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At least 109 records · Page 6Linked to original sources
PubMed2003

Serotonergic modulation of bladder afferent pathways.

Normal bladder function is based on activation and maintenance of a sophisticated reflex mechanism involving sympathetic, parasympathetic, and somatic control of the lower urinary tract. The spinal and supraspinal neuronal pathways involved can be modulated by activation or inhibition of neurons in the periphery, at the lumbosacral and thoracolumbar spinal levels, and at supraspinal regulatory sites. Activation of the primary afferent neurons that innervate the lower urinary tract is the first step on this reflex pathway. Under conditions in which bladder function is compromised, abnormal activity in these afferent neurons can induce changes in these circuits, resulting in bladder dysfunction. Control and modulation of afferent pathways is a recent focus for the development of novel treatments for lower urinary tract disorders. This review focuses on the central regulation of bladder function by central serotonergic modulation of sensory pathways. Modulation of this monoaminergic system has dramatic effects on bladder activity and can be a target for pharmacologic treatment of bladder disorders.

Adrenergic Uptake Inhibitors↗
PubMed2000

Activation of intrinsic afferent pathways in submucosal ganglia of the guinea pig small intestine.

The enteric nervous system contains intrinsic primary afferent neurons that allow mucosal stimulation to initiate reflexes without CNS input. We tested the hypothesis that submucosal primary afferent neurons are activated by 5-hydroxytryptamine (5-HT) released from the stimulated mucosa. Fast and/or slow EPSPs were recorded in submucosal neurons after the delivery of exogenous 5-HT, WAY100325 (a 5-HT(1P) agonist), mechanical, or electrical stimuli to the mucosa of myenteric plexus-free preparations (+/- extrinsic denervation). These events were responses of second-order cells to transmitters released by excited primary afferent neurons. After all stimuli, fast and slow EPSPs were abolished by a 5-HT(1P) antagonist, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide, and by 1.0 microM tropisetron, but not by 5-HT(4)-selective antagonists (SB204070 and GR113808A) or 5-HT(3)-selective antagonists (ondansetron and 0.3 microM tropisetron). Fast EPSPs in second-order neurons were blocked by hexamethonium, and most slow EPSPs were blocked by an antagonist of human calcitonin gene-related peptide (hCGRP(8-37)). hCGRP(8-37) also inhibited the spread of excitation in the submucosal plexus, assessed by measuring the uptake of FM2-10 and induction of c-fos. In summary, data are consistent with the hypothesis that 5-HT from enterochromaffin cells in response to mucosal stimuli initiates reflexes by stimulating 5-HT(1P) receptors on submucosal primary afferent neurons. Second-order neurons respond to these cholinergic/CGRP-containing cells with nicotinic fast EPSPs and/or CGRP-mediated slow EPSPs. Slow EPSPs are necessary for excitation to spread within the submucosal plexus. Because some second-order neurons contain also CGRP, primary afferent neurons may be multifunctional and also serve as interneurons.

Afferent Pathways↗
PubMed1999

Bladder afferent pathway and spinal cord injury: possible mechanisms inducing hyperreflexia of the urinary bladder.

Lower urinary tract dysfunction is a common problem in patients with spinal cord injury (SCI). Since the coordination of the urinary bladder and urethra is controlled by the complex mechanisms in spinal and supraspinal neural pathways, SCI rostral to the lumbosacral level disrupts voluntary and supraspinal control of voiding and induces a considerable reorganization of the micturition reflex pathway. Following SCI, the urinary bladder is initially areflexic. but then becomes hyperreflexic because of the emergence of a spinal micturition reflex pathway. Recent electrophysiologic and histologic studies in rats have revealed that chronic SCI induces various phenotypic changes in bladder afferent neurons such as: (1) somal hypertrophy along with increased expression of neurofilament protein; and (2) increased excitability due to the plasticity of Na+ and K+ ion channels. These results have now provided detailed information to support the previous notion that capsaicin-sensitive, unmyelinated C-fiber afferents innervating the urinary bladder change their properties after SCI and are responsible for inducing bladder hyperreflexia in both humans and animals. It is also suggested that the changes in bladder reflex pathways following SCI are influenced by neural-target organ interactions probably mediated by neurotrophic signals originating in the hypertrophied bladder. Thus, increased knowledge of the plasticity in bladder afferent pathways may help to explain the pathogenesis of lower urinary tract dysfunctions after SCI and may provide valuable insights into new therapeutic strategies for urinary symptoms in spinal cord-injured patients.

Afferent Pathways↗
PubMed1993

Dual afferent pathways of vasodilator reflex induced by lingual stimulation in the cat.

We investigated whether two groups of afferent fibers in the combined chorda tympani (CT) and lingual (LN) nerve that emanate from the facial and trigeminal nerves function in the vasodilator reflex in the cat lip. Experiments were conducted on 18 cats weighing 1-3 kg which were anesthetized with pentobarbital sodium (30 mg/kg, i.v.) and artificially ventilated (pancuronium bromide 0.2 mg/kg/h, i.v.). Blood flow changes in the lower lip adjacent to the canine tooth on both sides of the mouth were monitored with a laser Doppler flowmeter. Electrical (0-50 V, 2 ms, 40 Hz, 10 s) and capsaicin (1%) stimulation of the tongue or chorda-lingual nerve after cutting the chorda tympani evoked an increase in blood flow in the ipsilateral lower lip (LN-response). Electrical stimulation of the central cut ends of the chorda tympani nerve also caused an increase in blood flow in the ipsilateral lip (CT-response). Capsaicin application to the CT, however, did not elicit a blood flow increase. Both the LN- and CT-responses of the different afferent fibers were reduced by prior treatment with the autonomic ganglion blocking agent hexamethonium (1 mg/kg, i.v.). Results suggest that capsaicin-insensitive fibers in the chorda tympani branch of the facial nerve, as well as capsaicin-sensitive ones in the lingual branch of the trigeminal nerve, participate as afferents of the parasympathetic vasodilator reflex in cat lip.

Afferent Pathways↗
PubMed1993

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

To establish the mechanism(s) and site(s) of action of cholecystokinin (CCK) on pancreatic secretion under physiological conditions, we used an in vivo model using anesthetized rats with pancreaticobiliary cannulas. Infusion of CCK-8 (10-160 pmol/kg per h) produced a dose-dependent increase in plasma CCK levels. CCK-8 infusion at 40 pmol/kg per h produced a plasma CCK level of 7.9 +/- 1.5 pM and an 80% increase in pancreatic protein output over basal. This level was closely approximated by a postprandial peak plasma CCK level by 6.2 +/- 1.1 pM. Pretreatment with atropine or hexamethonium completely abolished pancreatic protein response to low doses of CCK-8 (10-40 pmol/kg per h) but had only partial effect on doses > 40 pmol/kg per h. Bilateral vagotomy also abolished the pancreatic responses to low doses of CCK-8. Similarly perivagal treatment with a sensory neurotoxin, capsaicin, caused a complete inhibition of pancreatic protein secretion in response to CCK-8 infusion. In contrast, pancreatic protein responses to bethanechol were similar in control and capsaicin-treated rats. In separate studies we demonstrated that gastroduodenal but not jejunal application of capsaicin for 30 min abolished pancreatic protein secretion in response to physiological doses of CCK-8. In conclusion, CCK at physiological levels stimulates pancreatic enzyme secretion via a capsaicin-sensitive afferent vagal pathway originating from the gastroduodenal mucosa.

Afferent Pathways↗
PubMed2000

Evidence for VIP(1)/PACAP receptors in the afferent pathway mediating surgery-induced fundic relaxation in the rat.

We previously reported activation of an inhibitory adrenergic and a non-adrenergic non-cholinergic (NANC) pathway during abdominal surgery relaxing the rat gastric fundus. In the present study, we investigated the possible role of nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) in the NANC part of the surgery-induced fundic relaxation. The effect of the NO biosynthesis inhibitor N(G)-nitro-L-arginine (L-NOARG), the non-selective VIP receptor antagonist [D-p-Cl-Phe(6),Leu(17)]-VIP and the selective VIP(1) receptor antagonist [Acetyl-His(1),D-Phe(2),Lys(15),Arg(16), Leu(17)]-VIP was investigated on the non-adrenergic fundic relaxation induced by manipulation of the small intestine followed by resection of the caecum. Guanethidine partly reduced the manipulation-induced fundic relaxation. Addition of L-NOARG reduced this non-adrenergic component, whereas the non-selective VIP receptor antagonist had no significant effect. Combination of L-NOARG and the non-selective VIP antagonist however further reduced the relaxation to manipulation. The selective VIP(1) receptor antagonist reduced the mean and maximal relaxation induced by abdominal surgery in the presence of guanethidine. When combined with L-NOARG, the relaxation of the gastric fundus was almost completely abolished. The VIP(1) receptor antagonist alone had no significant effect on the mean and maximal relaxation, but enhanced recovery of fundic tone. In conclusion, as VIP(1) receptors are not present in the rat gastric fundus, these results suggest that the NANC inhibitory pathway activated during abdominal surgery involves VIP(1) receptors, most likely in the afferent limb. The inhibitory neurotransmitters released at the level of the gastric fundus smooth muscle are NO and a substance different from VIP.

Abdomen↗