TY - JOUR
T1 - Ionic currents and ion channels of lobster olfactory receptor neurons
AU - McClintock, Timothy S.
AU - Ache, Barry W.
PY - 1989/12/1
Y1 - 1989/12/1
N2 - The role of the soma of spiny lobster olfactory receptor cells in generating odor-evoked electrical signals was investigated by studying the ion channels and macroscopic currents of the soma. Four ionic currents; a tetrodotoxin-sensitive Na+ current, a Ca++ current, a Ca++-activated K+ current, and a delayed rectifier K+ current, were isolated by application of specific blocking agents. The Na+ and Ca++ currents began to activate at -40 to -30 mV, while the K+ currents began to activate at - 30 to - 20 mV. The size of the Na+ current was related to the presence of a remnant of a neurite, presumably an axon, and not to the size of the soma. No voltage-dependent inward currents were observed at potentials below those activating the Na+ current, suggesting that receptor potentials spread passively through the soma to generate action potentials in the axon of this cell. Steady-state inactivation of the Na+ current was half-maximal at -40 mV. Recovery from inactivation was a single exponential function that was half-maximal at 1.7 ms at room temperature. The K+ currents were much larger than the inward currents and probably underlie the outward rectification observed in this cell. The delayed rectifier K+ current was reduced by GTP-γ-S and AlF4−, agents which activate GTP-binding proteins. The channels described were a 215-pS Ca++-activated K+ channel, a 9.7-pS delayed rectifier K+ channel, and a 35-pS voltage-independent Cl− channel. The Cl− channel provides a constant leak conductance that may be important in stabilizing the membrane potential of the cell.
AB - The role of the soma of spiny lobster olfactory receptor cells in generating odor-evoked electrical signals was investigated by studying the ion channels and macroscopic currents of the soma. Four ionic currents; a tetrodotoxin-sensitive Na+ current, a Ca++ current, a Ca++-activated K+ current, and a delayed rectifier K+ current, were isolated by application of specific blocking agents. The Na+ and Ca++ currents began to activate at -40 to -30 mV, while the K+ currents began to activate at - 30 to - 20 mV. The size of the Na+ current was related to the presence of a remnant of a neurite, presumably an axon, and not to the size of the soma. No voltage-dependent inward currents were observed at potentials below those activating the Na+ current, suggesting that receptor potentials spread passively through the soma to generate action potentials in the axon of this cell. Steady-state inactivation of the Na+ current was half-maximal at -40 mV. Recovery from inactivation was a single exponential function that was half-maximal at 1.7 ms at room temperature. The K+ currents were much larger than the inward currents and probably underlie the outward rectification observed in this cell. The delayed rectifier K+ current was reduced by GTP-γ-S and AlF4−, agents which activate GTP-binding proteins. The channels described were a 215-pS Ca++-activated K+ channel, a 9.7-pS delayed rectifier K+ channel, and a 35-pS voltage-independent Cl− channel. The Cl− channel provides a constant leak conductance that may be important in stabilizing the membrane potential of the cell.
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U2 - 10.1085/jgp.94.6.1085
DO - 10.1085/jgp.94.6.1085
M3 - Article
C2 - 2482328
AN - SCOPUS:0024801907
SN - 0022-1295
VL - 94
SP - 1085
EP - 1099
JO - Journal of General Physiology
JF - Journal of General Physiology
IS - 6
ER -