Nmda Ampa and Kainate are the receptors of Glutamate.
MGlu and glu receptors fall in the category of the above mentioned.
Too much glutamate is harmful i.e. destroys the Brain.
Search in google or even here on longecity for DXM, Ketamine or Angeldust "victims" ( those are all nmda inhibiotrs)
-> Monoamine receptors like dopamine d2 d3, Adrenaline a1,a2 and a few 5-ht ( Serotonine) receptors and ion channels e.g. Calcium channels
decrease Glutamate to various extends
-> Risperdal decreases/destroys some of those monoamine receptors
-> By blocking e.g. Nmda receptors, more Glutamate is avaiable, dosedependly, to such extend that it overactivates the Ampa and kainate receptors,
so that the Braincells die.
-> by using Nmda blockers and having a decreased number of one of those receptors ( caused by Risperdal or other Antipsychotics)
You have even more glutamate released and therefore cell death is increased or at least the possibility.
As said, this would not regrowth.
Some reproted that Wellbrutin has actually a dulling effect and others say that this isnt even comparable to Ritalin
http://www.socialanx...932-post15.html
DRI cant work in certain areas if Dopamine is not released by 5-ht2a receptor activation
(which act like autoreceptors in the mesocortical area) or there arent enough receptors
You could try besides Trazodone a low dose (50mg) of Amisulpride
which is a dopamine autoreceptor inhibitor but beyond 100mg, a dopamine receptor antagonist like Risperdal
5-Ht1a blockade could be helpful.
http://www.ncbi.nlm....pubmed/19435548
http://www.propeciah...opic.php?t=7009
Ask Area-1255 for 5-ht1a antagonists.
Afaik cyproheptadine does also block 5-ht1a ( or perhaps only the presynaptic ? Dunno)
Serotonin neurons from the dorsal raphe project to the substantia nigra, the ventral tegmentum, the dorsal and ventral striatum, and to the frontal cortex. These terminal areas contain 5-HT1B/1D,5-HT2A, and 5-HT3 receptors. Serotonin may induce local release of dendritic nigral DA (131). Serotonin stimulation of 5-HT2A receptors inhibits the activity of DA neurons in the substantia nigra. 5-HT2A antagonistss increase activity of DA neurons in the ventral tegmental area (VTA) and substantia nigra DA neurons, and thus increase DA release in terminal areas (24,53,87). VTA neurons respond to lower concentrations of 5-HT2 antagonistss (33).5-HT2A antagonistss may also increase DA release in the prefrontal cortex by a direct action at 5-HT2A receptors on DA nerve terminals (82,93,117). 5-HT2A. antagonistss may also prevent the effect of decreased prefrontal glutamatergic activity that inhibits burst firing of VTA DA neurons. This might be a mechanism by which 5-HT2A antagonistss decrease negative symptoms (36,117).
http://www.acnp.org/...0117/CH115.html
Edited by Flex, 13 September 2014 - 08:22 PM.