Abstract
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 (PKMζ). Whereas the role of PKMζ in animal models of declarative knowledge is established, its effect on procedural knowledge is not well understood. Here we show that PKMζ 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.
Highlights
Memories have been classified into several varieties characterized by different acquisition paradigms, temporal stability, and neural and molecular substrates
Five zeta inhibitory peptide (ZIP)/ control pairs were injected in the sensorimotor cortex at posterior: 1.5 mm; lateral: 1.5 mm and 2.5 mm, relative to Bregma, while the remaining six pairs were injected in the motor cortex: anterior 1.5 mm; lateral: 1.5 mm and 2.5 mm, relative to Bregma
Of the animals injected in posterior sensorimotor cortex, ZIP was injected with a 24 hr delay after the last training episode for two rats, and with a 4 hr delay for three rats; the results were indistinguishable and combined
Summary
Memories have been classified into several varieties characterized by different acquisition paradigms, temporal stability, and neural and molecular substrates. Procedural memories, like the skill of riding a bicycle, are thought to be fundamentally different from declarative (explicit) memories because they accumulate slowly through repetition, are expressed automatically in performance, rather than consciously through explicit knowledge, and are subserved by a separate neural system [1,2] Both forms of long-term memory have been proposed to be mediated by the strengthening of synaptic connections through long-term potentiation (LTP) [3,4,5]. We tested whether the PKMf inhibitor, zeta inhibitory peptide (ZIP), disrupts performance on a rat reach-to-grasp and retrieve task This task has previously been associated with changes in sensorimotor cortex cutaneous receptive field size, baseline level of synaptic transmission and the ability to induce LTP, and the number and stability of dendritic spines [8,9,10,11,12,13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
