M1 muscarinic receptor‐mediated facilitation of acetylcholine release in the rat urinary bladder.

Somogyi, George T.; Tanowitz, Michael; Groat, William C. de

doi:10.1113/jphysiol.1994.sp020342

Cited by 91 publications

(88 citation statements)

References 29 publications

(41 reference statements)

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“…There is evidence for the presence of both facilitatory and inhibitory prejunctional muscarinic receptors of the M 1 subtype on both sympathetic and/or parasympathetic neurones supplying other genito-urinary organs (Eltze, 1988;Somogyi & de Groat, 1990;Somogyi et al, 1994;. In our study the putatively M 1 receptor-selective agonist McN-A-343 was without eect on neurotransmission to the guinea-pig prostate smooth muscle.…”

Section: Discussionmentioning

confidence: 65%

Cholinergic facilitation of neurotransmission to the smooth muscle of the guinea‐pig prostate gland

Lau

Pennefather

Mitchelson

2000

British J Pharmacology

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1 Functional experiments have been conducted to assess the eects of acetylcholine and carbachol, and the receptors on which they act to facilitate neurotransmission to the stromal smooth muscle of the prostate gland of the guinea-pig. 2 Acetylcholine and carbachol (0.1 mM ± 0.1 mM) enhanced contractions evoked by trains of electrical ®eld stimulation (20 pulses of 0.5 ms at 10 Hz every 50 s with a dial setting of 60 V) of nerve terminals within the guinea-pig isolated prostate. In these concentrations they had negligible eects on prostatic smooth muscle tone. The facilitatory eects of acetylcholine, but not those of carbachol, were further enhanced in the presence of physostigmine (10 mM). 3 The facilitatory eects of carbachol were unaected by the neuropeptide Y Y 1 receptor antagonist BIBP 3226 ((R)-N 2 -(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininamide) (0.3 mM, n=3) or suramin (100 mM, n=5). Prazosin (0.1 mM, n=5) and guanethidine (10 mM, n=5) alone and in combination (n=4), reduced responses to ®eld stimulation and produced rightward shifts of the log concentration-response curves to carbachol. 4 The rank orders of potency of subtype-preferring muscarinic receptor antagonists in inhibiting the facilitatory actions of acetylcholine and carbachol were: pirenzepine 4 HHSiD (hexahydrosiladifenidol) 4 pF-HHSiD (para-¯uoro-hexahydrosiladifenidol) 5 himbacine, and pirenzepine 4 HHSiD 4 himbacine 5 pF-HHSiD, respectively. These pro®les suggest that muscarinic receptors of the M 1 -subtype mediate the facilitatory eects of acetylcholine and carbachol on neurotransmission to the smooth muscle of the guinea-pig prostate.

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Section: Discussionmentioning

confidence: 65%

Cholinergic facilitation of neurotransmission to the smooth muscle of the guinea‐pig prostate gland

Lau

Pennefather

Mitchelson

2000

British J Pharmacology

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“…This effect which has been demonstrated in several species including rat, rabbit, and human is mediated by activation of prejunctional muscarinic receptors (108,(578)(579)(580).…”

Section: Modulation Of Efferent Neurotransmissionmentioning

confidence: 99%

“…ACh release in rat urinary bladder strips is influenced by various stimulation parameters including frequency, pattern, and number of stimuli (108,232,580,582,641,642). During intermittent field stimulation (IS), consisting of short trains (10 shocks) separated by 5 s quiescent periods, the duration of stimulation (5-360 shocks) had little effect on the total ACh output (nonfacilitatory stimulation).…”

Section: Modulation Of Efferent Neurotransmissionmentioning

confidence: 99%

“…The facilitation of ACh release is blocked by atropine or pirenzepine (an M1 selective antagonist) indicating that it is mediated by M1 muscarinic receptors. The lower range of CS (10 Hz, 100 shocks) which mimics the physiological firing rate of bladder parasympathetic neurons (155) and which produces maximal bladder contractions elicits a marked recruitment of ACh release (580).…”

Section: Modulation Of Efferent Neurotransmissionmentioning

confidence: 99%

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Neural Control of the Lower Urinary Tract

1997

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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“…Several subtypes of muscarinic receptors controlling release of acetylcholine have been demonstrated on cholinergic nerves in the detrusor muscle of several animal species (Somogyi & de Groat, 1992;Somogyi et al 1994;Alberts, 1995;D'Agostino et al 1997). M, inhibitory receptors dominated in untreated rat preparations, whereas in physostigminetreated bladder strips, where the concentrations of acetylcholine were elevated, facilitatory M, receptors were also demonstrated.…”

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confidence: 99%