MEMBRANE POTENTIAL CHANGE AND MEMBRANE CURRENT IN SUPRAMEDULLARY NERVE CELL OF PUFFER

1959 ◽  
Vol 22 (2) ◽  
pp. 204-221 ◽  
Author(s):  
Susumu Hagiwara ◽  
Nozomu Saito
2007 ◽  
Vol 23 (6) ◽  
pp. 348-356 ◽  
Author(s):  
Vincent Cazenave-Loustalet ◽  
Qing-Li Qiao ◽  
Li-Ming Li ◽  
Qiu-Shi Ren

1986 ◽  
Vol 56 (3) ◽  
pp. 702-717 ◽  
Author(s):  
M. Takahata ◽  
M. Hisada

The occurrence of the uropod steering response as one of the equilibrium reflexes to body rolling in crayfish is significantly facilitated if the stimulus is given while the animal is performing the abdominal posture movement. This facilitation of the descending statocyst pathway by the abdominal posture system takes place between the uropod motor neurons and the statocyst interneurons, which directly project from the brain to the terminal abdominal ganglion where the motor neurons originate. To elucidate the synaptic mechanisms underlying the postural facilitation of the steering response, we analyzed in this study the activity of an identified set of uropod motor neurons during the fictive abdominal extension movement in the whole-animal preparation. Intracellular recordings from the dendritic branches of uropod motor neurons revealed that they were continuously excited during the fictive abdominal extension. The large fast motor neurons usually showed a sustained depolarization of the subthreshold magnitude. The small slow ones showed a suprathreshold sustained depolarization with spikes superimposed. Putative inhibitory motor neurons, on the other hand, showed a sustained hyperpolarization with their spontaneous spike discharge suppressed. The discrete synaptic potentials could hardly be distinguished and, instead, small fluctuations of the membrane potential were observed during the sustained depolarization of both the fast and slow motor neurons. Occasionally, large discrete synaptic potentials could be observed to be superimposed on the sustained depolarization. The occurring frequency of these synaptic potentials showed, however, no significant increase associated with the sustained depolarization. It hence seemed unlikely that these potentials were responsible for producing the sustained depolarization. Their amplitude during the sustained depolarization was smaller than that observed during the quiescent state. The sustained membrane potential change during the fictive abdominal movement was also observed in many neurons other than motor neurons, including local nonspiking interneurons and mechanosensory spiking interneurons. Both motor neurons and interneurons showed a decrease in their membrane resistance during the sustained membrane potential change. We concluded that the sustained depolarization of uropod motor neurons during the fictive abdominal extension was produced by the summation of small chemically transmitted postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)


1994 ◽  
Vol 4 (2) ◽  
pp. 101-113 ◽  
Author(s):  
Kazunori Odashima ◽  
Ryuichi Naganawa ◽  
Hanna Radecka ◽  
Masamitsu Kataoka ◽  
Eiichi Kimura ◽  
...  

1973 ◽  
Vol 62 (5) ◽  
pp. 535-549 ◽  
Author(s):  
Hiroshi Kitasato

Membrane current responses to sudden potential changes were recorded in solutions of various [K]o on 52 internodal cells of Nitella clavata. The membrane current after sudden depolarization had a component sensitive to [K]o which increased with time from 0.3 to 2.0 s and remained steady thereafter. This late current became zero at values of E and [K]o which suggests that the current was nearly all carried by K+. The potassium conductivity represented by this current increased with depolarization, with a half-maximum value at about -70 mV, and saturation at about -30 to -20 mV. The potassium conductance also increased with increasing [K]o, but less rapidly than predicted for constant potassium permeability. This failure of the conductance to increase with [K]o was relatively the same at all membrane potentials and may be explained by a model with a finite number of channels. No attempt was made to model the dependence of gK on time after depolarization or on membrane potential. However, the finding that the membrane potential did not affect the way in which the permeability depended on [K]o suggests that the membrane potential change does not affect the affinity of the sites, and that the increase in gK with time after depolarization is brought about by an increase in the number of channels with such sites.


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