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Decrease of GSK 3β phosphorylation in the rat nucleus accumbens core enhances cocaine‐induced hyper‐locomotor activity
Author(s) -
Kim Wha Y.,
Jang Ju K.,
Lee Jung W.,
Jang Hyunduk,
Kim JeongHoon
Publication year - 2013
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.12222
Subject(s) - nucleus accumbens , phosphorylation , locomotor activity , gsk 3 , stimulant , microinjection , chemistry , pharmacology , neuroscience , endocrinology , psychology , biology , dopamine , biochemistry
Glycogen synthase kinase 3β ( GSK 3β), which is abundantly present in the brain, is known to contribute to psychomotor stimulant‐induced locomotor behaviors. However, most studies have been focused in showing that GSK 3β is able to attenuate psychomotor stimulants‐induced hyperactivity by increasing its phosphorylation levels in the nucleus accumbens ( NA cc). So, here we examined in the opposite direction about the effects of decreased phosphorylation of GSK 3β in the NA cc core on both basal and cocaine‐induced locomotor activity by a bilateral microinjection into this site of an artificially synthesized peptide, S9 (0.5 or 5.0 μg/μL), which contains sequences around N‐terminal serine 9 residue of GSK 3β. We found that decreased levels of GSK 3β phosphorylation in the NA cc core enhance cocaine‐induced hyper‐locomotor activity, while leaving basal locomotor activity unchanged. This is the first demonstration, to our knowledge, that the selective decrease of GSK 3β phosphorylation levels in the NA cc core may contribute positively to cocaine‐induced locomotor activity, while this is not sufficient for the generation of locomotor behavior by itself without cocaine. Taken together, these findings importantly suggest that GSK 3β may need other molecular targets which are co‐activated (or deactivated) by psychomotor stimulants like cocaine to contribute to generation of locomotor behaviors.