title: Facilitation at neuromuscular junctions: contribution to habituation and dishabituation of the Aplysia gill withdrawal reflex.
abstract: The gill withdrawal reflex of Aplysia has been used as a model for studying the neuronal mechanisms of habituation, a behavioral plasticity. We have assessed the contribution of neuromuscular facilitation, an elementary synaptic plasticity, during habituation of the reflex by recording gill muscle potentials, which we show are caused by excitatory junctional potentials. These potentials show systematic frequency-dependent changes in amplitude. The gill withdrawal evoked by central motor neuron firing during each habituation trial is determined by facilitation of the excitatory junctional potentials during the trial and the facilitated state of the initial excitatory junctional potential in a trial, determined by neuron activity prior to the trial. The neuromuscular junctions, therefore, act like a frequency-dependent amplifier of central motor activity. They are fully responsive to the dynamic changes of motor neuron firing that occurs during habituation and especially after dishabituation.
mesh_terms: D000200:Action Potentials; D000818:Animals; D005880:Gills / Q000502:physiology; D006185:Habituation, Psychophysiologic / Q000502:physiology*; D008974:Mollusca; D009046:Motor Neurons / Q000502:physiology; D009132:Muscles / Q000502:physiology; D009469:Neuromuscular Junction / Q000502:physiology*; D012018:Reflex
references.citation: Nature. 1975 Mar 6;254(5495):53-5
references.pmid: 1113876
references.citation: J Neurobiol. 1975 Mar;6(2):183-200
references.pmid: 1185181
references.citation: Science. 1976 Jan 30;191(4225):396-9
references.pmid: 1246622
references.citation: J Exp Biol. 1969 Feb;50(1):29-46
references.pmid: 4304852
references.citation: Science. 1971 Aug 13;173(3997):645-50
references.pmid: 4327600
references.citation: Science. 1971 Dec 17;174(4015):1252-6
references.pmid: 4332285
references.citation: Int J Neurosci. 1971 Aug;2(2):79-98
references.pmid: 4347410
references.citation: J Neurophysiol. 1974 Sep;37(5):996-1019
references.pmid: 4370172
references.citation: J Neurophysiol. 1974 Sep;37(5):1020-40
references.pmid: 4370262
references.citation: J Neurophysiol. 1974 Sep;37(5):1041-64
references.pmid: 4370315
references.citation: Proc Natl Acad Sci U S A. 1974 Dec;71(12):5004-8
references.pmid: 4373738
references.citation: Science. 1972 Dec 22;178(4067):1306-8
references.pmid: 4640071
references.citation: J Neurobiol. 1974;5(3):191-212
references.pmid: 4835399
references.citation: J Neurophysiol. 1972 Sep;35(5):621-37
references.pmid: 5054507
references.citation: Science. 1970 Mar 27;167(3926):1740-2
references.pmid: 5416541
references.citation: Science. 1970 Mar 27;167(3926):1743-5
references.pmid: 5416542
references.citation: Science. 1970 Mar 27;167(3926):1745-8
references.pmid: 5416543
references.citation: Science. 1970 Jul 3;169(3940):92-4
references.pmid: 5447541
references.citation: Science. 1970 Jul 24;169(3943):379-81
references.pmid: 5450371
references.citation: Science. 1969 May 16;164(3881):847-50
references.pmid: 5767790
references.citation: J Physiol. 1965 Nov;181(1):28-47
references.pmid: 5866285
references.citation: J Neurophysiol. 1966 Mar;29(2):253-74
references.pmid: 5927461
references.citation: Nature. 1966 Apr 2;210(5031):37-9
references.pmid: 5956349
references.citation: Science. 1969 Nov 28;166(3909):1167-72
references.pmid: 17775576