Inhibition of PKMζ in the nucleus accumbens core blocks the expression of locomotor sensitization induced by amphetamine

• Published in: Behavioural brain research 2013-03, Vol.241, p.139-143
• Main Authors: Song, Min Ji, Jang, Ju Kyong, Kim, Wha Young, Yoon, Hyung Shin, Kim, Jeong-Hoon
• Format: Article
• Language: English
• Subjects: Amphetamine; Amphetamine - pharmacology; Animals; Behavior, Animal - drug effects; Behavioral psychophysiology; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Locomotion - drug effects; Locomotor sensitization; Male; Medical sciences; Microinjections; Motor Activity - drug effects; Neuropharmacology; Nucleus accumbens; Nucleus Accumbens - drug effects; Nucleus Accumbens - metabolism; Pharmacology. Drug treatments; PKMζ; Protein Kinase C - antagonists & inhibitors; Protein Kinase C - metabolism; Protein Kinase Inhibitors - pharmacology; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease); Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopharmacology; Rats; Rats, Sprague-Dawley
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2012.12.007

► Repeated injection of amphetamine produces behavioral sensitization. ► PKMζ is known to play a role in the maintenance of long-term memory. ► The nucleus accumbens core is more likely involved in behavioral sensitization. ► Inhibition of PKMζ in this site blocks the expression of behavioral sensitization. ► PKMζ may have a regulatory role in non-associative long-term memory. Behavioral sensitization is a form of drug-induced, long-lasting, non-associative memory. Protein kinase M zeta (PKMζ) has been shown to play a role in maintaining associative long-term memory in various brain regions. In the present study, rats were pre-exposed to either saline or amphetamine (AMPH) (1mg/kg, i.p.). After 1 week of drug-free withdrawal period, they were challenged with AMPH (1mg/kg, i.p.) following a bilateral microinjection of either saline or zeta inhibitory peptide (ZIP) (5nmole/side) into the NAcc core. In the AMPH pre-exposed group, the ZIP microinjection blocked the enhanced increase of locomotion by AMPH challenge. These results suggest that PKMζ in the NAcc core plays a role in the expression of AMPH-induced locomotor sensitization, and further extend the role of PKMζ in long-term memory to non-associative form of drug-related memory.