scholarly journals RGK protein-mediated impairment of slow depolarization- dependent Ca2+entry into developing myotubes

Channels ◽  
2014 ◽  
Vol 8 (3) ◽  
pp. 243-248 ◽  
Author(s):  
Christin F Romberg ◽  
Donald Beqollari ◽  
Ulises Meza ◽  
Roger A Bannister
Keyword(s):  
Slow Depolarization

Drugs Affecting the Calcium-Dependent Slow Depolarization Mechanism of the Cardiac Cell Membrane

1982 ◽  
pp. 205-214
Author(s):  
V. Kecskeméti ◽  
K. Kelemen ◽  
R. Marko ◽  
J. Knoll
Keyword(s):  
Cell Membrane ◽  
Cardiac Cell ◽  
Calcium Dependent ◽  
Slow Depolarization

Insemination of rabbit eggs is associated with slow depolarization and repetitive diphasic membrane potentials

1983 ◽  
Vol 95 (2) ◽  
pp. 372-377 ◽  
Author(s):  
David H. McCulloh ◽  
Caird E. Rexroad ◽  
Herbert Levitan
Keyword(s):  
Membrane Potentials ◽  
Slow Depolarization

G-protein mediating the slow depolarization induced by FMRFamide in the ganglion cells of Aplysia

1992 ◽  
Vol 15 (4) ◽  
pp. 255-264 ◽  
Author(s):  
Osamu Chiba ◽  
Kazuhiko Sasaki ◽  
Hirobumi Higuchi ◽  
Koichiro Takashima
Keyword(s):  
G Protein ◽  
Ganglion Cells ◽  
Slow Depolarization

scholarly journals Substance P modulates nicotinic responses of intracardiac neurons to acetylcholine in the guinea pig

2001 ◽  
Vol 281 (6) ◽  
pp. R1792-R1800 ◽  
Author(s):  
Lili Zhang ◽  
John D. Tompkins ◽  
John C. Hancock ◽  
Donald B. Hoover
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Neuronal Excitability ◽  
Action Potential Generation ◽  
Potential Generation ◽  
Local Pressure ◽  
Slow Depolarization ◽  
Intracardiac Neurons

—Application of substance P (SP) to intracardiac neurons of the guinea pig causes slow depolarization and increases neuronal excitability. The present study was done to determine the influence of SP on fast excitatory responses of intracardiac neurons to ACh. Intracellular recording methods were used to measure responses of intracardiac neurons in whole mount preparations of atrial ganglionated nerve plexus from guinea pig hearts. Local pressure ejection of 100 μM SP (1 s) from a glass micropipette caused slow depolarization of all neurons ( n = 38) and triggered action potential generation in 47% of the cells tested. Bath application of SP (0.5–100 μM) caused a dose-dependent depolarization of intracardiac neurons but rarely evoked action potentials, even at the highest concentration. However, such treatment with SP enhanced nicotinic responses evoked by local pressure ejections of ACh (10 mM, 10- to 100-ms duration) in 77% of intracardiac neurons studied ( n = 52). A significant increase in amplitude of ACh-evoked fast depolarization occurred during treatment with 0.5 μM SP (13.0 ± 1.8 mV for control vs. 17.7 ± 1.9 mV with SP present, n = 7, P = 0.019). At higher concentrations of SP, enhancement of the response to ACh resulted mainly in action potential generation. However, responses to ACh were attenuated by SP in 15% of the intracardiac neurons studied. This attenuation occurred primarily during exposure to 10 and 100 μM SP and was manifest as a reduction in amplitude of nicotinic fast depolarization or inhibition of ACh-evoked action potentials. These findings support the conclusion that SP could function as a neuromodulator and neurotransmitter in intracardiac ganglia of the guinea pig.

Slow depolarization in cells presumed to be glia in cerebral cortex of cat.

1973 ◽  
Vol 36 (5) ◽  
pp. 869-878 ◽  
Author(s):  
B R Ransom ◽  
S Goldring
Keyword(s):  
Cerebral Cortex ◽  
Slow Depolarization ◽  
In Cells

Persistent Enhancement of Neuron–Glia Signaling Mediated by Increased Extracellular K+ Accompanying Long-Term Synaptic Potentiation

2007 ◽  
Vol 97 (3) ◽  
pp. 2564-2569 ◽  
Author(s):  
Woo-Ping Ge ◽  
Shumin Duan
Keyword(s):  
Neuronal Activity ◽  
Neural Development ◽  
Long Term Potentiation ◽  
Nmda Receptor Antagonist ◽  
Neuronal Synapses ◽  
Term Potentiation ◽  
Physiological Relevance ◽  
Persistent Elevation ◽  
Slow Depolarization

Neuron–glia signaling is important for neural development and functions. This signaling may be regulated by neuronal activity and undergo modification similar to long-term potentiation (LTP) of neuronal synapses, a hallmark of neuronal plasticity. We found that tetanic stimulation of Schaffer collaterals (Sc) in the hippocampus that induced LTP in neurons also resulted in LTP-like persistent elevation of Sc-evoked slow depolarization in perisynaptic astrocytes. The elevated slow depolarization in astrocytes was abolished by NMDA receptor antagonist and K+ channel inhibitors, but not by Ca2+ chelator BAPTA loaded in the recorded astrocytes, suggesting involvement of an increased extracellular K+ accumulation accompanying LTP of neuronal synapses. The increased K+ accumulation and astrocyte depolarization after LTP induction may reduce the efficiency of glial glutamate transporters, which may contribute to the enhanced synaptic efficacy. The neuronal activity–induced persistent enhancement of neuron–glia signaling may thus have important physiological relevance.

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