title: Repetition priming-induced changes in sensorimotor transmission.
abstract: When a behavior is repeated performance often improves, i.e., repetition priming occurs. Although repetition priming is ubiquitous, mediating mechanisms are poorly understood. We address this issue in the feeding network ofAplysia Similar to the priming observed elsewhere, priming inAplysiais stimulus specific, i.e., it can be either "ingestive" or "egestive." Previous studies demonstrated that priming alters motor and premotor activity. Here we sought to determine whether sensorimotor transmission is also modified. We report that changes in sensorimotor transmission do occur. We ask how they are mediated and obtain data that strongly suggest a presynaptic mechanism that involves changes in the "background" intracellular Ca(2+)concentration ([Ca(2+)]i) in primary afferents themselves. This form of plasticity has previously been described and generated interest due to its potentially graded nature. Manipulations that alter the magnitude of the [Ca(2+)]iimpact the efficacy of synaptic transmission. It is, however, unclear how graded control is exerted under physiologically relevant conditions. In the feeding system changes in the background [Ca(2+)]iare mediated by the induction of a nifedipine-sensitive current. We demonstrate that the extent to which this current is induced is altered by peptides (i.e., increased by a peptide released during the repetition priming of ingestive activity and decreased by a peptide released during the repetition priming of egestive activity). We suggest that this constitutes a behaviorally relevant mechanism for the graded control of synaptic transmission via the regulation of the [Ca(2+)]iin a neuron.
authors.affiliation: Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
authors.forename: Erik
authors.initials: E
authors.lastname: Svensson
authors.affiliation: Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
authors.forename: Colin G
authors.initials: CG
authors.lastname: Evans
authors.affiliation: Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York elizabeth.cropper@gmail.com.
authors.forename: Elizabeth C
authors.initials: EC
authors.lastname: Cropper
mesh_terms: D000200:Action Potentials; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004095:Dihydropyridines / Q000494:pharmacology; D017952:Ganglia, Invertebrate / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D017774:Long-Term Potentiation; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009475:Neurons, Afferent / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009479:Neuropeptides / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D060865:Repetition Priming; D009435:Synaptic Transmission
chemical_list: D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D009479:Neuropeptides; C038806:1,4-dihydropyridine; C041307:small cardioactive peptide B; D009543:Nifedipine; D002118:Calcium
keywords: Aplysia; cerebral peptide 2; invertebrate; mollusc; small cardioactive peptide