This upregulation of D1 receptors might be secondary to a sustained deficit in prefrontal DA function, as postmortem studies revealed deficits in DA innervation in the prefrontal cortex in schizophrenia.
Together, these observations led to a reformulation of the classical DA hypothesis postulating that the excess DA transmission is restricted to subcortical areas of the brain, rich in D2 receptors, and associated with positive symptoms of the illness, while a deficit in DA transmission at D1 receptors in the PFC might be implicated in the cognitive impairments and negative symptoms (8,9). This was supported by the lack of efficacy of D2 receptor antagonism in the treatment of negative and cognitive symptoms.
I had a lecturer mention this a few years ago and it’s interesting. But most likely, I think, dopamine is not the cause of either the cognitive deficits or the positive symptoms, but just a correlate of both. Cognitive deficits precede the dopamine dysregulation and APs that barely affect dopaminergic transmission are about as effective as those that do.
Of sz or of APs?
Of sz. And they are probably more fundamental to sz than positive symptoms.
All I know from experience is that anything that increase my dopamine improves my negative symptoms. Like LDopa etc
nevermind 555555
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