During the psychosis irrespective of particular diagnosis the dopamine synthesis capacity is increased (https://www.ncbi.nlm.nih.gov/pubmed/?term=A+Test+of+the+Transdiagnostic+Dopamine+Hypothesis+of+Psychosis+Using+Positron+Emission+Tomographic+Imaging+in+Bipolar+Affective+Disorder+and+Schizophrenia).
But, would not be better in the case of psychosis to talk about increased dopamine release instead of increased dopamine synthesis capacity, if we do not know directly, whether the hyperdopaminergic striatal state is caused by increased dopamine synthesis or only by increased dopamine release or even disruption of termination of synaptic dopamine action (https://www.ncbi.nlm.nih.gov/pubmed/?term=Putative+presynaptic+dopamine+dysregulation+in+schizophrenia+is+supported+by+molecular+evidence+from+post-mortem+human+midbrain)?
No, it would not be better because the mechanism is very complex. DAT plays a role, so do environmental and a lot of other factors.
But that is why I propose to talk about the increased dopamine release rather than the dopamine synthesis elevated. It seems to me a more complex and general concept.
I know it's not the same, that's why I am asking. For the hyperdopaminergic state, the increased striatal presence of dopamine is important, am I right? The release of dopamine from synaptic vesicles is more important phenomenon than dopamine synthesis capacity itself, as vesicular dopamine may also be reuptaken, it may not only have a source in cytoplasmic synthesis mechanisms.
However, it is true that increased dopamine synthesis can be a direct mechanism, leading to its increased release.
I agree with you. Actually many psychotropic drugs work not just in the production of a neurotransmitter but also in different levels of his pathways.
My understanding is that dopamine is released from dopamine cells under conditions of stress or anticipation of reward. On the postsynaptic side, dopamine D2 receptors are, in psychosis, more often in the "avid" or high sensitivity state so that an excess of dopamine is transmitted through the neuronal membrane of the next cell and less of it stays in the synapse from where it is taken back up by the presynaptic neuron. The smaller 'take back' , in turn, stimulates more production.
It is not only dopamine inculded in pathogenesis of sch'like behaviour!
Yes, sure. But whether we like it or not, every new theory is still somewhat related to dopamine.
@Michal Patarak. Indeed, to my knowledge every theory about psychosis is somewhat related to dopamine. And, I would suggest to the SEEK system. The antipsychotic action of clozapine, then would seem at the moment unexplained.