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Neuronal and behavioural abnormalities in striatal function in DARPP-32-mutant mice.
N Hiroi1, A A Fienberg, C N Haile
1Laboratory of Molecular Psychiatry, Center for Genes and Behaviour, Yale University School of Medicine, New Haven, CT 06508, USA.
The European Journal of Neuroscience
|April 2, 1999
Summary
Dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) influences substance P levels and cocaine-induced behavioral changes. DARPP-32 knockout mice exhibit altered responses to chronic cocaine, impacting plasticity.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- DARPP-32 is a key protein phosphatase inhibitor in the striatum.
- Its role in neuropeptide expression and drug-induced plasticity is not fully understood.
Purpose of the Study:
- To investigate the function of DARPP-32 in striatal neuropeptide expression.
- To examine the involvement of DARPP-32 in the biochemical and behavioral effects of repeated cocaine administration.
Main Methods:
- Utilized DARPP-32 knock-out mice and wild-type littermates.
- Measured striatal neuropeptide levels (substance P, others).
- Assessed DeltaFosB induction and locomotor activity following cocaine exposure.
Main Results:
- DARPP-32 mutant mice displayed heightened substance P levels.
- Cocaine-induced DeltaFosB increase in the striatum was abolished in mutants.
- Mutant mice showed increased locomotor sensitization to repeated cocaine.
Conclusions:
- DARPP-32 regulates substance P expression in the striatonigral pathway.
- DARPP-32 is crucial for cocaine-induced biochemical and behavioral plasticity.