scholarly journals 1P204 Involvement of NMDA-Rs in developmental change of spontaneous action potential pattern in a rat hippocampal dissociated neurons(Chemoreception, neuron and sensory system, neural network, and brain computing,Oral Presentations)

2007 ◽  
Vol 47 (supplement) ◽  
pp. S74
Author(s):  
Ai Kyohara ◽  
Takahisa Taguchi ◽  
Suguru N. Kudoh
Keyword(s):  
Neural Network ◽  
Action Potential ◽  
Developmental Change ◽  
Sensory System ◽  
Spontaneous Action Potential ◽  
Spontaneous Action ◽  
Oral Presentations

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
Keyword(s):  
Action Potential ◽  
Atrioventricular Node ◽  
Spontaneous Action Potential ◽  
Spontaneous Action

Propofol and Sevoflurane Depress Spinal Neurons In Vitro via  Different Molecular Targets

2004 ◽  
Vol 101 (5) ◽  
pp. 1167-1176 ◽  
Author(s):  
Christian Grasshoff ◽  
Bernd Antkowiak
Keyword(s):  
Spinal Cord ◽  
Action Potential ◽  
Gabaa Receptors ◽  
Molecular Targets ◽  
Glycine Receptors ◽  
Spinal Neurons ◽  
Action Potential Firing ◽  
Spontaneous Action Potential ◽  
Potential Firing ◽  
Spontaneous Action

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.

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