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Cell-specific MSN gene transcription is altered during the pathogenesis and treatment of many neuropsychiatric diseases, including Huntington disease, Parkinson disease, drug addiction, affective disorders, attention deficit hyperactivity disorder, and schizophrenia (4–7).
Despite the obvious clinical significance of gene regulation in MSNs and the requirement for cell-specific transcription in the development of the nervous system, few details are available regarding how the MSN phenotype is specified at the molecular level.
It also appears that PI3K is upstream of cdk5/p35, and its activation can lead to an increase in p35 protein levels.
Based on our data demonstrating regulation of DARPP-32 m RNA levels by BDNF (18, 19) and findings for a role for pathophysiological decreases in BDNF levels in depression and subsequent elevation during its treatment (reviewed in Refs.
24 and 25), it has been hypothesized that altered transcription of DARPP-32 by BDNF is implicated.
The potentiation of target protein phosphorylation, mediated by DARPP-32 regulation of protein phosphatase-1, appears to be a required action of the dopaminergic signaling pathway under physiologic conditions.
In the absence of DARPP-32, striatal neurons show marked neurophysiological abnormalities in response to dopamine D1 agonists, including decreased spike height in dissociated neurons and a reduced response -aspartic acid NR1 subtype.
DARPP-32 induction by BDNF requires phosphatidylinositide 3-kinase (PI3K), but inhibition of phosphorylation of protein kinase B/Akt does not entirely abolish expression of DARPP-32.