Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells

2001 ◽  
Vol 66 (4) ◽  
pp. 551-558 ◽  
Author(s):  
Zhi-Zhong Guan ◽  
Xiao Zhang ◽  
Malahat Mousavi ◽  
Jian-Ying Tian ◽  
Christina Unger ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Early Stages

Dynorphins directly inhibit neuronal nicotinic acetylcholine receptors in PC12 cells

2000 ◽  
Vol 12 (4) ◽  
pp. 1253-1262 ◽  
Author(s):  
Hideki Itoh ◽  
Tomio Andoh ◽  
Itaru Watanabe ◽  
Tosio Sasaki ◽  
Yoshinori Kamiya ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Nicotinic Acetylcholine

Inhibitory Effects of Isoflurane and Nonimmobilizing Halogenated Compounds on Neuronal Nicotinic Acetylcholine Receptors

2002 ◽  
Vol 97 (6) ◽  
pp. 1541-1549 ◽  
Author(s):  
Takayuki Matsuura ◽  
Yoshinori Kamiya ◽  
Hideki Itoh ◽  
Tomoko Higashi ◽  
Yoshitsugu Yamada ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Volatile Anesthetics ◽  
Dependent Manner ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Halogenated Compounds ◽  
Concentration Dependent Manner ◽  
Amnesic Effect ◽  
Nicotinic Acetylcholine

Background Neuronal nicotinic acetylcholine receptors (nAchRs) are inhibited by low concentrations of volatile anesthetics. However, it is not clear whether this phenomenon contributes to the anesthetic effects of volatile anesthetics. Effects of a volatile anesthetic (isoflurane) and structurally related nonimmobilizers (F6: 1,2-dichlorohexafluorocyclobutane, F8: 2,3-dichlorooctafluorobutane) on the current mediated through neuronal nAchRs were studied. Method This study investigated neuronal nAchRs in PC12 cells and acutely dissociated rat medial habenula (MHb) neurons. Whole cell currents elicited by 30 microm nicotine were recorded in the absence and presence of the halogenated agents. The minimum alveolar concentrations (MACs) for F6 and F8 were predicted from Meyer-Overton correlation. Results All halogenated compounds inhibited the nicotine-induced current in a concentration-dependent manner in PC12 cells. In MHb neurons, while isoflurane and F6 significantly inhibited the nicotine-induced peak current, F8 failed to inhibit it. The peak currents in the presence of isoflurane at 1.7 MAC, of F6 at 2.4 MAC, and of F8 at 2.2 MAC were 12, 31, and 97% of control, respectively. Conclusions Isoflurane, F6, and F8 inhibited ganglion-type nAchRs in PC12 cells independent from their abilities to produce the anesthetic state. In MHb neurons, isoflurane and F6, which lack the immobilizing effect but has the amnesic effect, inhibited nAchRs. Native brain nicotinic receptors in MHb neurons were almost insensitive to F8, which lacks both the immobilizing and the amnesic effect. These results are consistent with the hypothesis that inhibition of nAchRs in MHb neurons is not important for the anesthetic effect but may contribute to the amnesic effect of these agents.

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.

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