scholarly journals The Spontaneous Action Potential of Rabbit Atrioventricular Node Cells

1980 ◽  
Vol 30 (4) ◽  
pp. 529-540 ◽  
Author(s):  
Shinichiro KOKUBUN ◽  
Masao NISHIMURA ◽  
Akinori NOMA ◽  
Hiroshi IRISAWA
2004 ◽  
Vol 101 (5) ◽  
pp. 1167-1176 ◽  
Author(s):  
Christian Grasshoff ◽  
Bernd Antkowiak

Background The capacity of general anesthetics to produce immobility is primarily spinally mediated. Recently, compelling evidence has been provided that the spinal actions of propofol involve gamma-aminobutyric acid type A (GABAA) receptors, whereas the contribution of glycine receptors remains uncertain. The relevant molecular targets of the commonly used volatile anesthetic sevoflurane in the spinal cord are largely unknown, but indirect evidence suggests a mechanism of action distinct from propofol. Methods The effects of sevoflurane and propofol on spontaneous action potential firing were investigated by extracellular voltage recordings from ventral horn interneurons in cultured spinal cord tissue slices obtained from embryonic rats (embryonic days 14-15). Results Propofol and sevoflurane reduced spontaneous action potential firing of neurons. Concentrations causing half-maximal effects (0.11 microm propofol, 0.11 mm sevoflurane) were lower than the median effective concentration immobility (1-1.5 microm propofol, 0.35 mm sevoflurane). At higher concentrations, complete inhibition of action potential activity was observed with sevoflurane but not with propofol. Effects of sevoflurane were mediated predominantly by glycine receptors (45%) and GABAA receptors (38%), whereas propofol acted almost exclusively via GABAA receptors (96%). Conclusions The authors' results suggest that glycine and GABAA receptors are the most important molecular targets mediating depressant effects of sevoflurane in the spinal cord. They provide evidence that sevoflurane causes immobility by a mechanism distinct from the actions of the intravenous anesthetic propofol. The finding that propofol acts exclusively via GABAA receptors can explain its limited capacity to depress spinal neurons in the authors' study.


1985 ◽  
Vol 63 (5) ◽  
pp. 784-788 ◽  
Author(s):  
Kim J. Burchiel ◽  
Lisa C. Russell

✓ The effect of topical glycerol application on normal and previously injured saphenous nerves was tested in 20 Sprague-Dawley rats. Anhydrous glycerol treatment of five normal nerves showed a rapid loss of C-fiber conduction within 5 minutes of application, while after 10 to 30 minutes, a complete conduction blockade in all fiber types was produced. The effect of anhydrous glycerol on both spontaneous firing from the neuroma and impulse propagation within the nerve was examined in 11 rats that had undergone saphenous neurotomy 7 days previously. In these animals, cessation of spontaneous action potential production from the neuroma was the earliest electrophysiological change noted, followed by loss first of C-fiber, then of A-fiber conduction. Graded concentrations of glycerol (25%, 50%, 75%, and 100%) were used in four rats with saphenous neuromas, which allowed selective blockade of spontaneous action potential generation and C-fiber conduction with minimal effect on A-fibers. The neurophysiological mechanism of glycerol neurolysis appears to be a nonspecific conduction blockade of large and small fibers, which is established within minutes of its application. Spontaneous firing within damaged axons, which may play a role in a variety of cranial and peripheral nerve sensorimotor syndromes, is also exquisitely sensitive to glycerol application.


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