scholarly journals THE EXPERIMENTAL STUDIES ON THE ELECTRIC STIMULATION OF CILIARY CELL OF THE EPITHELIUM AND ITS MOTOR NERVE IN THE PALATE OF FROG

1970 ◽  
Vol 24 (4) ◽  
pp. 361-370
Author(s):  
Pai ih LIOU
Keyword(s):  
Electric Stimulation ◽  
Motor Nerve ◽  
Experimental Studies ◽  
Ciliary Cell ◽  
Stimulation Of

scholarly journals Electrical Stimulation of Injected Muscles to Boost Botulinum Toxin Effect on Spasticity: Rationale, Systematic Review and State of the Art

Toxins ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 303
Author(s):  
Alessandro Picelli ◽  
Mirko Filippetti ◽  
Giorgio Sandrini ◽  
Cristina Tassorelli ◽  
Roberto De Icco ◽  
...  
Keyword(s):  
Systematic Review ◽  
Electrical Stimulation ◽  
Botulinum Toxin ◽  
Current Literature ◽  
Electric Stimulation ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Botulinum Toxins ◽  
Stimulation Of

Botulinum toxin type A (BoNT-A) represents a first-line treatment for spasticity, a common disabling consequence of many neurological diseases. Electrical stimulation of motor nerve endings has been reported to boost the effect of BoNT-A. To date, a wide range of stimulation protocols has been proposed in the literature. We conducted a systematic review of current literature on the protocols of electrical stimulation to boost the effect of BoNT-A injection in patients with spasticity. A systematic search using the MeSH terms “electric stimulation”, “muscle spasticity” and “botulinum toxins” and strings “electric stimulation [mh] OR electrical stimulation AND muscle spasticity [mh] OR spasticity AND botulinum toxins [mh] OR botulinum toxin type A” was conducted on PubMed, Scopus, PEDro and Cochrane library electronic databases. Full-text articles written in English and published from database inception to March 2021 were included. Data on patient characteristics, electrical stimulation protocols and outcome measures were collected. This systematic review provides a complete overview of current literature on the role of electrical stimulation to boost the effect of BoNT-A injection for spasticity, together with a critical discussion on its rationale based on the neurobiology of BoNT-A uptake.

Homosynaptic depression and transmitter turnover in spinal monosynaptic pathway

1977 ◽  
Vol 40 (1) ◽  
pp. 95-105 ◽  
Author(s):  
R. Capek ◽  
B. Esplin
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Drug Effects ◽  
Medial Gastrocnemius ◽  
Lateral Gastrocnemius ◽  
Homosynaptic Depression ◽  
Dorsal Root Reflex ◽  
Frequency Of Stimulation ◽  
Fractional Release ◽  
Stimulation Of

1. The transmission in the spinal monosynaptic pathway was studied during repetitive stimulation of a motor nerve by 10 stimuli at 2, 5, or 10 Hz in spinal cats. Initially, the amplitudes of the monosynaptic responses rapidly declined, reaching a plateau after a few stimuli. The level of the plateau was inversely related to the frequency of stimulation. 2. This depression of monosynaptic response was seen only when the same pathway was stimulated; the response elicited from the lateral gastrocnemius was not depressed when preceded by stimulation of the medial gastrocnemius nerve and vice versa. Pretreatment with semicarbazide left the homosynaptic depression unchanged while suppressing the dorsal root reflex. The participation of a depolarization of primary afferents in the described depression is, therefore, unlikely. 3. The decrease of transmitter release by successive volleys, which is the cause of the observed depression, could conceivably be related to the depletion of transmitter stores. 4. A procedure is described, based on this assumption, which allows the calculation of transmitter turnover. The input-output relation in the spinal monosynaptic pathway is used to convert the amplitudes of monosynaptic responses to the amounts of transmitter, both relative to the maximum response. The changes of transmitter release are analyzed under the assumption that each volley releases instantaneously a constant fraction of the transmitter store available for release and that this store is replenished at a constant fraction of the depleted part per second. 5. The values of fractional release per volley were about 0.4, irrespective of frequency of stimulation. 6. The values of fractional replenishment per second ranged from about 1 to 5 on the average, depending directly on the frequency of stimulation. 7. It is suggested that the described procedure might be useful in analyzing drug effects on synaptic transmission.

ATP concentrations and muscle tension increase linearly with muscle contraction

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Motor Nerve ◽  
Muscle Tension ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Ventral Roots ◽  
Root Stimulation ◽  
Stimulation Of

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

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