Calcium Spike in the Longitudinal Muscle of the Lobworm, Tylorrynchus Heterochaetus, (Nereidae)

1970 ◽  
Vol 53 (3) ◽  
pp. 597-609
Author(s):  
Y. ITO ◽  
N. TASHIRO

1. The mechanical and electrical activities of the longitudinal somatic muscle of the nereid Tylorrynchus heterochaetus were studied by intra- and extracellular stimulating methods. 2. The contraction elicited by electrical stimulation under isometric conditions consisted of two components, i.e. early phasic contraction and sustained contraction. The sustained contraction lasted more than 1 min after the cessation of the tetanic stimulation. 3. The membrane potential was 62.8 mV, and spontaneous discharges with overshoot (mean 18 mV) were recorded. A similar amplitude of the spike could be recorded by the intra-cellular polarizing method. 4. The maximum slope of the membrane potential change against a tenfold change in [K]o was 39 mV in the presence of Na+ and 48 mV in the absence of Na+. 5. The membrane was hyperpolarized by reduction of [Na]o but not by reduction of [Cl]o. 6. Tetrodotoxin (10-5 g/ml) blocked neither spontaneous spike generation nor spikes evoked by electrical stimulation. 7. The spike amplitude (overshoot) was proportionally increased with increased [Ca]o in the absence of Na+. The electrical threshold and the membrane potential remained the same in the ranges of 2 and 200 mM [Ca]o in the absence of Na+. 8. Sr2+ and Ba2+ could produce spike generation in the absence of Na+ and Ca2+. Prolongation of the spike (plateau) was observed when 20 mM Ba2+ was added to the solution containing no Na2+ and Ca2+. 9. The electrical and mechanical properties of the muscle were discussed in comparison with those observed of the longitudinal muscle of the earthworm.

1969 ◽  
Vol 50 (2) ◽  
pp. 405-415
Author(s):  
T. HIDAKA ◽  
Y. ITO ◽  
H. KURIYAMA ◽  
N. TASHIRO

1. The properties of the membrane, in both the resting and the active state, of the longitudinal muscle of the earthworm were studied under various ionic environments. 2. The maximum slope of the membrane potential change against a tenfold change in the external potassium concentration was 27 mV. in the presence of external sodium and 42 mV. in the absence of external sodium. 3. In the normal external potassium concentration the removal of sodium hyper-polarized the membrane from a normal resting potential of -36 to -58 mV. 4. Reduction of the external calcium concentration to a tenth of its normal value depolarized the membrane by about 16 mV. 5. In excess of external potassium the spike height and the after-hyperpolarization were decreased and the duration of the spike was prolonged. 6. In sodium-free solution spikes with an overshoot potential were generated both spontaneously and under the stimulus of an intracellularly depolarizing current. 7. The amplitude and the maximum rate of rise of the spike were dependent on the external calcium concentration, whether or not sodium was present externally. 8. Manganese modified the membrane activity by competition with calcium.


1969 ◽  
Vol 50 (2) ◽  
pp. 431-443 ◽  
Author(s):  
T. HIDAKA ◽  
H. KURIYAMA ◽  
T. YAMAMOTO

1. A study of the mechanical properties of longitudinal muscle in relation to the membrane properties was carried out under isometric conditions. 2. When the stimulus duration exceeded 50 msec., active tension development was followed by sustained contraction. The sustained contractions were not related to spike generation. 3. The critical potassium concentration to produce the contracture depolarized the membrane from -36 to -20 mV. 4. Reduced sodium concentration and increased calcium and increased potassium (up to 27 mM) concentrations enhanced the amplitude of the active tension. 5. Reduced sodium concentration enhanced the amplitude and duration of the sustained tension, but increased potassium and calcium concentrations reduced them. 6. Caffeine (12 mM) induced contractures of the muscle, and reduced the membrane resistance and capacitance. 7. Spikes were not elicited by intracellular stimulation. 8. 5-Hydroxytryptamine (10-5 g./ml.) blocked the generation of the sustained contraction but no effect was observed on the phasic tension.


1969 ◽  
Vol 50 (2) ◽  
pp. 387-403
Author(s):  
T. HIDAKA ◽  
Y. ITO ◽  
H. KURIYAMA

1. The membrane properties of the longitudinal muscle fibre of the earthworm Pheretima communissima were investigated by intra- and extracellular stimulating methods. 2. The membrane potential was -35.4 mV., and spontaneous discharges with overshoot (mean +18 mV.) and after-hyperpolarization (-60 mV.) were recorded. 3. Tetrodotoxin (10-7 g./ml.) blocked nervous activity but did not influence the spontaneous discharges or the spikes elicited in the muscle fibre by intracellular stimulation. 4. The critical membrane potential required to elicit a spike was not constant, and the falling phase of the spikes was markedly dependent on the level of the membrane potential. 5. The chronaxie, measured from the intensity-duration relation to elicit a spike by intracellular stimulation, was 55 msec. 6. When nervous activity was excluded the propagation of excitation in longitudinal muscles was decremental.


2007 ◽  
Vol 23 (6) ◽  
pp. 348-356 ◽  
Author(s):  
Vincent Cazenave-Loustalet ◽  
Qing-Li Qiao ◽  
Li-Ming Li ◽  
Qiu-Shi Ren

1987 ◽  
Vol 58 (6) ◽  
pp. 1259-1274 ◽  
Author(s):  
A. J. Berger ◽  
T. E. Dick

1. Intracellular recordings were made from 50 dorsal respiratory group (DRG) neurons in the region of the ventrolateral nucleus of the solitary tract in anesthetized, paralyzed cats ventilated with a cycle-triggered pump whose inflation stroke was triggered by the onset of phrenic nerve inspiratory (I) discharge. Activity was recorded simultaneously in the ipsilateral nodose ganglion from sensory cell bodies of slowly adapting pulmonary stretch receptors (PSRs). 2. Respiratory cycle-related membrane potential changes of DRG neurons were recorded. Twenty-six neurons that did not exhibit spikes were classified as I alpha, I beta or pump (P)-cells by comparing their membrane potential trajectories during I in the presence of lung inflation with that observed during I, but with lung inflation withheld. The remaining 24 neurons were classified similarly, but the classification was based upon a comparison of their I-phase spike activity responses with and without lung inflation. I phase-related histograms of either membrane potential or spike activity were constructed to facilitate DRG neuronal classification. Additionally, steady lung inflation of varying magnitudes was applied during the expiratory phase. This prolonged expiration and produced different responses in the neurons. Generally, I beta and P-cells were depolarized, whereas I alpha cells were hyperpolarized. 3. Low-intensity electrical stimulation of the ipsilateral vagus nerve evoked excitatory postsynaptic potentials (EPSPs) in all three DRG neuronal types. P-cells and I beta cells exhibited EPSPs in response to the lowest intensity; generally this intensity was below threshold for the simultaneously recorded PSR. Overall, EPSPs in I alpha cells had the highest thresholds, but some EPSPs could be evoked at thresholds similar to those of the I beta cells. The distributions of the average onset latency of the evoked EPSP overlapped considerably. Thus vagal electrical stimulation cannot be used for unequivocal classification of DRG neurons into I alpha, I beta, and P-cell subpopulations. 4. Using intracellular spike-triggered averaging, single PSRs were shown to generate monosynaptic EPSPs in I beta neurons and P-cells but not I alpha cells. Divergence of single PSR afferents also was observed. Relationships between EPSP shape factors, amplitudes, and PSR afferent conduction velocity are similar to those previously observed for monosynaptic EPSPs in hindlimb motoneurons generated by spinal afferents.


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)


1989 ◽  
Vol 257 (4) ◽  
pp. G532-G538 ◽  
Author(s):  
T. Takeda ◽  
K. Taniyama ◽  
S. Baba ◽  
C. Tanaka

The mechanism of action of somatostatin on the motility of intestine was examined in the entire preparation and the longitudinal muscle attached with Auerbach's plexus (LA) preparation of guinea pig ileum, in relation to the cholinergic neuron and gamma-aminobutyric acid (GABA)ergic neuron. Somatostatin produced a transient potentiation of electrical stimulation-induced twitch contractions followed by an inhibition. The excitatory effect of somatostatin was associated with an increase in the release of [3H]acetylcholine (ACh) from the preparations preloaded with [3H]choline. Bicuculline, a GABAA antagonist, inhibited the somatostatin-induced excitatory effect. Somatostatin inhibited the electrical stimulation-induced twitch contraction and release of [3H]ACh, and the inhibition was greater in the entire preparation than in the LA. Phaclofen, a GABAB antagonist, prevented the inhibitory effects of somatostatin. Somatostatin induced a Ca2+ -dependent, tetrodotoxin-sensitive release of [3H]GABA from the preparations preloaded with [3H]GABA. Therefore somatostatin exerts excitatory and inhibitory effects on the cholinergic neuron due to the stimulation of the GABAergic neuron, and the motility of the intestine is regulated.


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

2012 ◽  
Vol 303 (2) ◽  
pp. G240-G246 ◽  
Author(s):  
Xue-Dao He ◽  
Raj K. Goyal

The ionic basis of nitrergic “slow'” inhibitory junction potential (sIJP) is not fully understood. The purpose of the present study was to determine the nature and the role of calmodulin-dependent protein kinase II (CaMKII)-dependent ion conductance in nitrergic neurotransmission at the intestinal smooth muscle neuromuscular junction. Studies were performed in guinea pig ileum. The modified Tomita bath technique was used to induce passive hyperpolarizing electrotonic potentials (ETP) and membrane potential change due to sIJP or drug treatment in the same cell. Changes in membrane potential and ETP were recorded in the same smooth muscle cell, using sharp microelectrode. Nitrergic IJP was elicited by electrical field stimulation in nonadrenergic, noncholinergic conditions and chemical block of purinergic IJP. Modification of ETP during hyperpolarization reflected active conductance change in the smooth muscle. Nitrergic IJP was associated with decreased membrane conductance. The CAMKII inhibitor KN93 but not KN92, the Cl− channel blocker niflumic acid (NFA), and the KATP-channel opener cromakalim hyperpolarized the membrane. However, KN93 and NFA were associated with decreased and cromakalim was associated with increased membrane conductance. After maximal NFA-induced hyperpolarization, hyperpolarization associated with KN93 or sIJP was not seen, suggesting a saturation block of the Cl− channel signaling. These studies suggest that inhibition of CaMKII-dependent Cl− conductance mediates nitrergic sIJP by causing maximal closure of the Cl− conductance.


2001 ◽  
Vol 149 (23) ◽  
pp. 707-711 ◽  
Author(s):  
N. P. H. Hudson ◽  
I. G. Mayhew ◽  
G. T. Pearson

Intracellular microelectrode recordings were made from smooth muscle cells in cross-sectional preparations of equine ileum, superfused in vitro. Membrane potential oscillations and spike potentials were recorded in all preparations, but recordings were made more readily from cells in the longitudinal muscle layer than from cells in the circular layer. The mean (se) resting membrane potential (RMP) of smooth muscle cells in the longitudinal muscle layer was -51.9 (1.2) mV, and the membrane potential oscillations in this layer had a mean amplitude of 4.8 (0.4) mV, a frequency of 9.0 (0.1) cycles per minute and a duration of 5.8 (0.2) seconds. The membrane potential oscillations were preserved in the presence of tetrodotoxin. A waxing and waning pattern of membrane potential oscillation activity was observed. Nifedipine abolished the spiking contractile activity of the smooth muscle, did not abolish the membrane potential oscillations but did alter their temporal characteristics.


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