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PubMed1977

Determination of muscle cable parameters from a single membrane voltage response.

Computer techniques have been developed to achieve a least-squares fit of the Hodgkin and Rushton one time-constant cable equation to the recorded responses of muscle cells to the intracellular injection of square current pulses. In the rat diaphragm the response of the muscle fiber to square current pulses is well fit by a one time-constant model. This makes possible the estimation of the passive electrical properties of muscle sarcolemma using the response of the fiber to a single stimulus. A comparison of the results of this method and the older method of spatial decay in the rat diaphragm shows no significant differences. Average values obtained using the one-point method for estimating membrane resistance and capacitance are 520 omega cm2 and 4.6 micronF/cm2, respectively. An estimation of the average specific resistivity of the cytoplasm was made using this method, and it was found to be 213 omega cm. At levels of injected currents producing large membrane hyperpolarizations where delayed conductance changes make the spatial decay method useless, the one-point method continues to give consistent results since it utilizes only the early portion of the membrane response. Work with the frog sartorius muscle, which is known to display the characteristics of a two time-constant system, shows that this method is capable of estimating the slower components of this system by using only the later portion of the response curve. The immunity of this method to delayed conductance changes and its experimental facility make it useful in estimating the passive electrical properties of muscle fibers, particularly when working with tissues that are small and delicate or that have poor in vitro viability.

Animals↗
PubMed1999

A weakly coupled version of the Huxley crossbridge model can simulate energetics of amphibian and mammalian skeletal muscle.

This study aimed to establish whether quantitatively accurate predictions of the rate of crossbridge-dependent energy output from shortening muscle could be made on the basis of a 2-state model of crossbridge kinetics incorporating weak coupling between mechanical cycles and ATP hydrolysis. The model was based on Huxley's (1957) model but included rapid detachment, without ATP hydrolysis, of crossbridges when their strain energy increased sufficiently that crossbridge free energy exceeded that of the unbound state (Cooke et al., 1994). An expression was derived relating force to steady-state velocity in terms of the model's rate constants. The values of the rate constants that both provided the best fit through force-velocity data and correctly predicted crossbridge-dependent rate of energy output during an isometric contraction were found and used to predict the variation in rate of energy liberation with shortening velocity. The model predictions closely matched the estimated crossbridge energetics of frog sartorius muscle, including the decline in rate of enthalpy output at high shortening velocities. Data from fast- and slow-twitch muscles of the mouse were also simulated. The velocity-dependence of rate of energy liberation from fast-twitch EDL muscle was well described by the model. The model overestimated crossbridge-dependent energy output from slow-twitch soleus at low shortening velocities but provided accurate predictions of energy output at high velocities. In terms of this model, the distinctive energetics of fast and slow muscles cannot be explained exclusively by differences in cross-bridge detachment rate; differences in the relative rates of crossbridge attachment must also be considered to explain the different relations between energy output and shortening velocity.

Animals↗
PubMed1987

Effect of hypertonic saline on quantal size and synaptic vesicles in identified neuromuscular junction of the frog.

Miniature endplate potential amplitude distributions, miniature endplate potential frequencies and the percentage of sub-miniature endplate potentials were studied during treatment with hypertonic saline (with sucrose) during the initial high frequencies of release and after fatigue. Small muscle fibers were selected which had normal miniature endplate potential frequencies of 0.1/s to 1/s so that the miniature endplate potential amplitude distributions could be determined at the height of the hypertonic effect (first 5-15 min) at which time the miniature endplate potential frequency increased two-hundredfold. During the first few minutes of the effect, there was little change in miniature endplate potential amplitude or in the profiles of their amplitude histograms. Subsequently, after the occurrence of as few as 10(4) miniature endplate potentials, the size of the mean bell-miniature endplate potentials decreased. Later (25 min) the amplitude profiles became uniform, and finally (45 min) the percentage of sub-miniature endplate potentials and smaller miniature endplate potentials increased until many miniature endplate potentials (30-70%) were of the sub-miniature endplate potential class and the overall distributions were skewed. The mean sub-miniature endplate potential amplitude did not appear to change. After the initial high frequency of release, many miniature endplate potentials showed a definite break on the rising phase and the amplitude of the break was usually that of the sub-miniature endplate potential. The rapid decrease in miniature endplate potential size, change in miniature endplate potential amplitude profile and breaks on the miniature endplate potential rising phase can be explained with the subunit hypothesis. The edge fibers of the sartorius muscle were used so that physiologically studied edge junctions that were producing various miniature endplate potential histograms could be identified for electron microscopy. Synaptic vesicle diameters and the coefficient of variation of vesicle diameters were not changed either during high miniature endplate potential frequencies or in those junctions that generated mainly sub-miniature endplate potentials. Thus, the quantal class (i.e. sub-miniature endplate potential or bell-miniature endplate potential) cannot be determined from the vesicle diameter.

Action Potentials↗
PubMed1977

Endotoxin alters spontaneous transmitter release at the frog neuromuscular junction.

The direct neurotoxic effects of E. coli endotoxin (ETX) on spontaneous transmitter release were tested at the frog sartorius muscle neuromuscular junction. Spontaneous transmitter release was monitored by intracellularly recording miniature end-plate potentials (MEPPs). Junctions were continuously exposed to standard concentrations of 10 microgram/ml of 3 ETX samples, 2 of which produced a significant elevation of MEPP frequency followed by a decline of frequency to very low rates. The third ETX sample, known to have a decreased canine lethality, was without effect on MEPP frequency. No significant changes in MEPP amplitude were evident. The rate of change in MEPP frequency, but not the peak frequency, was reduced by lowering ETX concentrations. Alterations in MEPP frequency induced by ETX were prevented by removing Ca++ and antagonized by high [K+]out. The results suggest that ETX alters ion conductance channels, particularly those for Ca++, in the presynaptic terminal membrane.

Action Potentials↗
PubMed2002

Rationale and definition of the lateral extension of the inguinal lymphadenectomy for vulvar cancer derived from an embryological and anatomical study.

BACKGROUND AND OBJECTIVES: The objective of the present study was to define the location of the most lateral superficial inguinal node lying along the inguinal ligament, through an embryological and anatomotopographical study, in order to rationalize the lateral extension of the groin lymphadenectomy in vulvar cancer. METHODS: Sections of the upper portion of the femoral triangle belonging to three human fetuses, whose crown-rump (CR) length ranged from 70 to 310 mm, corresponding to a developmental age of 11 and 35 weeks, were studied. In addition, for an objective topographical evaluation of the disposition of the superficial inguinal lymph nodes, adult cadavers photographs of dissected Scarpa's triangle, reported in anatomical atlases, were analyzed. RESULTS: Both the embryological investigation and the anatomotopographical evaluation on cadavers photographs demonstrate that the most lateral superficial inguinal lymph node does not rise above the medial margin of the sartorius muscle, nor far lateral to the point where the superficial circumflex iliac vessels cross the inguinal ligament. CONCLUSIONS: On the basis of the present study, the authors believe that the superficial circumflex iliac vessels could represent the lateral surgical landmark, easily detectable, at which the inguinal lymphadenectomy should cease. Therefore, there is no need to extend the lateral excision to the anterior superior iliac spine. Finally, leaving the fatty tissue laterally to these vessels, some lymphatic channels could be preserved, decreasing the incidence and the entity of wound seroma and lymphedema.

Fascia↗
PubMed1977

Permeability of the endplate membrane activated by acetylcholine to some organic cations.

The ability of various organic cations to depolarize the ACh-activated endplate membrane in the absence of Na ions was examined on frog sartorius muscle by measuring the endplate potential on the muscle surface with the moving electrode technique. The ACh-activated endplate membrane was very permeable to ammonium and its methyl and hydroxy derivatives, and moderately permeable to guanidine derivatives and Tris (hydroxymethyl) aminomethane. The permeability of alkylol derivatives of ammonium diminished progressively with increase in molecular size. The present results suggested that the endplate ionic channels can be represented by a pore of about 6.4 A in diameter.

Acetylcholine↗
PubMed1987

Synaptic competition and the persistence of polyneuronal innervation at frog neuromuscular junctions.

Mechanisms governing the elimination of polyneuronal innervation were examined by correlating the morphology and physiology of competing nerve terminals at identified dually innervated neuromuscular junctions in sartorius muscles of adult frogs (Rana pipiens). Synaptic efficacy (endplate potential amplitude per unit nerve terminal length) was presumed to reflect the ability of a terminal to compete for synaptic space. The synaptic efficacies of two terminals at the same synaptic site were found to be surprisingly equal, with a median difference of 33%. Much more variation would be expected if dually innervated junctions were randomly innervated by pairs of terminals having the same range of synaptic efficacy as that found at singly innervated junctions in the same muscle. This finding supports the hypothesis that the weaker input is eliminated from dually innervated junctions when there is a large discrepancy in competitive efficacy, and that both inputs may persist if competitive efficacies are relatively equal. We also tested but failed to find support for the hypothesis that spatial proximity between competing terminals intensifies competition for synaptic space during synapse elimination.

Animals↗
PubMed1997

Low-dose automated electron tomography: a recent implementation.

Low-dose automated tomography has been implemented on a 400-kV JEOL intermediate voltage electron microscope. Instrumentation and procedures for automatic tomographic series data collection are described. Difficulties encountered and ways to overcome them are discussed. A low-dose tomographic projection series of a triad junction of frog sartorius muscle was semiautomatically collected and a 3-D reconstruction of this organelle was made.

Animals↗
PubMed1997

Evidence for K+ channels involvement in capillary sensing and for bidirectionality in capillary communication.

Although the capillary sensing and communication phenomenon has been characterized, its mechanism is not clear. It has been hypothesized that capillary sensing involves a membrane potential change in the capillary endothelium and/or pericyte and that communication represents an electrotonic spread of this change along the capillary. The goal of the present study was to address this hypothesis by examining the presence of K+ channels on the capillary and by determining bidirectionality of communication. Using intravital microscopy, we locally applied K+ (100 mM), acetylcholine (ACh; 3 mM), and norepinephrine (NE; 0.3 mM) on capillaries, 400-500 microns downstream from the arteriole, at the surface of the sartorius muscle in anesthetized frogs. Responses were measured in terms of red blood cell velocity (VRBC) changes in the stimulated capillary (control prestimulation VRBC ranged from 110 to 770 microns/sec). K+ and ACh caused significant 19 and 38% increases in VRBC, while NE caused a -46% decrease, respectively. The K+ response was blocked by local pretreatment with K+ channel blocker BaCl2 (1 microM) and by pretreatment with tetraethyl ammonium chloride (TEA; 5 mM). Responses to ACh and NE were attenuated by pretreatment with 1 microM BaCl2 (to 1%) and with 50 mM TEA (to -25%), respectively. In a separate experiment, NE (3 mM) application on the capillary 500 microns away from the draining venule (capillary occluded) caused a 19% venular constriction (i.e., similar to a reported 21% arteriolar constriction caused by the NE stimulus). We concluded that (i) K+ channels were present on the capillary and (ii) capillary communication was bidirectional. We interpreted these results to be consistent with the above hypothesis of membrane potential change and electrotonic spread.

Acetylcholine↗
PubMed1996

Effects of 4-aminopyridine on saxitoxin intoxication.

Effects of 4-aminopyridine (4-AP) on neurotoxicity induced by saxitoxin (STX) are investigated in this study. In vitro, twitch tension evoked by nerve stimulation was depressed by STX (1.35 nM) in rat phrenic nerve-diaphragm preparations, and this inhibition was antagonized by 4-AP (0.1 mM). In addition, 4-AP (0.1 mM) restored the firing of membrane action potentials that were suppressed or even abolished by 0.334 nM STX in frog sartorius muscles. In vivo studies showed that 4-AP (0.3 mg/kg, iv) significantly reversed the respiratory rate, tidal volume, and blood pressure to normal values in anesthetized STX-toxicosis rats. Furthermore, 4-AP (0.75-6 mg/kg, ip) not only prolonged the survival time but also decreased the mortality of mice (71-43%) at a normally lethal dose (30 micrograms/kg, ip) of STX. The results suggest that 4-AP may be useful as an antidote for STX intoxication.

4-Aminopyridine↗
PubMed1991

The effects of muscarine and atropine reveal that inhibitory autoreceptors are present on frog motor nerve terminals but are not activated during transmission.

The role of presynaptic muscarinic receptors in modulating neuromuscular transmission was studied in the isolated sartorius muscle of the frog using electrophysiological techniques. In low calcium solutions muscarine reduced mEPP frequency and the quantal of EPPs. In solutions containing the normal calcium concentration the effect of muscarine on quantal content, but not the effect on mEPP frequency, was somewhat attenuated. Muscarine-induced reductions in the parameters of ACh release were prevented by atropine. Irrespective of the calcium concentration, atropine had no effect on mEPP frequency except where fibres were pretreated with glycerol. In experiments where evoked acetylcholine release was maintained at physiologically relevant levels, atropine had no effect on the quantal content of EPPs evoked at low frequency or on the extent of rundown in trains of EPPs evoked at high frequency.

Acetylcholine↗
PubMed1975

Pre- and postjunctional neuromuscular blockade by carbachol.

Carbachol, when applied to the bathing Ringer solution of frog sartorius muscles, caused depolarization of the endplate and a blockade of endplate potentials (EPP's), miniature EPP's (mepp's) and the iontophoretic acetylcholine potential. In muscles treated with an analog of hemicholinium-3, alpha, alpha'bis(dimethylammonium acetaldehyde diethylacetal)-p-p'-diacetylbiphenyl dibromide (DMAE), depolarization of the endplate by carbachol was blocked and the blockade by carbachol of the iontophoretic acetylcholine potential was prevented. These responses to carbachol were attributed to a postjunctional action that was antagonized by DMAE. In contrast, the blockade by carbachol of EPP's and mepp's was enhanced in DMAE-treated muscles at a time when carbachol-induced depolarization was blocked. This response to carbachol was attributed to a pre-junctional action. Carbachol either blocked transmitter release by a mechanism that was insensitive to DMAE or enhanced the prejunctional blocking actions of DMAE. Succinylcholine had actions similar to carbachol. DMAE prevented depolarization by succinylcholine but enhanced neuromuscular blockade by succinylcholine. SKF 525-A (beta-diethylaminoethyl diphenylpropylacetate hydrochloride), like DMAE, prevented depolarization but not transmission blockade caused by carbachol.

Acetylcholine↗
PubMed1981

Multiple actions of beta-bungarotoxin on acetylcholine release at amphibian motor nerve terminals.

The action of beta-bungarotoxin (beta-BuTX) on spontaneous transmitter release, as monitored by miniature endplate potential (MEPP) frequency, and nerve-stimulated release, which relates directly to endplate potential (EPP) amplitude, was studied at frog sciatic nerve-sartorius muscle junctions. Three phases were found for both spontaneous and evoked release: a transient decrease followed by an increase and a later decrease leading to complete failure. The initial inhibitory phase for both spontaneous and neurally-evoked release occurred at the same time and was independent of stimulation frequency. Both the excitatory and late inhibitory phases for both types of release had a more rapid onset when stimulation frequency was increased, with the effects on evoked release occurring more rapidly than the effects on spontaneous release. Even though EPP amplitude decreased to low levels while MEPP frequency was still high, EPPs did not completely fail until the MEPPs had also declined to very low levels. In elevated K+ solutions, the number of quanta released after toxin application was only about half that released during the control experiment. During the terminal part of the late inhibitory phase of beta-BuTX action on MEPP frequency, no effect or only small transient increases were observed after La3+ administration, elevated [K+]0, or increased osmotic pressure. The present study suggests that depolarization of nerve terminals by the toxin is responsible for initiation of the excitatory phases of both types of release followed by inhibition of nerve-evoked release, and then depletion of vesicular transmitter accounts for the eventual disappearance of both MEPPs and EPPs.

Acetylcholine↗
PubMed1979

Excitation-contraction coupling in frog sartorius and the role of the surface charge due to the carboxyl group of sialic acid.

Frog sartorius muscle fibres were incubated with the enzyme neuraminidase which is known to remove surface-bound sialic acids. The sialic acid content of the incubation media was analysed, and the relationship between the threshold of contraction and the altered pH and divalent cation concentration was investigated. The threshold potential of fibres treated with 3.3, 5 or 6.7 units of neuraminidase (at pH 5.5 and 30 degrees C for 2 h) was more positive than that of the control muscle fibres incubated under the same conditions, but without the enzyme. The potential shift is positively correlated with the enzyme concentration and with the amount of sialic acid released. After incubation with 5 units of neuraminidase the potential shift rose to +8.5 mV, depending on [Ca2+]0, [Mg2+]0 and pH. The threshold shift is greatest at low divalent cation concentration (0.5 mM), and not significant at high concentrations of divalent cations (50 mM). In both neuraminidase-treated and control muscles, the effectiveness of Mg2+ is half of that of Ca2+. The dependence of the contraction threshold on pH in the range 5.5--10 is even more pronounced in enzyme-treated than in control muscle fibres. Resting potential, time-course and overshoot of action potential are not affected by treatment with neuraminidase. Threshold shifts are explained by shifts of an external surface potential upon variation of [Ca2+]0, [Mg2+]0 and pH. Treating the muscles with neuraminidase diminishes the net negative charge density, and hence shifts the surface potential to more positive values, by release of negatively charged sialic acid. The different effectiveness of Ca2+ and Mg2+ is ascribed to their different effectiveness of Ca2+ Mg2+ is ascribed to their different binding behaviour towards the negative surface charges.

Animals↗
PubMed1987

The effect of anticholinesterase drugs on the ionophoretically-evoked end-plate currents.

In order to study the sensitivity of acetylcholine (ACh) receptors exposed to anticholinesterase drugs, the ionophoretically evoked end-plate currents (e.p.c.i) in frog sartorius muscle were studied. During treatment with prostigmine (PST, 3 microM) or methanesulfonyl fluoride (MSF, 1-2 mM), the amplitude of the e.p.c.i evoked by ACh was first increased, reaching its maximum (200-400%) after 20-30 min and then decreased. If these experiments were repeated by applying carbachol (CCh) instead of ACh, an increase, although less pronounced (30-100%), was also observed. The results obtained by applying CCh cannot be ascribed to the inhibition of ACh-esterase, as CCh is not hydrolysed by this enzyme. Therefore, a direct action of both drugs on the ACh-receptor channel complex is suggested. From the comparison of the effects of PST and MSF on the responses to CCh and ACh applications, it is calculated that 20-25% of the increased response to ACh during PST treatment can be ascribed to the direct effect on the ACh-receptor channel complex. During MSF treatment, this amount results in 13-15%. The changes of the time course of the e.p.c.i (evoked by CCh or ACh), which is prolonged in the presence of PST and shortened during the maximum effect of MSF, suggest that the direct action of both studied drugs is different.

Animals↗
PubMed1983

Facilitation and the conduction of the nerve action potential at the frog neuromuscular junction.

We have measured the time intervals (latencies) between the delivery of paired stimuli and the appearance of the extracellularly recorded nerve terminal action potentials (n.a.p.s) and end-plate currents (e.p.c.s) at different temperatures in the sciatic nerve, sartorius muscle preparation of the frog. When the interstimulus interval was 70 ms, the n.a.p. and e.p.c. latencies following the second stimulus of the pair were shorter than following the first at 10 degrees C and 15 degrees C, and facilitation of the e.p.c. was observed. The shortened latency was also observed at 20 degrees C by Barton and Cohen (1982), who suggested that this may be related to facilitation. At 5 degrees C, however, the n.a.p. and e.p.c. latencies following the second stimulus were longer than following the first, and facilitation was still observed. When a 30 ms interstimulus interval was used, the changes in latency were even greater at the temperatures studied. The changes in e.p.c. latency were due to changes in the conduction velocity of the n.a.p., not changes in synaptic delay. At all temperatures and interstimulus intervals studied, the larger amplitude n.a.p.s were conducted more slowly, however, facilitation was always observed. We conclude that changes in the amplitude and conduction velocity of the nerve action potential do not obviously affect facilitation at the frog neuromuscular junction.

Action Potentials↗
PubMed1990

Repeated, in vivo observation of frog neuromuscular junctions: remodelling involves concurrent growth and retraction.

The fluorescent dye 4-(4-diethylaminostyryl)-N-methylpyridinium iodide was used as a vital stain to study remodelling of motor nerve terminals in sartorius muscles of living frogs (Rana pipiens). Identified terminals were observed twice in vivo at intervals of 87-192 days. After the second observation, muscles were fixed and stained with the nitroblue tetrazolium method for nerve terminals and with cholinesterase stain. Observations were made of 243 junctions in 26 frogs. Most nerve terminals grew during the observation interval, with an average increase in total terminal length of 29%. This growth involved substantial remodelling. Within single junctions, the change in size was the net result of differing degrees of growth or shrinkage in individual nerve terminal branches. At least one new terminal branch appeared in 25% of the junctions. Terminal retraction was also common, with branch shortening seen in 60% of junctions and the complete disappearance of a branch in 12%. In one case the original axonal input retracted completely and the junction was partially reinnervated by a terminal sprout from a junction on an adjacent fibre. Some discrepancies between histological and in vivo observations of remodelling were noted. These observations confirm that frog neuromuscular junctions are highly dynamic synapses, subject to profound structural remodelling throughout adult life.

Animals↗
PubMed1982

The effects of chronic stimulation on the morphology of the frog neuromuscular junction.

A quantitative study was made of the effects of 24 h continuous stimulation on the morphology of the frog neuromuscular junction. The synaptic vesicle concentration in the nerve endings of frog sartorius muscles stimulated in vitro for 24 h at 2 Hz was the same as that in controls stimulated for only 0.3 h at 2 Hz. The control preparations were either freshly dissected or maintained at rest in vitro for 23 h prior to stimulation. Chronically stimulated terminals differed from their controls only in having more cisternae and fewer dense cored vesicles. Varying the lengths of the nerves to both chronically stimulated an in vitro control muscles had little effect on the morphology of the nerve endings. Continuous recording of muscle twitch tension demonstrated that neurotransmission was effective throughout the 24 h period of stimulation. Additional evidence that nerve failure or degeneration was not a factor in the results came from a second set of control and chronically stimulated preparations that were tetanized at 30 Hz for 0.3 h before fixation. Changes attributable to rapid stimulation were evident in 87 to 100% of their nerve terminals. Although the distribution of membrane among various membrane organelles differed from one treatment group to another, the total amount of measurable membrane in the nerve terminals was the same in all of the treatment groups; that is, the total amount of membrane was not altered by maintenance in vitro, chronic stimulation at 2 Hz, rapid stimulation at 30 Hz, reduced nerve length, or any tested combination of these treatments. This conservation of total membrane suggests that membrane exchange between axon and nerve terminal occurs at a relatively slow rate which is unaffected by synaptic activity, and that the local mechanism for recycling synaptic vesicle membrane in frog neuromuscular junctions is more autonomous and durable than has been suspected.

Animals↗