An investigation of the activity of opiate drug receptors located on frog skeletal muscle fibre membrane

1978 ◽  
Vol 56 (3) ◽  
pp. 501-508 ◽  
Author(s):  
G. B. Frank ◽  
J. Marwaha

Extracellular and intracellular microelcctrode studies were conducted to test the actions and interactions of opiate agonists, antagonists, and procaine on action potentials in frog sartorius muscles. Extracellular studies showed that morphine, methadone, propoxyphene, and procaine all depressed action potential production. Low concentrations of naloxone or naltrexone antagonized the excitability depression produced by the three opiate agonists but not the depression produced by procaine. Intracellular studies revealed that certain concentrations of the opiate agonists produced a biphasic decline in the stimulus-induced increase in sodium conductance (gNa). Naloxone or naltrexone antagonized only the second phase of this decline. These results show that part of the excitability depression produced by opiate agonists is due to an action on opiate drug receptors.

2004 ◽  
Vol 21 (3) ◽  
pp. 251-255
Author(s):  
Atsuko Suzuki ◽  
Ibuki Shirakawa ◽  
Kazunari Noguchi ◽  
Hirohiko Kishi ◽  
Haruo Sugi

1988 ◽  
Vol 92 (5) ◽  
pp. 601-612 ◽  
Author(s):  
L Csernoch ◽  
C L Huang ◽  
G Szucs ◽  
L Kovacs

The effects of tetracaine on charge movements and on antipyrylazo III signals monitoring intracellular delta [Ca2+] were compared in cut frog semitendinosus muscle fibers in a single vaseline gap-voltage clamp. Low tetracaine concentrations (25-40 microM) markedly reduced delta [Ca2+] signals and shifted the rheobase. However, they neither influenced charge movement nor that peak delta [Ca2+] value associated with the contractile threshold. Higher tetracaine concentrations (100-200 microM) partly inhibited charge movements in cut fibers. They separated a steeply voltage-sensitive charge, some of whose features resembled 'q gamma' reported in intact fibers, and whose movement preceded delta [Ca2+] signals at threshold. These findings: (a) directly confirm an earlier suggestion that tetracaine acts on steps in excitation-contraction coupling rather than myofilament activation; (b) show that tetracaine at low concentrations can directly interfere with sarcoplasmic reticular calcium release without modifying charge movement; (c) show that the tetracaine-sensitive charge, first found in intact fibers, also exists in cut fibers; and (d) make it unlikely that tetracaine-sensitive charge transfer is a consequence of Ca2+ release as suggested on earlier occasions.


1967 ◽  
Vol 50 (6) ◽  
pp. 1565-1583 ◽  
Author(s):  
Nick Sperelakis ◽  
Martin F. Schneider ◽  
E. J. Harris

The action of Ba++ on membrane potential (Em) and resistance (Rm) of frog (R. pipiens) sartorius fibers was studied. In normal Cl- Ringer's, Ba++ (<9 mM) did not depolarize or induce contractions, but increased Rm slightly above the control value of 3.8 ± 0.6 KΩ-cm2. In Cl--free Ringer's (methane sulfonate) Rm was 28.8 ± 2.8 KΩ-cm2, and low concentrations of Ba++ (0.05–5.0 mM) depolarized and induced spontaneous contractions (fibrillation), even in tetrodotoxin. To stop disturbance of the microelectrodes, contractions were prevented by using two Cl--free solutions: (a) twice hypertonic with sucrose (230 mM), or (b) high K+ (83 mM) partially replacing Na+. In the hypertonic solution, the fiber diameters decreased, Em increased slightly, and Rm decreased to 9.0 ± 0.6 KΩ-cm2 (perhaps due to swelling of sarcotubules). Ba++ (0.5 mM) rapidly increased Rm to 31.3 ± 3.8, decreased Em (e.g., to -30 mv), and induced spontaneous "action potentials;" Sr++ had no effect. In the high K+ solution, the fibers were nearly completely depolarized, and Rm was decreased markedly to 1.5 ± 0.2 KΩ-cm2; Ba++ increased Rm to 6.7 ± 0.5 KΩ-cm2. The Ba++ actions usually began within 0.5 min and reached a maximum within 5 min. Addition of SO4=, to precipitate the Ba++, rapidly reversed the increase in Rm. Ba++ must act by decreasing K+ conductance (gK). In Cl- Ringer's, the high gCl/gK ratio masked the effect of Ba++ on gK. Thus, small concentrations of Ba++ specifically and rapidly decrease gK.


1987 ◽  
Vol 65 (12) ◽  
pp. 2488-2491 ◽  
Author(s):  
M. J. Mason

The present results demonstrate the sensitivity of the Corning chloride liquid ion exchanger 477913 to L-lactate. Microelectrodes filled with this exchanger showed responses to changes in L-lactate concentration in chloride-free solutions. In these experiments L-lactate replaced gluconate in equimolar amounts. Microelectrodes filled with this exchanger were used to qualitatively detect changes in intracellular anion in chloride-depleted frog sartorius muscle fibres during exposure to extracellular concentrations of L-lactate. The increase in intracellular anion concentration is consistent with the movement of L-lactate into the cell. This microelectrode enables one to qualitatively monitor changes in intracellular L-lactate in chloride-free experiments without incorporating selectivity coefficients.


1994 ◽  
Vol 266 (5) ◽  
pp. C1291-C1300 ◽  
Author(s):  
J. A. Sanchez ◽  
J. Vergara

Action potentials and intracellular Ca2+ transients were monitored in current-clamped segments of frog skeletal muscle fibers using the triple vaseline-gap technique. Calcium signals were measured with the fluorescent indicator rhod 2. Action potentials produced a transient increase in intracellular Ca2+ that was estimated, by deconvolution of the fluorescence signals, to range between 3 and 12 microM. The comparative effects of flash photolysis of caged adenosine 3',5'-cyclic monophosphate (cAMP) and caged ATP on action potentials and Ca signals in muscle were investigated. The photorelease of both nucleotides produced a reduction in the amplitude of the afterpotential that follows the spike. Photorelease of cAMP and ATP prolonged the rate of decay of the Ca signals. No changes in either the rate of rise or in the latent period between stimulation and onset of the Ca signal were observed. Release of cAMP reduced the amplitude of Ca signals, whereas release of ATP had the opposite effect. Our results show that cAMP and ATP, released above their endogenous levels, modulate intracellular Ca2+ release. The cAMP modulation is more significant and may be of physiological importance.


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