scholarly journals Mitochondrial Reactive Oxygen Species Inactivate Neuronal Nicotinic Acetylcholine Receptors and Induce Long-Term Depression of Fast Nicotinic Synaptic Transmission

2008 ◽  
Vol 28 (7) ◽  
pp. 1733-1744 ◽  
Author(s):  
V. A. Campanucci ◽  
A. Krishnaswamy ◽  
E. Cooper
Keyword(s):  
Reactive Oxygen Species ◽  
Synaptic Transmission ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Oxygen Species ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Mitochondrial Reactive Oxygen Species ◽  
Long Term Depression ◽  
Nicotinic Acetylcholine

scholarly journals Nicotinic Acetylcholine Receptors Interact with Dopamine in Induction of Striatal Long-Term Depression

2002 ◽  
Vol 22 (7) ◽  
pp. 2541-2549 ◽  
Author(s):  
John G. Partridge ◽  
Subbu Apparsundaram ◽  
Greg A. Gerhardt ◽  
Jennifer Ronesi ◽  
David M. Lovinger
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Long Term Depression ◽  
Nicotinic Acetylcholine

Differential Effects of Thiopental on Neuronal Nicotinic Acetylcholine Receptors and P2XPurinergic Receptors in PC12 Cells 

1997 ◽  
Vol 87 (5) ◽  
pp. 1199-1209 ◽  
Author(s):  
Tomio Andoh ◽  
Ryousuke Furuya ◽  
Keikou Oka ◽  
Satoshi Hattori ◽  
Itaru Watanabe ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Pc12 Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Whole Cell ◽  
Inward Current ◽  
Steady Current ◽  
Neuronal Nachr

Background PC12 cells, derived from rat pheochromocytoma, express neuronal nicotinic acetylcholine receptors (nAchRs) and P2X purinergic receptors, both of which resemble the receptors in postganglionic sympathetic neurons. The former is the established and the latter is the putative receptor to mediate fast synaptic transmission. The authors investigated effects of thiopental on these two ligand-gated ion channels. Methods Whole cell currents were recorded in PC12 cells without treatment of nerve growth factor, using conventional whole cell patch clamp technique. Nicotine or adenosine triphosphate (ATP) 30 microM was applied for 4-5 s in the absence or presence of thiopental 3-300 microM. Results Nicotine induced the rapidly decaying inward current at -60 mV, which exhibited the characteristics of the neuronal nAchR-mediated current. Thiopental inhibited the nicotine-induced inward current and accelerated the current decay in a dose-dependent manner, resulting in the greater effects on the steady current than the peak current. IC50s for the peak and steady current were 56.7 and 7.4 microM, when the anesthetic was coapplied with nicotine. Thiopental's inhibition was not associated with a change in the reversal potential and was voltage-independent at membrane potential of -30 to -70 mV. Most of thiopental's effects seemed to require channel opening. In contrast to the nicotine-induced current, thiopental had little effect on the current elicited by ATP. Conclusions Thiopental, whose reported EC50 for general anesthesia is 25 microM, inhibited the neuronal nAchR-mediated current but not the P2X receptor-mediated response in PC12 cells at clinically relevant concentrations. Inhibition may result in suppression of synaptic transmission in sympathetic ganglia.

Potentiation and inhibition of subtypes of neuronal nicotinic acetylcholine receptors by Pb2+

1995 ◽  
Vol 291 (3) ◽  
pp. 399-406 ◽  
Author(s):  
Ruud Zwart ◽  
Regina G.D.M. Van Kleef ◽  
Jacob M. Milikan ◽  
Marga Oortgiesen ◽  
Henk P.M. Vijverberg
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Nicotinic Acetylcholine
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