scholarly journals The "late" Ca channel in squid axons.

1981 ◽  
Vol 78 (6) ◽  
pp. 683-700 ◽  
Author(s):  
L J Mullins ◽  
J Requena
Keyword(s):  
Steady State ◽  
Repetitive Stimulation ◽  
Test Solution ◽  
Ca Channel ◽  
Normal Concentration ◽  
Giant Axons ◽  
Light Production ◽  
High K ◽  
K Response ◽  
Stimulation Of

Squid giant axons were injected with aequorin and then treated with seawater containing 50 mM Ca and 100-465 mM K+. Measurements of light production suggested a phasic entry of Ca as well as an enhanced steady-state aequorin glow. After a test K+ depolarization, the aequorin-injected axon was stimulated for 30 min in Li seawater that was Ca-free, a procedure known to reduce [Na]i to about one-half the normal concentration. Reapplication of the elevated K+ test solution now showed that the Ca entry was virtually abolished by this stimulation in Li. A subsequent stimulation of the axon in Na seawater for 30 min resulted in recovery of the response to depolarization by high K+ noted in a normal fresh axon. In axons first tested for a high K+ response and then stimulated in Na seawater for 30 min (where [Na]i increases approximately 30%), there was approximately eight fold enhancement in this response to a test polarization. Axons depolarized with 465 mM K seawater in the absence of external Ca for several minutes were still capable of producing a large phasic entry of Ca when [Ca]0 was made 50 mM, which suggests that it is Ca entry itself rather than membrane depolarization that produced inactivation. Responses to stimulation at 60 pulses/s in Na seawater containing 50 mM Ca are at best only 5% of those measured with high K solutions. The response to repetitive stimulation is not measurable if [Ca]o is made 1 mM, whereas the response to steady depolarization is scarcely affected.

Tetanic hyperpolarization of single medullated nerve fibers in sodium and lithium

1976 ◽  
Vol 231 (4) ◽  
pp. 1033-1038 ◽  
Author(s):  
GM Schoepfle
Keyword(s):  
Steady State ◽  
Interspike Interval ◽  
Nerve Fibers ◽  
Repetitive Stimulation ◽  
Time Dependent ◽  
Potassium Ions ◽  
Current Densities ◽  
Medullated Nerve Fiber ◽  
Sodium And Potassium ◽  
Stimulation Of

Repetitive stimulation of a single medullated nerve fiber of Xenopus yields a succession of postspike voltage-time curves which are nearly coincident until attainment of a voltage that corresponds to that of the maximum attained by the normal postspike undershoot. Initially the interspike potential returns toward a resting level after this brief phase of hyperpolarization. However, as tetanization proceeds, a pattern of hyperpolarization develops with the result that, in the tetanic steady state, there exists a progressive hyperpolarization throughout each interspike interval. Extent of postspike hyperpolarization in terms of a deviation deltaVm from the resting level of membrane potential is approximated by the variation deltaVm = delta[MNa + MK]/[GNa + GK] where MNa and MK are current densities associated with active pumping of sodium and potassium ions and GNa and GK are corresponding time-dependent leak conductances. Tetanic hyperpolarization is reversibly abolished by cyanide and by exposure to lithium Ringer. Eventual reappearance of tetanic hyperpolarization in the presence of lithium Ringer suggests lithium pumping.

Non-Homogeneous Conduction In Giant Axons Of The Nerve Cord Of Periplaneta Americana

1969 ◽  
Vol 50 (3) ◽  
pp. 635-649
Author(s):  
I. PARNAS ◽  
M. E. SPIRA ◽  
R. WERMAN ◽  
F. BERGMANN
Keyword(s):  
Nerve Cord ◽  
Periplaneta Americana ◽  
Repetitive Stimulation ◽  
Low Doses ◽  
Thoracic Region ◽  
Safety Factors ◽  
Suboesophageal Ganglion ◽  
Giant Axons ◽  
Physiological Conditions ◽  
Stimulation Of

Studies with intracellular electrodes show that the abdominal giant axons of the cockroach give ascending responses to stimulation of cercal nerves and descending responses to stimulation of S0-T1 connectives. 2. In the thoracic region one or more areas of low safety factors occur for descending conduction. 3. These areas, which are considered not to be synapses, are blocked by low doses of nicotine (2-5 µg./ml.) fatigued by repetitive stimulation and show conduction delays of 0·6-0·7 msec. 4. It is concluded that the abdominal giant axons extend continuously from A6 to suboesophageal ganglion. The possibility of bi-directional conduction under physiological conditions is discussed.

scholarly journals Receptor-operated Ca2+ channels in gastric parietal cells: gastrin and carbachol induce Ca2+ influx in depleting intracellular Ca2+ stores

1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous
Keyword(s):  
Steady State ◽  
Receptor Activation ◽  
Parietal Cells ◽  
The Other ◽  
Bivalent Cation ◽  
Gtp Binding ◽  
Gastric Parietal Cells ◽  
Type Receptor ◽  
Ca2 Channels ◽  
Stimulation Of

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.

Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig

1989 ◽  
Vol 62 (6) ◽  
pp. 1225-1236 ◽  
Author(s):  
S. M. Gurahian ◽  
S. H. Chandler ◽  
L. J. Goldberg
Keyword(s):  
Reticular Formation ◽  
Short Duration ◽  
Field Potential ◽  
Membrane Potentials ◽  
Repetitive Stimulation ◽  
Jaw Movements ◽  
Postsynaptic Potentials ◽  
Duration Stimulus ◽  
Long Duration ◽  
Stimulation Of

1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.

Repetitive stimulation of optic nerve and lateral geniculate synapses

1959 ◽  
Vol 1 (6) ◽  
pp. 534-555 ◽  
Author(s):  
P.O. Bishop ◽  
W. Burke ◽  
W.R. Hayhow
Keyword(s):  
Optic Nerve ◽  
Repetitive Stimulation ◽  
Lateral Geniculate ◽  
Stimulation Of

Proportion of muscles spindles supplied by skeletofusimotor axons (beta-axons) in peroneus brevis muscle of the cat

1975 ◽  
Vol 38 (6) ◽  
pp. 1390-1394 ◽  
Author(s):  
F. Emonet-Denand ◽  
Y. Laporte
Keyword(s):  
Neuromuscular Junctions ◽  
Muscle Fibers ◽  
Repetitive Stimulation ◽  
Motor Axon ◽  
Dynamic Sensitivity ◽  
Conduction Velocities ◽  
Peroneus Brevis ◽  
Stimulation Of

Of 32 cat peroneus brevis spindles, 23 (72%) were found to be supplied by a least 1 skeletofusimotor or beta-axon. A motor axon was identified as skeletofusimotor when repetitive stimulation of it elicited both the contraction of extrafusal muscle fibers and as acceleration of the discharge of primary ending, which persisted after selective block of the neuromuscular junctions of extrafusal muscle fibers. The block was obtained by stimulating single axons at 400-500/s for a few seconds. Of 135 axons supplying extrafusal muscle fibers, 24 (18%) were shown to be beta-axons; 22 beta-axons had conduction velocities ranging from 45 to 75 m/s. All but three beta-axons increased the dynamic sensitivity of primary endings. Beta-innervated spindles may also be supplied by dynamic gamma-axons.

Effects of pyruvate on the energetics of rat ventricles stunned by ischemia–reperfusion

2014 ◽  
Vol 92 (5) ◽  
pp. 386-398 ◽  
Author(s):  
Patricia Bonazzola ◽  
María Inés Ragone ◽  
Alicia E. Consolini
Keyword(s):  
Confocal Microscopy ◽  
Heat Release ◽  
Dynamic Balance ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
High K ◽  
Energetic State ◽  
Contractile Recovery ◽  
Stimulation Of

Pyruvate (Pyr) was proposed as an additive to cold high-K+–low-Ca2+ cardioplegia (CPG) to protect the heart during surgery. We explored whether Pyr and CPG would work synergistically to protect rat hearts from stunning during ischemia–reperfusion (I/R). We measured the heat release and contractility of perfused ventricles during I/R, and the cytosolic and mitochondrial [Ca2+] in cardiomyocytes by confocal microscopy. We found that under cold-CPG (30 °C), 10 mmol·L−1 Pyr reduced the post-ischemic contractile recovery (PICR) as well as muscle economy, when added either before ischemia or during I/R, which was reversed by blockade of UCam. In noncardioplegic hearts, Pyr was cardioprotective when it was present during I/R, more so at 37 °C than at 30 °C, with improved economy. In cardiomyocytes, the addition of Pyr to CPG slightly increased the mitochondrial [Ca2+] but decreased cytosolic [Ca2+]. The results suggest that Pyr only protects hearts from stunning when present before ischemia and during reperfusion, and that it dampens the cardioprotective properties of CPG. The mechanisms underlying such different behavior depend on the dynamic balance between Pyr stimulation of the energetic state and mitochondrial Ca2+ uptake. Our results support the use of Pyr in stunned hearts, but not in cold high-K+ cardioplegia.

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