Chapter 7 Functional properties of spinal visceral afferents supplying abdominal and pelvic organs, with special emphasis on visceral nociception

Jänig, Wilfrid; Morrison, J.

doi:10.1016/s0079-6123(08)62758-2

Cited by 324 publications

(150 citation statements)

References 134 publications

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“…Afferent axons in the pelvic, hypogastric, and pudendal nerves transmit information from the LUT to second-order neurons in the lumbosacral spinal cord (145,292,701). Pelvic nerve afferents that innervate the bladder and urethra originate in caudal lumbosacral dorsal root ganglia (DRG) and are divided into two populations: small myelinated (Aδ) and unmyelinated C-fibers.…”

Section: Afferent Innervationmentioning

confidence: 99%

“…2A) (37,195,548,677) or the sacral dorsal roots (252,292), of the cat respond to both passive distension as well as active contraction of the bladder indicating that they are in series tension receptors. These afferents which have conduction velocities ranging between 2.5 and 15 m/s (252) are silent when the bladder is empty but during slow filling of the bladder display a graded increase in discharge frequency at intravesical pressures below 25 mmHg (83,292). Multiunit recordings exhibit a successive recruitment of mechanoreceptors with different thresholds during bladder filling.…”

Section: Afferent Innervationmentioning

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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Section: Afferent Innervationmentioning

confidence: 99%

Section: Afferent Innervationmentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

1997

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“…These effects are thought to be mediated both by direct effects of circulating hormones on the hypothalamus and by actions on vagal afferent neurons that project to the nucleus tractus solitarius (NTS). In addition, vagal afferent neurons may respond directly to mechanical, chemical, or inflammatory stimuli, whereas spinal afferent neurons serving the gastrointestinal tract are involved primarily in transmission of noxious stimuli (Andrews, 1986;Janig and Morrison, 1986;Holzer, 1998). The brain-gut peptide CCK is released from enteroendocrine cells by fat and protein and in turn acts at CCK-1 receptors on vagal afferent neurons (Smith et al, 1981;Ritter and Ladenheim, 1985;Moran et al, 1990;Moriarty et al, 1997;McLaughlin et al, 1999;Reidelberger et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Burdyga¹,

Lal²,

Varró³

et al. 2004

J. Neurosci.

251

224

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Both inhibitory (satiety) and stimulatory (orexigenic) factors from the gastrointestinal tract regulate food intake. In the case of the satiety hormone cholecystokinin (CCK), these effects are mediated via vagal afferent neurons. We now report that vagal afferent neurons expressing the CCK-1 receptor also express cannabinoid CB1 receptors. Retrograde tracing established that these neurons project to the stomach and duodenum. The expression of CB1 receptors determined by RT-PCR, immunohistochemistry and in situ hybridization in rat nodose ganglia was increased by withdrawal of food for Ն12 hr. After refeeding of fasted rats there was a rapid loss of CB1 receptor expression identified by immunohistochemistry and in situ hybridization. These effects were blocked by administration of the CCK-1 receptor antagonist lorglumide and mimicked by administration of CCK to fasted rats. Because CCK is a satiety factor that acts via the vagus nerve and CB1 agonists stimulate food intake, the data suggest a new mechanism modulating the effect on food intake of satiety signals from the gastrointestinal tract.

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“…The major sensory nerves distributed to the bladder are the group C and group Aδfibers. The group Aδfibers respond to the passive dilatation and active contraction of the bladder, and are also sensitive to the distention of the bladder mucosa 20) while group C fibers mainly respond to the chemical stimulation of the mucosa and also to strong mechanical stimulation 14) .The nociceptive group C fibers in the viscera are also referred as the "silent nociceptors" because they are inactive under normal conditions, and show voluntary firing in inflammation the bladder, and increase their firing rate during the distention of the bladder.…”

Section: Discussionmentioning

confidence: 99%