5HT2A receptor actually is highly effective for anhedonia as it increases da release and does other things, that's why psychedelics in threshold doses work for anhedonia, depression or anxiety, but activation of other neurotransmitters is involved too, that one they all act on tough.
5ht2a blockade can actually cause anhedonia(look at mirtazapine, trazodone, atypical aps) sure theres that book written by that pdoc that has spread that myth that 5ht2a is a bad anti dopaminergic receptor, sure aps increase da in the pfc, but that's caused by activation of 5ht2a and 5ht2c blockade if I remember correctly.
Offcourse it also depends on the type of depression,melancholic depression is alleviated by 5ht2a antagonism, and in that sense depression relief can cause anhedonia relief, that doesn't make 5ht2a a "evil" receptor, the brain is far more complicated then that, bloody hell that receptor does opposite things with dopamine in 1000 differened brainareas, the brain isn't just a simple straightforward organ>
5HT2A receptor actually is highly effective for anhedonia as it increases da release and does other things, that's why psychedelics in threshold doses work for anhedonia, depression or anxiety, but activation of other neurotransmitters is involved too, that one they all act on tough.
5ht2a blockade can actually cause anhedonia(look at mirtazapine, trazodone, atypical aps) sure theres that book written by that pdoc that has spread that myth that 5ht2a is a bad anti dopaminergic receptor, sure aps increase da in the pfc, but that's caused by activation of 5ht2a and 5ht2c blockade if I remember correctly.
Offcourse it also depends on the type of depression,melancholic depression is alleviated by 5ht2a antagonism, and in that sense depression relief can cause anhedonia relief, that doesn't make 5ht2a a "evil" receptor, the brain is far more complicated then that, bloody hell that receptor does opposite things with dopamine in 1000 differened brainareas, the brain isn't just a simple straightforward organ>
Jesus OP.. it would be sufficient to only mention the receptors or neurotransmitters known to blunt emotions or be necessary for emotions. Of them are dopamine, noradrenaline, serotonin, opioid, gaba, and possibly more.
The prime causes of blunted affect or flat affect are excessive opioid or gaba activation. A deficiency of glutamate activity can cause flat and blunted affect (creatine does this via depleting glutamate). Also serotonin is known to cause blunted and flat affect via the 5ht2a receptor and potentially more mechanisms.
Drugs that increase noradrenaline like male hormones also induce a degree of flatness.
Flat affect is the most severe of the affective dysfunctions, blunted precedes it I think, and so on. You can read on Wikipedia about this.
Ginseng is slightly effective for flat effect in shizo, and tada its a 5ht2a agonist.
