Modulatory effects of nitric oxide on synaptic depression in the crayfish neuromuscular system

2000 ◽  
Vol 203 (23) ◽  
pp. 3595-3602 ◽  
Author(s):  
H. Aonuma ◽  
T. Nagayama ◽  
M. Takahata
Keyword(s):  
Nitric Oxide ◽  
Neuromuscular Transmission ◽  
Procambarus Clarkii ◽  
Synaptic Depression ◽  
Physiological Property ◽  
Muscle Fibres ◽  
Flexor Muscle ◽  
Bath Application ◽  
Flexor Muscles ◽  
Stimulation Of

A characteristic physiological property of the neuromuscular junction between giant motor neurones (MoGs) and fast flexor muscles in crayfish is synaptic depression, in which repetitive electrical stimulation of the MoG results in a progressive decrease in excitatory junction potential (EJP) amplitude in flexor muscle fibres. Previous studies have demonstrated that l-arginine (l-Arg) modulates neuromuscular transmission. Since l-Arg is a precursor of nitric oxide (NO), we examined the possibility that NO may be involved in modulating neuromuscular transmission from MoGs to abdominal fast flexor muscles. The effect of a NO-generating compound, NOC7, was similar to that of l-Arg, reversibly decreasing the EJP amplitude mediated by the MoG. While NOC7 reduced the amplitude of the EJP, it induced no significant change in synaptic depression. In contrast, a scavenger of free radical NO, carboxy-PTIO, and an inhibitor of nitric oxide synthase, l-NAME, reversibly increased the EJP amplitude mediated by MoGs. Synaptic depression mediated by repetitive stimulation of MoGs at 1 Hz was partially blocked by bath application of l-NAME. Bath application of a NO scavenger, a NOS inhibitor and NO-generating compounds had no significant effects on the depolarisation of the muscle fibres evoked by local application of l-glutamate. The opposing effects on EJP amplitude of NOC7 and of carboxy-PTIO and l-NAME suggest that endogenous NO presynaptically modulates neuromuscular transmission and that it could play a prominent role at nerve terminals in eliciting MoG-mediated synaptic depression in the crayfish Procambarus clarkii.

scholarly journals The interaction between two trains of impulses converging on the same motoneurone

1929 ◽  
Vol 105 (738) ◽  
pp. 363-371 ◽  
Keyword(s):  
Mechanical Effect ◽  
The Other ◽  
Muscle Fibres ◽  
Flexor Muscle ◽  
Afferent Pathways ◽  
Afferent Nerves ◽  
Maximal Stimulation ◽  
The Common ◽  
The Relationship ◽  
Stimulation Of

It was shown in an earlier paper (7) that if maximal stimulation of either of two different afferent nerves can reflexly excite fractions of a given flexor muscle, there are generally, within the aggregate of neurones which innervate that muscle, motoneurones which can be caused to discharge by either afferent (i. e., motoneurones common to both fractions). The relationship which two such afferents bear to a common motoneurone was shown, by the isometric method of recording contraction, to be such that the activation of one afferent, at a speed sufficient to cause a maximal motor tetanus when trans­mitted to the muscle fibres, caused exclusion of any added mechanical effect when the other afferent was excited concurrently. This default in mechanical effect was called “occlusion.” Occlusion may conceivably be due to total exclusion of the effect of one afferent pathway on the common motoneurone by the activity of the other; but facilitation of the effect of one path by the activation of the other when the stimuli were minimal suggests that, in some circumstances at least, the effect of each could augment and summate with th at of the other at the place of convergence of two afferent pathways. Further investigation, using the action currents of the muscle as indication of the nerve impulses discharged by the motoneurone units, has now given some information regarding the effect of impulses arriving at the locus of convergence by one afferent path when the unit common to both is already discharging in response to impulses arriving by the other afferent path. Our method has been to excite both afferent nerves in overlapping sequence by series of break shocks at a rapid rate and to examine the action currents of the resulting reflex for evidence of the appearance of the rhythm of the second series in the discharge caused by the first when the two series are both reaching the motoneurone.

Contribution of hind limb flexor muscle afferents to the timing of phase transitions in the cat step cycle

1996 ◽  
Vol 75 (3) ◽  
pp. 1126-1137 ◽  
Author(s):  
G. W. Hiebert ◽  
P. J. Whelan ◽  
A. Prochazka ◽  
K. G. Pearson
Keyword(s):  
Electrical Stimulation ◽  
Stance Phase ◽  
Flexor Muscle ◽  
Step Cycle ◽  
Locomotor Rhythm ◽  
Ia Afferents ◽  
Group I ◽  
Flexor Muscles ◽  
Group Ii ◽  
Stimulation Of

1. In this investigation, we tested the hypothesis that muscle spindle afferents signaling the length of hind-leg flexor muscles are involved in terminating extensor activity and initiating flexion during walking. The hip flexor muscle iliopsoas (IP) and the ankle flexors tibialis anterior (TA) and extensor digitorum longus (EDL) were stretched or vibrated at various phases of the step cycle in spontaneously walking decerebrate cats. Changes in electromyogram amplitude, duration, and timing were then examined. The effects of electrically stimulating group I and II afferents in the nerves to TA and EDL also were examined. 2. Stretch of the individual flexor muscles (IP, TA, or EDL) during the stance phase reduced the duration of extensor activity and promoted the onset of flexor burst activity. The contralateral step cycle also was affected by the stretch, the duration of flexor activity being shortened and extensor activity occurring earlier. Therefore, stretch of the flexor muscles during the stance phase reset the locomotor rhythm to flexion ipsilaterally and extension contralaterally. 3. Results of electrically stimulating the afferents from the TA and EDL muscles suggested that different groups of afferents were responsible for the resetting of the step cycle. Stimulation of the TA nerve reset the locomotor step cycle when the stimulus intensity was in the group II range (2-5 xT). By contrast, stimulation of the EDL nerve generated strong resetting of the step cycle in the range of 1.2-1.4 xT, where primarily the group Ia afferents from the muscle spindles would be activated. 4. Vibration of IP or EDL during stance reduced the duration of the extensor activity by similar amounts to that produced by muscle stretch or by electrical stimulation of EDL at group Ia strengths. This suggests that the group Ia afferents from IP and EDL are capable of resetting the locomotor pattern generator. Vibration of TA did not affect the locomotor rhythm. 5. Stretch of IP or electrical stimulation of TA afferents (5 xT) during the flexion phase did not change the duration of the flexor activity. Stimulation of the EDL nerve at 1.8-5 xT during flexion increased the duration of the flexor activity. In none of our preparations did we observe resetting to extension when the flexor afferents were activated during flexion. 6. We conclude that as the flexor muscles lengthen during the stance phase of gait, their spindle afferents (group Ia afferents for EDL and IP, group II afferents for TA) act to inhibit the spinal center generating extensor activity thus facilitating the initiation of swing.

CRAYFISH SKELETAL MUSCLE REQUIRES BOTH INFLUX OF EXTERNAL Ca2+ AND Ca2+ RELEASE FROM INTERNAL STORES FOR CONTRACTION

1993 ◽  
Vol 181 (1) ◽  
pp. 95-105 ◽  
Author(s):  
H. Ushio ◽  
S. Watabe ◽  
M. Iino
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Sarcoplasmic Reticulum ◽  
Procambarus Clarkii ◽  
Isometric Tension ◽  
Resting Potential ◽  
Muscle Fibres ◽  
Flexor Muscle ◽  
Caffeine Treatment ◽  
Skeletal Muscle Fibres

The isometric tension and membrane potential of single skeletal muscle fibres from the flexor muscle of the carpopodite in the meropodite of crayfish Procambarus clarkii (Girard) were studied to determine whether crayfish muscle contraction requires Ca2+ release from the sarcoplasmic reticulum. Contraction elicited by brief extracellular electrical stimulation was reduced by the removal of Ca2+ or by the addition of 25 micromolar nicardipine in crayfish Ringer's solution. Addition of 30 micromolar ryanodine with 1 mmol l-1 caffeine induced a transient contracture, the peak tension of which was 10–30 % of that of the high-K+ induced contracture and which declined to the pretreatment level in 20–60 min. After ryanodine-caffeine treatment, 30 mmol l-1 caffeine failed to induce contraction, suggesting that intracellular Ca2+ stores had been exhausted by the treatment. Extracellular electrical stimulation also failed to induce contraction after ryanodine-caffeine treatment, although the resting potential was not changed. These results suggest that Ca2+ release from the sarcoplasmic reticulum, together with Ca2+ influx via nicardipine-sensitive Ca2+ channels, is essential to the contraction of crayfish leg muscle fibres after a brief membrane depolarization.

SOME ASPECTS OF MECHANISM OF SUCCINAMIDES INFLUENCE ON METABOLIC HOMEOSTASIS OF THE ORGANISM

2018 ◽  
pp. 27-31
Author(s):  
I. A. Palagina
Keyword(s):  
Nitric Oxide ◽  
Biological Activity ◽  
Antioxidant System ◽  
No Synthase ◽  
Antioxidant Potential ◽  
Metabolic Homeostasis ◽  
Energetic Metabolism ◽  
Complex Action ◽  
Energy Processes ◽  
Stimulation Of

Succinate containing compounds possess many types of biological activity and are used for the development of drugs with the target and complex action. This paper is devoted to some aspects of the mechanism of succinamides’ action in a dose of 100 mg/kg. We studied the influence of the compound with antidiabetic properties, -phenylethylamide of 2-oxysuccinanyl acid ( -PhEA-OSAA), and its metabolites such as 2-hydroxyphenylsuccinamide (2-HPhSA) and β-phenylethylsuccinamide ( -PhESA) on the marker indicators of energetic metabolism (EM), antioxidant system (AOS) and nitric oxide (NO) metabolism in subacute experiment on rats. Studies have shown that the action of -FEA-OSAKA on metabolic homeostasis is realized through stimulation of EM, reduction of intensity of NO-synthase metabolism and weakening of the AOS. The nature of the action of -FES and 2-GFS, taking into account the indicators of the state of homeostasis, largely coincides with β-FEA-OSAKA. It was found that the key links in the mechanism of toxic action of succinamides are the effect on antioxidant potential, NO metabolism and energy processes.

Nitric Oxide Activates Leak K+ Currents in the Presumed Cholinergic Neuron of Basal Forebrain

2007 ◽  
Vol 98 (6) ◽  
pp. 3397-3410 ◽  
Author(s):  
Youngnam Kang ◽  
Yoshie Dempo ◽  
Atsuko Ohashi ◽  
Mitsuru Saito ◽  
Hiroki Toyoda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Basal Forebrain ◽  
Reversal Potential ◽  
Soluble Guanylyl Cyclase ◽  
Outward Current ◽  
Pump Current ◽  
Atp Depletion ◽  
Equilibrium Potential ◽  
No Donor ◽  
Bath Application

Learning and memory are critically dependent on basal forebrain cholinergic (BFC) neuron excitability, which is modulated profoundly by leak K+ channels. Many neuromodulators closing leak K+ channels have been reported, whereas their endogenous opener remained unknown. We here demonstrate that nitric oxide (NO) can be the endogenous opener of leak K+ channels in the presumed BFC neurons. Bath application of 1 mM S-nitroso- N-acetylpenicillamine (SNAP), an NO donor, induced a long-lasting hyperpolarization, which was often interrupted by a transient depolarization. Soluble guanylyl cyclase inhibitors prevented SNAP from inducing hyperpolarization but allowed SNAP to cause depolarization, whereas bath application of 0.2 mM 8-bromoguanosine-3′,5′-cyclomonophosphate (8-Br-cGMP) induced a similar long-lasting hyperpolarization alone. These observations indicate that the SNAP-induced hyperpolarization and depolarization are mediated by the cGMP-dependent and -independent processes, respectively. When examined with the ramp command pulse applied at –70 mV under the voltage-clamp condition, 8-Br-cGMP application induced the outward current that reversed at K+ equilibrium potential ( EK) and displayed Goldman-Hodgkin-Katz rectification, indicating the involvement of voltage-independent K+ current. By contrast, SNAP application in the presumed BFC neurons either dialyzed with the GTP-free internal solution or in the presence of 10 μM Rp-8-bromo-β-phenyl-1,N2-ethenoguanosine 3′,5′-cyclic monophosphorothioate sodium salt, a protein kinase G (PKG) inhibitor, induced the inward current that reversed at potentials much more negative than EK and close to the reversal potential of Na+-K+ pump current. These observations strongly suggest that NO activates leak K+ channels through cGMP-PKG-dependent pathway to markedly decrease the excitability in BFC neurons, while NO simultaneously causes depolarization by the inhibition of Na+-K+ pump through ATP depletion.

Isokinetic Strength After ACL Reconstruction: Influence of Concomitant Anterolateral Ligament Reconstruction

2021 ◽  
pp. 194173812110054
Author(s):  
Benoit Gillet ◽  
Yoann Blache ◽  
Isabelle Rogowski ◽  
Grégory Vigne ◽  
Bertrand Sonnery-Cottet ◽  
...  
Keyword(s):  
Muscle Strength ◽  
Ligament Reconstruction ◽  
Knee Extensor ◽  
Anterolateral Ligament ◽  
Flexor Muscle ◽  
Knee Flexor ◽  
Strength Recovery ◽  
Flexor Muscles ◽  
Knee Muscle ◽  
Knee Muscle Strength

Background: To reduce the rate of anterior cruciate ligament (ACL) graft rupture, recent surgeries have involved anterolateral ligament reconstruction (ALLR). This reconstruction procedure harvests more knee flexor muscle tendons than isolated ACL reconstruction (ACLR), but its influence on knee muscle strength recovery remains unknown. This study aimed to assess the influence of ALLR with a gracilis graft on the strength of the knee extensor and flexor muscles at 6 months postoperatively. Hypothesis: The additional amount of knee flexor harvest for ALLR would result in impairment in knee flexor muscle strength at 6 months postoperatively. Study Design: Retrospective cohort study. Level of Evidence: Level 2. Methods: A total of 186 patients were assigned to 2 groups according to the type of surgery: ACL + ALLR (graft: semitendinosus + gracilis, n = 119) or isolated ACLR (graft: semitendinosus, n = 67). The strength of the knee extensor and flexor muscles was assessed using an isokinetic dynamometer at 90, 180, and 240 deg/s for concentric and 30 deg/s for eccentric contractions and compared between groups using analysis of variance statistical parametric mapping. Results: Regardless of the surgery and the muscle, the injured leg produced significantly less strength than the uninjured leg throughout knee flexion and extension from 30° to 90° for each angular velocity (30, 90, 180, and 240 deg/s). However, the knee muscle strength was similar between the ACL + ALLR and ACLR groups. Conclusion: The addition of ALLR using the gracilis tendon during ACLR does not alter the muscle recovery observed at 6 months postoperatively. Clinical Relevance: Although more knee flexor muscle tendons were harvested in ACL + ALLR, the postoperative strength recovery was similar to that of isolated ACLR.

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