Erasing sensorimotor memories via PKMzeta inhibition.
Sensorimotor cortex has a role in procedural learning. Previous studies suggested that this learning is subserved by long-term potentiation (LTP), which is in turn maintained by the persistently active kinase, protein kinase Mzeta (PKMzeta). Whereas the role of PKMzeta in animal models of declarative knowledge is established, its effect on procedural knowledge is not well understood. Here we show that PKMzeta inhibition, via injection of zeta inhibitory peptide (ZIP) into the rat sensorimotor cortex, disrupts sensorimotor memories for a skilled reaching task even after several weeks of training. The rate of relearning the task after the memory disruption by ZIP was indistinguishable from the rate of initial learning, suggesting no significant savings after the memory loss. These results indicate a shared molecular mechanism of storage for declarative and procedural forms of memory.
von Kraus
Lee Michael
LM
Graduate Program in Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, New York, United States of America.
Sacktor
Todd Charlton
TC
Francis
Joseph Thachil
JT
D000818:Animals; D005260:Female; D008568:Memory / Q000187:drug effects*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D051381:Rats; D020318:Rats, Long-Evans
D047428:Protein Kinase Inhibitors; D011493:Protein Kinase C; C504730:protein kinase M zeta, rat