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Published on: September 16, 2015
Decrease of GSK3β phosphorylation in the rat nucleus accumbens core enhances cocaine-induced hyper-locomotor activity
Wha Y Kim1, Ju K Jang, Jung W Lee
1Department of Physiology, Brain Korea 21 Project for Medical Science, Brain Research Institute, Yonsei University College of Medicine, Seoul, South Korea.
Journal of Neurochemistry
|February 27, 2013
Summary
Decreasing glycogen synthase kinase 3 beta (GSK3β) phosphorylation in the nucleus accumbens enhances cocaine-induced hyperactivity. This suggests GSK3β, when less phosphorylated, may facilitate stimulant-driven behaviors.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Glycogen synthase kinase 3 beta (GSK3β) is abundant in the brain and influences psychomotor stimulant responses.
- Previous research indicated GSK3β attenuates stimulant-induced hyperactivity via increased phosphorylation in the nucleus accumbens (NAcc).
Purpose of the Study:
- To investigate the effects of decreased GSK3β phosphorylation in the NAcc core on basal and cocaine-induced locomotor activity.
- To explore the role of reduced GSK3β phosphorylation in stimulant-related behaviors.
Main Methods:
- Bilateral microinjection of the S9 peptide into the NAcc core of the brain.
- The S9 peptide targets sequences around the N-terminal serine 9 residue of GSK3β, decreasing its phosphorylation.
- Assessment of basal and cocaine-induced locomotor activity.
Main Results:
- Decreased GSK3β phosphorylation in the NAcc core significantly enhanced cocaine-induced hyper-locomotor activity.
- Basal locomotor activity remained unchanged by the manipulation.
- This is the first study to show that reduced GSK3β phosphorylation in the NAcc core positively contributes to cocaine-induced locomotor activity.
Conclusions:
- Selective reduction of GSK3β phosphorylation in the NAcc core potentiates cocaine's locomotor effects.
- GSK3β phosphorylation levels in the NAcc core are critical for modulating stimulant-induced behaviors.
- GSK3β may require co-activation of other molecular targets by cocaine to fully mediate locomotor behaviors.
