scholarly journals An acetylcholine-induced potassium current in tail sensory neurons in the pleural ganglion of Aplysia.

1988 ◽  
Vol 38 (4) ◽  
pp. 563-568 ◽  
Author(s):  
Mitsuyuki ICHINOSE ◽  
Masashi SAWADA ◽  
Takashi MAENO
Keyword(s):  
Sensory Neurons ◽  
Potassium Current ◽  
Pleural Ganglion

Angiotensin II increases excitability and inhibits a transient potassium current in vagal primary sensory neurons

Neuropeptides ◽  
2009 ◽  
Vol 43 (3) ◽  
pp. 193-199 ◽  
Author(s):  
Thaís Helena Moreira ◽  
Jader Santos Cruz ◽  
Daniel Weinreich
Keyword(s):  
Angiotensin Ii ◽  
Sensory Neurons ◽  
Potassium Current ◽  
Primary Sensory Neurons

Prostaglandin e2 inhibits the potassium current in sensory neurons from hyperalgesic kv1.1 knockout mice

Neuroscience ◽  
2003 ◽  
Vol 119 (1) ◽  
pp. 65-72 ◽  
Author(s):  
X. Jiang ◽  
Y.H. Zhang ◽  
J.D. Clark ◽  
B.L. Tempel ◽  
G.D. Nicol
Keyword(s):  
Prostaglandin E2 ◽  
Sensory Neurons ◽  
Knockout Mice ◽  
Potassium Current

scholarly journals Prostaglandins Suppress an Outward Potassium Current in Embryonic Rat Sensory Neurons

1997 ◽  
Vol 77 (1) ◽  
pp. 167-176 ◽  
Author(s):  
G. D. Nicol ◽  
M. R. Vasko ◽  
A. R. Evans
Keyword(s):  
Steady State ◽  
Sensory Neurons ◽  
Potassium Current ◽  
Current Treatment ◽  
Resting Membrane Potential ◽  
Prostaglandin E ◽  
Patch Clamp Recording ◽  
Cellular Mechanisms ◽  
Steady State Inactivation ◽  
Outward Potassium Current

Nicol, G. D., M. R. Vasko, and A. R. Evans. Prostaglandins suppress an outward potassium current in embryonic rat sensory neurons. J. Neurophysiol. 77: 167–176, 1997. The cellular mechanisms giving rise to the enhanced excitability induced by prostaglandin E2 (PGE2) and carba prostacyclin (CPGI2) in embryonic rat sensory neurons were investigated using the whole cell patch-clamp recording technique. Exposing sensory neurons to 1 μM PGE2 produced a twofold increase in the number of action potentials elicited by a ramp of depolarizing current, but this eicosanoid had no effect on the resting membrane potential or the amplitude of the slow afterhyperpolarization. Characterization of the outward potassium currents in the embryonic sensory neurons indicated that the composition of the total current was variable among these neurons. A steady-state inactivation protocol was used to determine the extent of residual noninactivating current. A conditioning prepulse to +20 mV demonstrated that some of these neurons exhibited only a sustained potassium current with little steady-state inactivation whereas others exhibited some combination of a sustained as well as a rapidly inactivating I A-type current. Treatment with 1 μM PGE2 or 1 μM CPGI2, but not 1 μM prostaglandin F2α (PGF2α) produced a time-dependent suppression of the total potassium current. After a 20-min exposure, PGE2 and CPGI2 inhibited the maximal current obtained at +60 mV by 48 and 40%, respectively. The prostaglandin-induced suppression of the potassium current was not associated with a shift in the voltage dependence for activation. Subtraction of the currents remaining after PGE2 or CPGI2 treatment from their respective control recordings revealed that the prostaglandin-sensitive current had characteristics that were consistent with a sustained-type of potassium current. This idea is supported by the following observation. The steady-state inactivation protocol revealed that for prepulse voltages activating both rapidly inactivating and sustained currents, the relaxation of the current was accelerated after treatment with PGE2 or CPGI2 suggesting the removal of a slower component. This effect was not observed in neurons exhibiting only the sustained type current. These results suggest that pro-inflammatory prostaglandins enhance the excitability of rat sensory neurons, in part, through the suppression of an outward potassium current that may modulate the firing threshold for generation of the action potential.

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