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Biomedical subjects

K Kusano

Publications and source records attributed to K Kusano.

118 records · Page 7Linked to original sources
PubMed1968

Further study of the relationship between pre- and postsynaptic potentials in the squid giant synapse.

The minimal presynaptic depolarization (MPD) for producing a detectable postsynaptic potential (PSP) was lower than 25 mv in normal or tetrodotoxin (TTX)-containing seawater. The MPD was about 10 mv when a small amount of tetraethylammonium ions (TEA) was injected into the presynaptic terminal. Application of linearly increasing depolarizing current to the normal presynaptic terminal at times produced a PSP before a presynaptic spike was evoked; the rate of rise of the resulting PSP was much slower than that of a PSP triggered by the normal presynaptic spike. A brief depolarizing pulse that preceded the presynaptic spike in normal seawater or the initial transient presynaptic depolarization in TTX decreased the PSP. It increased the PSP when it was applied during the spike or initial transient depolarization. Hyperpolarizing pulses had the reverse effect. The Off-PSP was also modified by inserting pulses at an initial part of the recovery phase of the strong presynaptic depolarization. These results indicate further that increases in Na(+) and K(+) conductance during presynaptic spike activity are not a requirement for transmitter release; the rate of release of transmitter can be controlled by electrical manipulation of the presynaptic terminal; there is a superficial correspondence between the time courses of presynaptic depolarization and the resulting PSP. Thus presynaptic depolarization appears to be only the first step in the series of events constituting excitation-transmitter release coupling. It may not be a necessary step for the release mechanism.

Animals↗
PubMed1967

Tetraethylammonium ions: effect of presynaptic injection on synaptic transmission.

Tetraethylammonium ions were injected into the presynaptic axon of the squid giant synapse. Injection of these ions caused prolongation of the action potential with decreased out ward current. The prolonged spike was associated with increased release and prolonged activity of the transmitter substance. Although the amplitude of the postsynaptic potential increased with presynaptic depolarization, strong depolarization blocked transmitter re lease. In the injected presynaptic axon, transmitter release was blocked by 10(-6) gram of tetrodotoxin per milliliter. Transmitter release appears to be under control of presynaptic potential levels.

Animals↗
PubMed1967

Correlation of transmitter release with membrane properties of the presynaptic fiber of the squid giant synapse.

Depolarization of the presynaptic terminal by current produced a postsynaptic potential (PSP) which increased with increasing presynaptic polarization and then reached a plateau. Iontophoretic injection of tetraethylammonium ions (TEA) into the presynaptic axon near the terminal produced a prolonged presynaptic spike. The resulting PSP is increased in size and its time course closely followed that of the presynaptic spike. The presynaptic fiber no longer exhibited rectification and strong depolarizations revealed that the PSP reached a maximum with about 110 mv depolarization. Further depolarization produced a decrease in PSP amplitude and finally transmission was blocked. However, a PSP then always appeared on withdrawal of the depolarizing current. Under the conditions of these experiments, the PSP could be considered a direct measure of transmitter release. Bathing the TEA-injected synapse with concentrations of tetrodotoxin (TTX) sufficient to block spike activity in both pre- and postsynaptic axons did not greatly modify postsynaptic electrogenesis. However, doubling TTX concentration reversibly blocked PSP. Thus the permeability changes to Na and K accompanying the spike do not appear necessary for transmitter release. Some other processes related to the level of presynaptic polarization must be involved to explain the data. The inhibition of transmitter release by strong depolarizations appears to be related to Ca action. A membrane Ca current may also be necessary for normal transmitter release.

Action Potentials↗
PubMed1966

Behavior of delayed current under voltage clamp in the supramedullary neurons of puffer.

Depolarizations applied to voltage-clamped cells bathed in the normal solution disclose an initial inward current followed by a delayed outward current. The maximum slope conductance for the peak initial current is about 30 times the leak conductance, but the maximum slope conductance for the delayed current is only about 10 times the leak conductance. During depolarizations for as long as 30 sec, the outward current does not maintain a steady level, but declines first exponentially with a time constant of about 6 msec; it then tends to increase for the next few seconds; finally, it declines slowly with a half-time of about 5 sec. Concomitant with the changes of the outward current, the membrane conductance changes, although virtually no change in electromotive force occurs. Thus, the changes in the membrane conductance represent two phases of K inactivation, one rapidly developing, the other slowly occurring, and a phase of K reactivation, which is interposed between the two inactivations. In isosmotic KCl solution after a conditioning hyperpolarization there occurs an increase in K permeability upon depolarization. When the depolarizations are maintained, the increase of K permeability undergoes changes similar to those observed in the normal medium. The significance of the K inactivation is discussed in relation to the after-potential of the nerve cells.

Animals↗
PubMedDate not supplied

A case of dyskinetic cerebral palsy resembling post-anoxic action myoclonus.

Myoclonus after brain anoxia is more commonly observed in adults. Perinatal anoxia, however, on rare occasions causes myoclonus as the main neurologic abnormality. In this paper we described a case of cerebral palsy complicated by chorea and tremulous movements of the foot in which there were no risk factors except perinatal asphyxia. The patient had unique symptoms, action myoclonus associated with the movements of hyperkinésie volitionnelle. This case illustrated two points. One is that abnormal involuntary movements attributed to perinatal brain insults had changed as the brain matured. The other is that some movements were very similar to those of the post-anoxic action myoclonus, commonly seen in patients who sustain brain damage in adulthood.

Adult↗
PubMedDate not supplied

A sporadic case of very slow progressive leukodystrophy involving the cerebellar peduncles.

We describe a patient with infantile onset leukodystrophy involving the cerebellar peduncles. She had mild mental retardation, spastic diplegia and mild cerebellar ataxia. The peripheral nerves seemed to be normal. The characteristic MRI findings in this case were extensive lesions of the white matter involving the cerebellar peduncles. In addition there was ventricular enlargement with a markedly decreased volume of the white matter and a hypoplastic corpus callosum. The clinical and laboratory findings imply that the white matter lesions in this patient were the result of delayed myelination rather than demyelination. The patient was evaluated for known metabolic and degenerative diseases, but no abnormalities were observed. Her symptoms and neuroimaging findings did not fit the criteria for any defined leukodystrophy.

Adolescent↗