Sensory nerves

The unmyelinated axons in the cornea of the adult rat have been subject to electron-microscopic scrutiny after local capsaicin desensitization of the eye. This caused impairment of mitochondrial structure similar to 

Summary of Anatomical Observations after Various Methods of Capsaicin Administration 

intrathecal Axon terminal degeneration in dorsal horn 

topical Reduced vesicle content in corneal nerve 

Neonatal, s.c. Reduced type B neuron content in sensory ganglion 

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Allergic Seasonal or Perennial Rhinoconjunctivitis. Histamine can cause all pathologic features of allergic rhinitis (35—37), with the exception of late-phase inflammatory reactions. Pmritus is caused by stimulation of receptors on sensory nerve endings prostaglandins (qv) may also contribute. Sneering, like pmritus, is an H -mediated neural reflex and can also be mediated by eicosanoids. Mucosal edema, which manifests as nasal... 

As a neurotransmitter in the sensory nervous system, high levels of substance P are found in the dorsal horn of the spinal cord as well as in peripheral sensory nerve terminals. However, substance P also plays a significant role as a neuromodulator in the central, sympathetic, and enteric nervous system. NKA and NKB are also localized selectively in the CNS. 

C22H23NNa202, (17), both inhibit the effect of sensory nerve activation, thereby interfering with bronchoconstriction (101). 

P-Homochelidonine was examined by Meyer and von Engel, and the results, as quoted by Sehmidt, indicate that in frogs -homoehelidonine behaves like ehelidonine, and that in mammals it eauses slight nareosis and a transitory fall in blood pressme, followed by eonvulsions of the type indueed by camphor, slowing of the pulse and, in large doses, paralysis of the vaso-motor centres. It also paralyses the ends of the sensory nerves. ... 

Teudt considers that the nasal sensory nerves have electron vibrations which are increased by resonance when odoriferous substances having corresponding intramolecular electron vibrations are inspired with air, and he concludes that a chemical element can the more readily induce odour in... 

Airway hyperresponsiveness is an exaggerated airway narrowing in response to a variety of unspecific stimuli. It can be measured by bronchial provocation with histamine, methacholine or adenosine. The reason for hyperresponsiveness may be stimulation of sensory nerves that are located within the epithelium. They become easily accessible after denudation of the... 

Both disodium cromoglycate and nedocromil sodium have antitussive effects in humans. In this instance, their activity occurs by increasing the depolarisation of sensory nerves, which increases the threshold for an action potential and therefore inhibits the activity of these neurons. 

The neurokinin, substance P (SP), may be involved as a sensory transmitter in afferent vagal nerves involved in the vomiting reflex. Both SP and its receptors (NKi receptors) have been detected in several areas of the brain associated with vomiting, including the AP, NTS and dorsal motor vagal nucleus. The neurokinin can activate neurons in the AP and NTS. SP is present also in sensory nerves in the gut as well as being co-localised with serotonin in some enterochromaffin cells. 

The surrounding redness caused by the vasodilatation of local blood vessels in the skin (hyperaemia). Histamine released at the site of contact acts on sensory nerve endings in the skin. Impluses travel along the axon to other peripheral branches of the same neuron to cause release of vasodilataory peptide neurotransmitters from nerve endings serving a wider area of skin than the initial contact point. Impluses reaching the CNS are interpreted as itch and pain. 

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. 

Sensory nerves are peripheral nerves involved in the detection of exogenous and endogenous stimuli for transmission into the CNS. They can be subdivided into RARs and C-fibres according to their channel characteristics. 

Topical anesthetics temporarily inhibit the conduction of impulses from sensory nerve fibers. These drug s may be used to relieve itching and pain due to skin conditions, such as minor bums, fungus infections, insect bites, rashes, sunburn, and plant poisoning, such as poison ivy. Some are applied to mucous membranes as local anesthetics. Examples of local anesthetics include benzocaine (Lanacane), dibucadne (Nupereainal), and lidocaine (Xylocadne). 

Laine P. Naukkarinen A. Heikkila L, Pentilla A. Kovanen PT Adventitial mast cells cormect with sensory nerve fibers in atherosclerotic coronary arteries. Circulation 2000 101 1665. 

Fig. 1.—Diagrammatic Representation of the Three Steps in the Taste-cell Transduction. Step 1, interaction of stimulus (S) with membrane-bound receptor (R) to form stimulus-receptor complex (SR) step 2, conformational change (SR) to (SR), brought about by interaction of S with R (this change initiates a change in plasma-membrane conformation of taste cells, probably below the level of the tight junction) and step 3, conformational changes of the membrane result in lowered membrane resistance, and the consequential influx on intracellular ionic species, probably Na. This influx generates the receptor potential which induces synaptic vesicular release to the innervating, sensory nerve, leading to the generator potential.

TRPVl also plays a central role in intercellular pro-inflammatory feedback loops. An important example is mast cells and sensory nerves. Mast cells release tryptase that, in turn, activates the protease-activated receptor PAR-2 activation of PAR-2 then opens TRPVl via PKC [50]. In keeping with this, PAR-2 agonists reduce the heat activation threshold of TRPVl from 42 °C to below body temperature [51]. Excited nerve endings release SP that, as a positive feedback, binds to neurokinin NKl receptors on mast cells. Mast cells also express TRPVl [52]. Consequently, endovanilloids can act in concert to stimulate mast cells and activate capsaicin-sensitive nerve endings. Of relevance is the finding that PAR-2 is up-regulated in the bladder during experimental cystitis [53]. 

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