Voltage-dependent effect of tetraethylammonium on the nicotinic acetylcholine receptors of rat superior cervical ganglion neurons

1996 ◽  
Vol 27 (1) ◽  
pp. 50-53
Author(s):  
S. V. Voitenko
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Superior Cervical Ganglion ◽  
Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Dependent Effect ◽  
Voltage Dependent ◽  
Cervical Ganglion ◽  
Ganglion Neurons

scholarly journals α4β2 nicotinic acetylcholine receptors in the early postnatal mouse superior cervical ganglion

2011 ◽  
Vol 71 (5) ◽  
pp. 390-399 ◽  
Author(s):  
Petra Scholze ◽  
Anna Ciuraszkiewicz ◽  
Florian Groessl ◽  
Avi Orr-Urtreger ◽  
J. Michael McIntosh ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Superior Cervical Ganglion ◽  
Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Cervical Ganglion

Expression of nicotinic acetylcholine receptors in the rat superior cervical ganglion on mRNA and protein level

1994 ◽  
Vol 27 (1) ◽  
pp. 167-173 ◽  
Author(s):  
L. Klimaschewski ◽  
S. Reuss ◽  
R. Spessert ◽  
C. Lobron ◽  
A. Wevers ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Superior Cervical Ganglion ◽  
Protein Level ◽  
Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Cervical Ganglion

scholarly journals Activation of Nicotinic Acetylcholine Receptors Augments Calcium Channel-mediated Exocytosis in Rat Pheochromocytoma (PC12) Cells

1998 ◽  
Vol 111 (2) ◽  
pp. 257-269 ◽  
Author(s):  
Amy B. Harkins ◽  
Aaron P. Fox
Keyword(s):  
Pc12 Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Single Cells ◽  
Cellular Functions ◽  
Nicotinic Acetylcholine ◽  
Cellular Processes ◽  
Voltage Dependent ◽  
Vesicle Secretion ◽  
Ca2 Channels

The functional effect of activating Ca2+-permeable neuronal nicotinic acetylcholine receptors (nAChRs) on vesicle secretion was studied in PC12 cells. Single cells were patch-clamped in the whole-cell configuration and stimulated with either brief pulses of nicotine to activate the Ca2+-permeable nAChRs or with voltage steps to activate voltage-dependent Ca2+ channels. Membrane capacitance was used as a measure of vesicle secretion. Activation of nAChRs by nicotine application to cells voltage clamped at −80 mV evoked secretion. This secretion was completely abolished by nicotinic antagonists. When the cells were voltage clamped at +20 mV in the presence of Cd2+ to block voltage-activated Ca2+ channels, nicotine elicited a small amount of secretion. Most interestingly, when the nAChRs were activated coincidentally with voltage-dependent Ca2+ channels, secretion was augmented approximately twofold over the secretion elicited with voltage-dependent Ca2+ channels alone. Our data suggest that Ca2+ influx via nAChRs affects Ca2+-dependent cellular functions, including vesicle secretion. In addition to the secretion evoked by nAChR activation at hyperpolarized potentials, we demonstrate that even at depolarized potentials, nAChRs provide an important Ca2+ entry pathway underlying Ca2+-dependent cellular processes such as exocytosis.

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