title: Decreased response to acetylcholine during aging of aplysia neuron R15.
abstract: How aging affects the communication between neurons is poorly understood. To address this question, we have studied the electrophysiological properties of identified neuron R15 of the marine mollusk Aplysia californica. R15 is a bursting neuron in the abdominal ganglia of the central nervous system and is implicated in reproduction, water balance, and heart function. Exposure to acetylcholine (ACh) causes an increase in R15 burst firing. Whole-cell recordings of R15 in the intact ganglia dissected from mature and old Aplysia showed specific changes in burst firing and properties of action potentials induced by ACh. We found that while there were no significant changes in resting membrane potential and latency in response to ACh, the burst number and burst duration is altered during aging. The action potential waveform analysis showed that unlike mature neurons, the duration of depolarization and the repolarization amplitude and duration did not change in old neurons in response to ACh. Furthermore, single neuron quantitative analysis of acetylcholine receptors (AChRs) suggested alteration of expression of specific AChRs in R15 neurons during aging. These results suggest a defect in cholinergic transmission during aging of the R15 neuron.
authors.affiliation: Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, United States of America.
authors.forename: Komolitdin
authors.initials: K
authors.lastname: Akhmedov
authors.affiliation: Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, United States of America.
authors.forename: Valerio
authors.initials: V
authors.lastname: Rizzo
authors.affiliation: Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, United States of America.
authors.forename: Beena M
authors.initials: BM
authors.lastname: Kadakkuzha
authors.affiliation: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Carter
authors.affiliation: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
authors.forename: Neil S
authors.initials: NS
authors.lastname: Magoski
authors.affiliation: Division of Marine Biology and Fisheries, University of Miami Rosenstiel School of Marine and Atmospheric Science, Miami, Florida, United States of America.
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Capo
authors.affiliation: Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, United States of America.
authors.forename: Sathyanarayanan V
authors.initials: SV
authors.lastname: Puthanveettil
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001048:Aplysia / Q000166:cytology / Q000235:genetics / Q000378:metabolism*; D001483:Base Sequence; D016922:Cellular Senescence / Q000187:drug effects*; D018679:Cholinergic Agonists / Q000494:pharmacology*; D008969:Molecular Sequence Data; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000235:genetics / Q000378:metabolism*
chemical_list: D018679:Cholinergic Agonists; D011950:Receptors, Cholinergic; D000109:Acetylcholine