Abstract：
:To identify the molecular mechanisms underlying psychostimulant-elicited plasticity in the brain reward system, we undertook a phenotype-driven approach using genome-wide microarray profiling of striatal transcripts from three genetic and one pharmacological mouse models of psychostimulant or dopamine supersensitivity. A small set of co-affected genes was identified. One of these genes encoding the synaptic scaffolding protein PSD-95 is downregulated in the striatum of all three mutants and in chronically, but not acutely, cocaine-treated mice. At the synaptic level, enhanced long-term potentiation (LTP) of the frontocortico-accumbal glutamatergic synapses correlates with PSD-95 reduction in every case. Finally, targeted deletion of PSD-95 in an independent line of mice enhances LTP, augments the acute locomotor-stimulating effects of cocaine, but leads to no further behavioral plasticity in response to chronic cocaine. Our findings uncover a previously unappreciated role of PSD-95 in psychostimulant action and identify a molecular and cellular mechanism shared between drug-related plasticity and learning.
journal_name
Neuronjournal_title
Neuronauthors
Yao WD,Gainetdinov RR,Arbuckle MI,Sotnikova TD,Cyr M,Beaulieu JM,Torres GE,Grant SG,Caron MGdoi
10.1016/s0896-6273(04)00048-0subject
Has Abstractpub_date
2004-02-19 00:00:00pages
625-38issue
4eissn
0896-6273issn
1097-4199pii
S0896627304000480journal_volume
41pub_type
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