title: Switching off and on of synaptic sites at aplysia sensorimotor synapses.
abstract: Using the highly plastic synapses between mechanoreceptor sensory neurons and siphon motor neurons of Aplysia as a model, we have investigated whether switching off and on of individual synaptic release sites is a strategy that is used by neurons in forms of short-term synaptic modulation with a time course of minutes to hours. We have modified some of the techniques of classical quantal analysis and examined the kinetics of synaptic depression under different stimulation protocols to answer this question. Our analysis shows that both synaptic depression caused by homosynaptic activity and synaptic facilitation induced by an endogenous facilitatory transmitter occur by means of the shutting off and turning on, respectively, of synaptic sites, without intermediate changes in the probability of release. Our findings imply that other forms of plasticity at these synapses, such as post-tetanic potentiation, long-term facilitation, and long-term potentiation, are also expressed by all-or-none changes in activity at individual sites. We thus show that in addition to the mechanisms of synaptic integration that are known to operate in single cells and networks, neurons can exercise a further layer of fine control, at the level of individual release sites.
authors.affiliation: Clinical Research Institute of Montreal and University of Montreal, Centre de Recherches en Sciences Neurologiques, Montreal, Quebec H2W 1R7, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Royer
authors.forename: R L
authors.initials: RL
authors.lastname: Coulson
authors.forename: M
authors.initials: M
authors.lastname: Klein
mesh_terms: D000818:Animals; D001048:Aplysia; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology*; D017952:Ganglia, Invertebrate / Q000166:cytology / Q000502:physiology; D008959:Models, Neurological; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D011789:Quantum Theory; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*