title: On the ionic mechanisms of adaptation in an isolated mechanoreceptor --an electrophysiological study.
abstract: The ionic mechanisms of adaptation of the receptor potential, especially the early adaptation, was studied in an isolated mechanoreceptor, the slowly adapting crustacean stretch receptor, with electrophysiological methods including potential clamp technique. This receptor has frequently been used as a model to demonstrate general principles for the generation of signals in sensory receptors. The receptor potential is depolarizing and consists of an initial peak followed by a static phase in response to a ramp and hold stretch with a high rate of rise. The receptor current, defined as the stretch induced current, is inward and has a similar appearance. The adaptive fall of the receptor potential and receptor current occurs in two phases, an initial rapid fall from the peak (early adaptation) followed by a slow decline during the static phase (late adaptation). The two phases could be characterized by different time constants. By polarizing the cell to various steady potentials before stretch it was shown that the time constant of the early adaptive fall of the receptor potential varied with potential and had a minimum close to resting membrane potential. The time course of the late adaptive fall appeared to be independent of holding potential. These results suggest that ionic mechanisms play an important role during early adaptation, whereas late adaptation probably is governed by mechanical factors. Prolonged exposure to K+-free solutions or injection of TEA caused nearly complete abolition of the early adaptive fall of the receptor potential, making the response almost rectangular in shape. The outward current associated with a positive potential step was considerably reduced after injection of TEA. Intracellular injection of Ca2+ or exposure to isotonic Ca2+-saline decreased the amplitude of the static phase of the receptor potential, whereas injection of EGTA caused an increase in amplitude. Ion substitution experiments indicated that Ca2+ might enter the neuron through the transducer channels opened by stretch. It is concluded that the major cause of the early adaptive fall of the receptor potential is an outward K+ current activated by the stretch-induced depolarization. The effects of varied intra- and extracellular Ca2+ concentration suggest that a part of the K+ current might be activated by Ca2+ influx. Another possibility is that intracellular Ca2+ contributes to adaptation by inactivation of the transducer channels. The present results demonstrate a possible mechanism for adaptation in sensory receptors. A potential activated outward K+ current enhances the fall of the receptor potential from the initial peak.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects; D000818:Animals; D003400:Astacoidea; D002118:Calcium / Q000502:physiology; D007473:Ion Channels / Q000187:drug effects; D007477:Ions / Q000502:physiology*; D008465:Mechanoreceptors / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000502:physiology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors
chemical_list: D007473:Ion Channels; D007477:Ions; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D011188:Potassium; D002118:Calcium