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Repetition priming-induced changes in sensorimotor transmission.

Erik Svensson¹, Colin G Evans¹, Elizabeth C Cropper²

¹Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.

Journal of Neurophysiology

|January 15, 2016

Summary

Repetition priming improves performance through stimulus-specific changes in neural networks. This study reveals that synaptic transmission is modified by altering background intracellular calcium concentration ([Ca(2+)]i) in primary afferents.

Keywords:

Aplysia cerebral peptide 2 invertebrate mollusc small cardioactive peptide

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Area of Science:

Neuroscience
Behavioral Neuroscience
Cellular Neuroscience

Background:

Repetition priming enhances performance but its underlying mechanisms remain unclear.
Priming in the Aplysia feeding network is stimulus-specific (ingestive or egestive).
Previous work showed priming affects motor and premotor activity.

Purpose of the Study:

To investigate if repetition priming modifies sensorimotor transmission in the Aplysia feeding network.
To elucidate the mechanisms mediating these changes in synaptic transmission.
To explore the role of intracellular calcium concentration ([Ca(2+)]i) in graded synaptic plasticity.

Main Methods:

Examined synaptic transmission in the Aplysia feeding network.
Investigated changes in background intracellular calcium concentration ([Ca(2+)]i) in primary afferents.
Assessed the role of a nifedipine-sensitive current in regulating [Ca(2+)]i.
Analyzed the effects of behaviorally relevant peptides on this current and synaptic efficacy.

Main Results:

Repetition priming induces changes in sensorimotor transmission.
These changes are mediated by presynaptic mechanisms involving alterations in background intracellular calcium concentration ([Ca(2+)]i).
A nifedipine-sensitive current regulates [Ca(2+)]i, and its induction is modulated by specific peptides linked to ingestive and egestive priming.

Conclusions:

Synaptic plasticity underlies repetition priming in the Aplysia feeding system.
Regulation of background intracellular calcium concentration ([Ca(2+)]i) via a nifedipine-sensitive current provides a mechanism for graded control of synaptic transmission.
Peptides released during behavioral priming modulate this calcium-dependent plasticity, linking neural mechanisms to behavior.