Persistent Increases of PKMζ in Sensorimotor Cortex Maintain Procedural Long-Term Memory Storage
Peng Penny Gao,
Jeffrey H. Goodman,
Todd Charlton Sacktor,
Joseph Thachil Francis
Affiliations
Peng Penny Gao
Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA
Jeffrey H. Goodman
Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA; Department of Developmental Neurobiology, New York State Institute for Basic Research, Staten Island, NY 10314, USA; Department of Neurology, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA
Todd Charlton Sacktor
Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA; Department of Anesthesiology, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA; Department of Neurology, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA; Corresponding author
Joseph Thachil Francis
Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA; Department of Biomedical Engineering, Cullen College of Engineering, University of Houston, Houston, TX 77204, USA; Corresponding author
Summary: Procedural motor learning and memory are accompanied by changes in synaptic plasticity, neural dynamics, and synaptogenesis. Missing is information on the spatiotemporal dynamics of the molecular machinery maintaining these changes. Here we examine whether persistent increases in PKMζ, an atypical protein kinase C (PKC) isoform, store long-term memory for a reaching task in rat sensorimotor cortex that could reveal the sites of procedural memory storage. Specifically, perturbing PKMζ synthesis (via antisense oligodeoxynucleotides) and blocking atypical PKC activity (via zeta inhibitory peptide [ZIP]) in S1/M1 disrupts and erases long-term motor memory maintenance, indicating atypical PKCs and specifically PKMζ store consolidated long-term procedural memories. Immunostaining reveals that PKMζ increases in S1/M1 layers II/III and V as performance improved to an asymptote. After storage for 1 month without reinforcement, the increase in M1 layer V persists without decrement. Thus, the persistent increases in PKMζ that store long-term procedural memory are localized to the descending output layer of the primary motor cortex. : Neuroscience; Behavioral Neuroscience; Molecular Neuroscience Subject Areas: Neuroscience, Behavioral Neuroscience, Molecular Neuroscience
