance their clinical efficacy.[38][40][41] Enhancement of dopamine release in these areas may also play a major role in the antidepressant and anxiolytic effects seen upon postsynaptic activation of the 5-HT1A receptor.[42][43]

Activation of 5-HT1A receptors has been demonstrated to impair certain aspects of memory (affecting declarative and non-declarative memory functions) and learning (due to interference with memory-encoding mechanisms), by inhibiting the release of glutamate and acetylcholine in various areas of the brain.[44] 5-HT1A activation are known to improve cognitive functions associated with the prefrontal cortex, possibly via inducing prefrontal cortex dopamine and acetylcholine release.[45] Conversely, 5-HT1A receptor antagonists such as lecozotan have been shown to facilitate certain types of learning and memory in rodents, and as a result, are being developed as novel treatments for Alzheimer's disease.[46]

Other effects of 5-HT1A activation that have been observed in scientific research include:

Decreased aggression[47][48]
Increased sociability[30]
Decreased impulsivity[49]
Inhibition of drug-seeking behavior[50][51][52]
Facilitation of sex drive and arousal[53][54]
Inhibition of penile erection[55][56]
Diminished food intake[57]
Prolongation of REM sleep latency[58][59]
Reversal of opioid-induced respiratory depression[60]

Originariamente inviata da Wikipedia

Physiological processes mediated by the receptor include:

CNS: neuronal excitation (most likely responsible for the psychedelic effects associated with 5-HT2A receptor agonists such as LSD, DMT, etc.),[29] behavioural effects, learning, anxiety
smooth muscle: contraction (in bronchi and gastrointestinal tract)
vasoconstriction / vasodilation
platelets: aggregation
Activation of the 5-HT2A receptor with 2,5-Dimethoxy-4-iodoamphetamine (DOI) produces potent anti-inflammatory effects in several tissues including cardiovascular and gut. Other 5-HT2A agonists like LSD also have potent anti-inflammatory effects against TNF-alpha-induced inflammation.[30][31]
Activation of the 5-HT2A receptor in hypothalamus causes increases in hormonal levels of oxytocin, prolactin, ACTH, corticosterone, and renin.[32][33]
Role in memory and learning[15][34][35]

Originariamente inviata da Svers0 (Messaggio 2162294)

Più studio questo farmaco e meno ne capisco, si comporta in modo davvero strano.