THE ACTION OF CATECHOLAMINES IN SYMPATHETIC GANGLIA

1963 ◽  
Vol 41 (1) ◽  
pp. 2627-2636 ◽  
Author(s):  
Mervyn C. L. Weir ◽  
H. McLennan
Keyword(s):  
Synaptic Transmission ◽  
Sympathetic Ganglion ◽  
Sympathetic Ganglia ◽  
Physiological Significance ◽  
Preganglionic Stimulation

Injection of the catecholamines, and particularly adrenaline, has been found always to depress synaptic transmission in a sympathetic ganglion. Although an adrenaline-like substance is released upon preganglionic stimulation, this is not believed to have any physiological significance.

THE ACTION OF CATECHOLAMINES IN SYMPATHETIC GANGLIA

1963 ◽  
Vol 41 (12) ◽  
pp. 2627-2636 ◽  
Author(s):  
Mervyn C. L. Weir ◽  
H. McLennan
Keyword(s):  
Synaptic Transmission ◽  
Sympathetic Ganglion ◽  
Sympathetic Ganglia ◽  
Physiological Significance ◽  
Preganglionic Stimulation

Injection of the catecholamines, and particularly adrenaline, has been found always to depress synaptic transmission in a sympathetic ganglion. Although an adrenaline-like substance is released upon preganglionic stimulation, this is not believed to have any physiological significance.

Reversible Effects of Hyperosmolar Sucrose on Frog Sympathetic Ganglion

1973 ◽  
Vol 31 ◽  
pp. 534-535
Author(s):  
E. Minker ◽  
W. K. Riker ◽  
N. J. Russell
Keyword(s):  
Synaptic Transmission ◽  
Sympathetic Ganglion ◽  
Neuromuscular Junctions ◽  
Extracellular Recording ◽  
Sympathetic Ganglia ◽  
Discharge Frequency ◽  
Ringer’S Solution ◽  
Synaptic Structure ◽  
Structural Recovery ◽  
Saline Solutions

Saline solutions made hyperosmotic by addition of sucrose increase the discharge frequency of miniature spontaneous junctional potentials at neuromuscular junctions and sympathetic ganglia and can alter structure in both muscle and nerve. Since effects of such solutions on synaptic structure are unknown, we have investigated the influence of hyperosmolarity on function and ultrastructure in synaptic regions of isolated abdominal sympathetic ganglia of the bullfrog, Rana catesbiana.Synaptic transmission was monitored by extracellular recording of postganglionic responses to supramaximal.preganglionic stimulation (0.3 Hz). Ganglia were first equilibrated in normal frog Ringer's solution, then transferred to test solutions, and some ganglia were subsequently returned to normal Ringer's to examine functional and structural recovery.

Actions of ketamine on synaptic transmission in frog sympathetic ganglia

1976 ◽  
Vol 15 (2) ◽  
pp. 139-143 ◽  
Author(s):  
J.P. Gallaghert ◽  
N. Dun ◽  
H. Higashi ◽  
S. Nishi
Keyword(s):  
Synaptic Transmission ◽  
Sympathetic Ganglia

Modulation of Nicotinic AChR Channels by Prostaglandin E2 in Chick Sympathetic Ganglion Neurons

1998 ◽  
Vol 79 (2) ◽  
pp. 870-878 ◽  
Author(s):  
Wen Tan ◽  
Chuang Du ◽  
Steven A. Siegelbaum ◽  
Lorna W. Role
Keyword(s):  
Sympathetic Ganglion ◽  
Sympathetic Ganglia ◽  
Prostaglandin E ◽  
Channel Function ◽  
Endogenous Production ◽  
Open Time ◽  
Channel Opening ◽  
Ganglion Neurons ◽  
Channel Currents ◽  
Whole Cell Recordings

Tan, Wen, Chuang Du, Steven A. Siegelbaum, and Lorna W. Role. Modulation of nicotinic AChR channels by prostaglandin E2 in chick sympathetic ganglion neurons. J. Neurophysiol. 79: 870–879, 1998. The effects of prostaglandin E2 (PGE2), an important metabolite of arachidonic acid, were studied on the activity of nicotinic AChR channels in cultured chick sympathetic ganglion neurons. In whole cell recordings, PGE2 (25 nM) inhibited significantly the ACh-evoked macroscopic current. In cell-attached patch recordings, PGE2 significantly inhibited single AChR channel currents as a result of a decrease in the frequency of channel opening, with no change in open time and conductance. PGE2 did not alter the extent or rate of agonist-induced desensitization of the AChR channels. These effects are specific since the related compound PGD2 had no effect on AChR channel function. Because there is an abundant endogenous production of PGE2 within sympathetic ganglia in response to certain stimuli, the inhibition of AChR channel function by PGE2 could serve an important role to modulate synaptic transmission in the sympathetic nervous system.

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