Impairment of accessory nerves around major pelvic ganglion leading to overflow urinary incontinence in rats

2021 ◽  
Vol 40 (2) ◽  
pp. 624-631
Author(s):  
Kotomi Maeda ◽  
Yuji Hotta ◽  
Maaya Shibayama ◽  
Ryoya Kawata ◽  
Tomoya Kataoka ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Pelvic Ganglion ◽  
Major Pelvic Ganglion

1019: Visualization of the Neurovascular Bundles and Major Pelvic Ganglion with Fluorescent Proteins after Penile Injection

2006 ◽  
Vol 175 (4S) ◽  
pp. 328-328 ◽  
Author(s):  
Hugo H. Davila ◽  
Maggie Mamcarz ◽  
Irving Nadelhaft ◽  
Raoul Salup ◽  
Jorge Lockhart ◽  
...  
Keyword(s):  
Fluorescent Proteins ◽  
Pelvic Ganglion ◽  
Major Pelvic Ganglion ◽  
Neurovascular Bundles

Modulation of release of [3H]acetylcholine in the major pelvic ganglion of the rat

1993 ◽  
Vol 264 (6) ◽  
pp. R1084-R1088
Author(s):  
G. T. Somogyi ◽  
W. C. de Groat
Keyword(s):  
Inhibitory Effect ◽  
Facilitatory Effect ◽  
K Channel ◽  
Muscarinic Agonist ◽  
Ach Release ◽  
Pelvic Ganglion ◽  
M1 Receptor ◽  
Major Pelvic Ganglion ◽  
Electrophysiological Findings ◽  
Frequency Of Stimulation

Cholinergic modulation of [3H]acetylcholine release evoked by electrical stimulation was studied in the rat major pelvic ganglion, which was prelabeled with [3H]choline. Acetylcholine (ACh) release was independent of the frequency of stimulation; 0.3 Hz produced the same volley output as 10 Hz. Tetrodotoxin (1 microM) or omission of Ca2+ from the medium abolished ACh release. The M1 receptor agonist (4-hydroxy-2-butynyl)-1-trimethylammonium m-chlorocarbanilate chloride (McN-A 343, 50 microM) increased release (by 136%), whereas the M2 muscarinic agonist oxotremorine (1 microM) decreased ACh release (by 22%). The muscarinic antagonists, atropine (1 microM) or pirenzepine (M1 selective, 1 microM), did not change ACh release. However, pirenzepine (1 microM) blocked the facilitatory effect of McN-A 343, and atropine (1 microM) blocked the inhibitory effect of oxotremorine. The cholinesterase inhibitor physostigmine (1-5 microM), the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP, 10 microM), and the nicotinic antagonist D-tubocurarine (50 microM) did not change ACh release. 4-Aminopyridine, a K+ channel blocker, significantly increased the release (by 146%). Seven days after decentralization of the major pelvic ganglion, the evoked release of ACh was abolished. It is concluded that release of ACh occurs from the preganglionic nerve terminals rather than from the cholinergic cell bodies and is not modulated by actions of endogenous ACh on either muscarinic or nicotinic autoreceptors. These data confirm and extend previous electrophysiological findings indicating that synapses in the major pelvic ganglion have primarily a relay function.

Differential susceptibility to ageing of rat preganglionic neurones projecting to the major pelvic ganglion and of their afferent inputs

2002 ◽  
Vol 96 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Robert M Santer ◽  
Monica A Dering ◽  
Richard N Ranson ◽  
Henrietta N Waboso ◽  
Alan H.D Watson
Keyword(s):  
Differential Susceptibility ◽  
Pelvic Ganglion ◽  
Major Pelvic Ganglion ◽  
Afferent Inputs

Integrative properties of the major pelvic ganglion in the rat

1998 ◽  
Vol 69 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Bernadette Félix ◽  
Daniel Catalin ◽  
Jean-Pierre Miolan ◽  
Jean-Pierre Niel
Keyword(s):  
Pelvic Ganglion ◽  
Major Pelvic Ganglion
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