Cough Sensors. III. Opioid and Cannabinoid Receptors on Vagal Sensory Nerves

2009 ◽  
pp. 63-76 ◽  
Author(s):  
M. G. Belvisi ◽  
D. J. Hele
Keyword(s):  
Cannabinoid Receptors ◽  
Sensory Nerves ◽  
Vagal Sensory Nerves

scholarly journals Endocannabinoids in Bladder Sensory Mechanisms in Health and Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Stewart Christie ◽  
Simon Brookes ◽  
Vladimir Zagorodnyuk
Keyword(s):  
Overactive Bladder ◽  
Sensory Neurons ◽  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Endocannabinoid System ◽  
Sensory Nerves ◽  
Sensory Innervation ◽  
Bladder Function ◽  
Painful Bladder ◽  
Bladder Diseases

The recent surge in research on cannabinoids may have been fueled by changes in legislation in several jurisdictions, and by approval for the use of cannabinoids for treatment of some chronic diseases. Endocannabinoids act largely, but not exclusively on cannabinoid receptors 1 and 2 (CBR1 and CBR2) which are expressed in the bladder mainly by the urothelium and the axons and endings of motor and sensory neurons. A growing body of evidence suggests that endocannabinoid system constitutively downregulates sensory bladder function during urine storage and micturition, under normal physiological conditions. Similarly, exogenous cannabinoid agonists have potent modulatory effects, as do inhibitors of endocannabinoid inactivation. Results suggest a high potential of cannabinoids to therapeutically ameliorate lower urinary tract symptoms in overactive bladder and painful bladder syndromes. At least part of this may be mediated via effects on sensory nerves, although actions on efferent nerves complicate interpretation. The sensory innervation of bladder is complex with at least eight classes identified. There is a large gap in our knowledge of the effects of endocannabinoids and synthetic agonists on different classes of bladder sensory neurons. Future studies are needed to reveal the action of selective cannabinoid receptor 2 agonists and/or peripherally restricted synthetic cannabinoid receptor 1 agonists on bladder sensory neurons in animal models of bladder diseases. There is significant potential for these novel therapeutics which are devoid of central nervous system psychotropic actions, and which may avoid many of the side effects of current treatments for overactive bladder and painful bladder syndromes.

Roles of right versus left vagal sensory nerves in cardiopulmonary reflexes of conscious dogs

1985 ◽  
Vol 249 (3) ◽  
pp. R301-R307 ◽  
Author(s):  
K. W. Barron ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Sensory Nerves ◽  
Inhibitory Influence ◽  
Relative Pressure ◽  
Intracoronary Administration ◽  
The Right ◽  
Vagal Sensory Nerves ◽  
Change In Mean

This study examined the relative roles of the right vs. left vagi in mediating the inhibitory influence of vagal sensory input on sympathetic outflow to the cardiovascular system. This objective was pursued through examination of responses to 1) interruption of tonic vagal input and 2) intracoronary administration of veratridine (Bezold-Jarisch effect). Bilateral vagal cold block (BVB) (n = 16) increased arterial pressure 25 +/- 3 mmHg and heart rate 66 +/- 7 beat/min, whereas right vagal cold block (RVB) and left vagal cold block (LVB) increased arterial pressure 13 +/- 2 and 4 +/- 2 mmHg, respectively. The relative differences in the change in mean arterial pressure were independent of heart rate since similar changes in arterial pressure were observed with preelevation of heart rate with atropine. Sinoaortic baroreceptor denervation augmented the pressure responses approximately fourfold, with the relative pressure changes produced by BVB, RVB, or LVB remaining proportionally the same. Intracoronary administration of veratridine (0.1 g/kg) produced a hypotension action (-44 +/- 6 mmHg), bradycardia (-48 +/- 8 beat/min), and a negative intropic effect (-482 +/- 68 mmHg/s, left ventricular (LV) (dP/dt)max. During RVB the depressor effect of veratridine was reduced to -18 +/- 5 mmHg, and changes in heart rate or LV (dP/dt)max were abolished. Veratridine administration during LVB decreased arterial pressure (-39 +/- 6 mmHg), heart rate (-22 +/- 6 beat/min), and LV (dP/dt)max (-250 +/- 60 mmHg). We conclude that in the conscious dog the tonic inhibitory influence of vagal afferent nerves on vasomotor outflow is predominantly associated with the right vagus as in Bezold-Jarisch effect.

Abdominal vagal mediation of the satiety effects of CCK in rats

2004 ◽  
Vol 286 (6) ◽  
pp. R1005-R1012 ◽  
Author(s):  
Roger D. Reidelberger ◽  
Jessica Hernandez ◽  
Bernd Fritzsch ◽  
Martin Hulce
Keyword(s):  
Food Intake ◽  
Blood Brain Barrier ◽  
Sensory Nerves ◽  
Brain Barrier ◽  
Cck1 Receptor ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Vagal Nerves ◽  
Inhibit Food Intake ◽  
Vagal Sensory Nerves

CCK type 1 (CCK1) receptor antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCK1 receptors on vagal sensory nerves innervating the small intestine. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Nα-3-quinolinoyl-d-Glu- N,N-dipentylamide, does not. At dark onset, non-food-deprived control rats and rats with subdiaphragmatic vagotomies received a bolus injection of devazepide (2.5 μmol/kg iv) or a 3-h infusion of A-70104 (3 μmol·kg−1·h−1 iv) either alone or coadministered with a 2-h intragastric infusion of peptone (0.75 or 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. In control rats both antagonists stimulated food intake and attenuated the anorexic response to intragastric infusion of peptone. In contrast, only devazepide was effective in stimulating food intake in vagotomized rats. Thus endogenous CCK appears to act both at CCK1 receptors beyond the blood-brain barrier and by a CCK1 receptor-mediated mechanism involving abdominal vagal nerves to inhibit food intake.

scholarly journals Store-operated calcium entry in vagal sensory nerves is independent of Orai channels

2013 ◽  
Vol 1503 ◽  
pp. 7-15 ◽  
Author(s):  
Justin Shane Hooper ◽  
Stephen H. Hadley ◽  
Adithya Mathews ◽  
Thomas E. Taylor-Clark
Keyword(s):  
Calcium Entry ◽  
Sensory Nerves ◽  
Store Operated Calcium Entry ◽  
Vagal Sensory Nerves ◽  
Orai Channels

Cannabinoid receptors undergo axonal flow in sensory nerves

Neuroscience ◽  
1999 ◽  
Vol 92 (4) ◽  
pp. 1171-1175 ◽  
Author(s):  
A.G Hohmann ◽  
M Herkenham
Keyword(s):  
Cannabinoid Receptors ◽  
Sensory Nerves ◽  
Axonal Flow

Galanin in porcine vagal sensory nerves: Immunohistochemical and immunochemical study

Peptides ◽  
1990 ◽  
Vol 11 (5) ◽  
pp. 989-993 ◽  
Author(s):  
C. Philippe ◽  
J.C. Cuber ◽  
A. Bosshard ◽  
O. Rampin ◽  
J.P. Laplace ◽  
...  
Keyword(s):  
Sensory Nerves ◽  
Immunochemical Study ◽  
Vagal Sensory Nerves

Membrane-associated microtubular areays induced in proximal myelinated processes of dorsal root ganglia by large doses of vitamin B6

1986 ◽  
Vol 44 ◽  
pp. 368-369
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin
Keyword(s):  
Animal Model ◽  
Endoplasmic Reticulum ◽  
Dorsal Root Ganglia ◽  
Rough Endoplasmic Reticulum ◽  
Dorsal Root ◽  
Vitamin B6 ◽  
Morphological Changes ◽  
Model System ◽  
Sensory Nerves ◽  
Peripheral Sensory

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

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