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Biomedical subjects

H Yawo

Publications and source records attributed to H Yawo.

27 records · Page 2Linked to original sources
PubMed1990

Voltage-activated calcium currents in presynaptic nerve terminals of the chicken ciliary ganglion.

1. Calcium currents (ICa) were recorded from presynaptic calyces of ciliary ganglia of the chick embryo under whole-cell voltage clamp. 2. Only high-threshold ICa was recorded without any evidence for the presence of low-threshold Ca2+ channels. 3. High-threshold (high-voltage-activated, HVA) ICa could be classified into non-inactivating (HVAn) and inactivating (HVAi) components. The mean inactivation time constant of the HVAi component was 213 ms (at 0 mV). The threshold for activation by depolarizing pulses was more negative for the HVAn component than for the HVAi component. The HVAi component was inactivated by 19% at a holding potential of -60 mV, while the HVAn component was little affected under this condition. 4. The activation of HVAn component was faster than that of the HVAi component. 5. Both the HVAn and HVAi components were blocked by Cd2+ (50 microM) and La3+ (1 microM). Both components were only slightly affected by Ni2+ (100 microM). The order of potency in blocking was La3+ greater than Cd2+ greater than Ni2+ for both components. Both the HVAi and HVAn components were irreversibly blocked by omega-conotoxin GVIA(omega-CgTX, 10 microM). 6. The two components could pharmacologically be distinguished by selective blockade of the HVAn component with nifedipine (2 microM) and D600 (100-250 microM). 7. HVAn and HVAi components are suggested to represent two different subpopulations of Ca2+ channels. The HVAn subpopulation may be responsible for persistent Ca2+ influx during subthreshold depolarization of the nerve terminal.

Animals↗
PubMed1989

Rectification of synaptic and acetylcholine currents in the mouse submandibular ganglion cells.

1. Synaptic currents and responses to acetylcholine (ACh) were recorded from mouse submandibular ganglion (SMG) cells under whole-cell voltage clamp. 2. The peak amplitude of excitatory synaptic currents (ESCs) as well as the currents evoked by the ionophoretic application of ACh followed a unique non-linear current-voltage (I-V) relation. The chord conductance of the whole-cell currents decreased with depolarization of the membrane potential and became virtually 0 at 50 mV. 3. The decay of ESCs was described by two exponential functions. Both the fast (tau f) and slow (tau s) time constants were sharply decreased at depolarizing potentials beyond -40 mV, being insensitive to hyperpolarizing potentials more than -50 mV. 4. Single ACh receptor channels were characterized by the whole-cell current noise analysis. The single-channel currents followed Ohm's law at negative membrane potentials but tended to reach a plateau at positive membrane potentials. The mean slope conductance measured between -40 and -20 mV was 28.5 pS. 5. The product of the number of functional channels (N) and the probability of a channel being open (p) showed a steep voltage dependence. The value of Np at 20 mV was only 31% of that at -20 mV. 6. The noise power spectrum was best fitted by a double-Lorentzian function. Both the fast (tau f) and slow (tau s) time constants were sharply decreased by depolarizations beyond -20 mV. being less sensitive to membrane potentials more negative than -30 mV. 7. The non-linear I-V relation of ESCs was attributed in part to the voltage dependence of p and in part to the voltage dependence of the single-channel conductance (gamma) of ACh receptor channels.

Acetylcholine↗
PubMed1987

Nerve terminal remodeling visualized in living mice by repeated examination of the same neuron.

The distribution of presynaptic endings on the surfaces of autonomic ganglion cells was mapped in living mice after intravenous administration of a styryl pyridinium dye. The staining and imaging techniques did not appear to damage the ganglion cells, or the synapses on them; these procedures could therefore be repeated after an arbitrary period. Observations of the same neurons at intervals of up to 3 weeks indicate that the pattern of preganglionic terminals on many of these nerve cells gradually changes.

Action Potentials↗
PubMed1987

Changes in the dendritic geometry of mouse superior cervical ganglion cells following postganglionic axotomy.

The dendritic geometry of mouse superior cervical ganglion cells was studied over periods of up to 3 months after postganglionic axotomy. Intracellular injection of HRP showed that total dendritic length and complexity were reduced by 60-70%, on average, among cells whose postganglionic axons had been crushed 2 weeks before. Both parameters gradually recovered in parallel with ganglion cell reinnervation of the periphery. These results indicate that neuronal interactions with peripheral targets influence the configuration of ganglion cell dendrites throughout life. The implications of this conclusion are discussed.

Animals↗
PubMed1985

Low-threshold, slow-inactivating Na+ potentials in the cockroach giant axon.

Electrophysiological properties of the ventral giant axon in the abdominal nerve cord of the cockroach were studied by recording intracellular potentials following partial or complete block of the K+ conductance. When the K+ conductance was completely blocked by tetraethylammonium (TEA) and 3,4-diaminopyridine, the intensity of depolarizing currents necessary for eliciting the action potential was markedly decreased, and the action potential was followed by a prolonged plateau potential. During the plateau potential following the spike, the input resistance was significantly reduced. The plateau potential was not affected by changing the external Ca2+ concentration but depended on the external Na+ concentration in a manner expected from the Nernst equation and was blocked by tetrodotoxin (TTX). During the plateau potential, the Na+ conductance responsible for the spike was inactivated, whereas immediately after the plateau potential a newly evoked spike was not followed by a plateau potential, suggesting different inactivation kinetics between the spike and plateau Na+ conductances. When the K+ conductance was partially blocked by TEA alone, slow depolarizing responses were evoked at voltage levels a few millivolts more positive than the resting potential. The "threshold" for the slow potential was much lower than that for the spike potential. The slow potential produced after partial block of the K+ conductance was not affected by alterations of the external Ca2+ concentration but was blocked by TTX or in a Na+-free solution. Even in normal medium, a small TTX-sensitive depolarizing response was discernible. This response was similar in its time course and threshold to the slow potential observed after partial block of the K+ conductance. It is concluded that the cockroach giant axon has two populations of Na+ channels, which can be distinguished by differences in time course and voltage levels for activation and that the slow, low-threshold Na+-dependent potential is largely masked by delayed increases in the K+ conductance under normal conditions. It remains uncertain whether the low-threshold slow potential and the plateau potential originate from the same or different populations of Na+ channels.

4-Aminopyridine↗
PubMed1985

Calcium dependence of membrane sealing at the cut end of the cockroach giant axon.

Following transection of a nerve fiber, the ruptured membrane must be resealed before regeneration from the proximal cut end. However, it is not certain how fast the cut end is resealed or how it is resealed. We have examined the membrane sealing process following transection of the cockroach giant axon, using recovery of decreased membrane potential and input resistance as criteria. The cable analysis and the injury current profile measured under voltage clamp suggested that the injured site is resealed by a structure with high electrical resistances 5 to 30 min after the transection. This recovery of membrane properties roughly coincided in time with the appearance of a partition-like structure formed near the cut end. The membrane resealing process was highly dependent upon temperature and extracellular Ca2+. Substitution of Ca2+ by equimolar Mg2+, Mn2+, or Sr2+ failed to induce the membrane sealing following transection. However, even in a Ca2+-free solution, the membrane resealing occurred if Ca2+ was injected into the axoplasm near the cut end. Thus, the membrane resealing appears to require Ca2+ entry into the axoplasm. The resealing process was not affected by colchicine or cytochalasin. However, the resealing was prevented by the application of phospholipase A2 inhibitors. These results suggest that the membrane resealing is triggered by phospholipase A2, which is activated by excess Ca2+ entering the axoplasm at the injured site.

Animals↗
PubMed1983

How a nerve fiber repairs its cut end: involvement of phospholipase A2.

Following transection of a giant axon, the nerve membrane at the cut end is resealed within 5 to 30 minutes. This membrane resealing process is highly dependent upon temperature and extracellular calcium ions. The membrane resealing is triggered by excess calcium entering the axoplasm at the site of transection but is prevented by the application of phospholipase A2 inhibitors. We propose that calcium activated phospholipase A2 plays a central role in resealing of the ruptured nerve membrane.

Acetophenones↗
PubMed1981

Phagocytic activity and hyperpolarizing responses in L-strain mouse fibroblasts.

1. Fibroblastic L cells not only respond with a slow hyperpolarizing potential change to a mechanical or electrical stimulus but also show spontaneous, repetitive hyperpolarizations (i.e. membrane potential oscillation). 2. Almost all the cells can actively take up latex beads whose surfaces were treated by U.V. irradiation. 3. Non-phagocytic L cells hardly showed hyperpolarizing responses, while hyperpolarizing responses were obtained in all the phagocytic L cells. The exposure of the cell surface to beads, however, did not trigger the generation of hyperpolarizing responses. 4. Metabolic inhibitors, low temperature and cytochalasin B inhibited both the uptake of beads and the hyperpolarizing responses. 5. Increasing the external concentration of Ca2+ induced a remarkable stimulation of the phagocytosis of beads. Mg2+ and Ba2+, which inhibited hyperpolarizing responses due to competition for Ca2+ sites on the outer surface of the membrane, significantly suppressed the uptake of beads. 6. Verapamil, a Ca2+ channel blocker, inhibited not only hyperpolarizing membrane responses but also ingestion of beads. 7. It is concluded that the Ca2+ inflow on the hyperpolarizing membrane responses is closely associated with the phagocytic activity in L cells, probably through activation of the microfilament assembly.

Animals↗