Übersetzung für "Nociceptors" in Deutsch

Following capsaicin exposure, cutaneous nociceptors become less sensitive to a variety of stimuli.

Another criterion is the possession of drivers like nociceptors.

Most nociceptors react to the following harmful stimuli:

The density of nociceptors in humans is greater than that of all other skin receptors.

Nociceptors and afferent nerve fibres are in a permanent state of irritation.

Instead, what's really happening is that certain compounds in spicy foods activate the type of sensory neurons called polymodal nociceptors.

This means that it stimulates the TRPV1 receptor, which is found in the nociceptors (pain receptors) in the skin.

This would mean that such pains are produced by the nociceptors existing in the epidermis.

The expression of the receptor was detected on peripheral nerve endings of nociceptors, on macrophages and neutrophils.

The nociceptors are then more sensitive and the person is more likely to perceive pain, and to a greater extent.

It is clear that these thermal stimuli stimulate nociceptors which lead to a reflex-like retraction behaviour.

The initial effect of capsaicin is the activation of TRPV1-expressing cutaneous nociceptors, which results in pungency and erythema due to the release of vasoactive neuropeptides.

Capsaicin-induced alterations in cutaneous nociceptors are reversible and it has been reported and observed that normal function (the detection of noxious sensations) returns within weeks in healthy volunteers.

They are the result of secondary side effects of a nociceptive somatomotoric blocking effect having its origin in the pain sensors (nociceptors) of the affected articular capsules, tendom attachments, of the periosteum and other tissues.

Inflammatory tissue hormones and transmitters (histamine, serotonin, prostaglandins, interleukin-1) secreted by local inflamed cells in the vicinity of the nocisensor may result in sensitisation of the nociceptors with a reduced threshold of stimulus and increased spontaneous activity, wherein persistent inflammation with constant stimuli ultimately results in the development of adaptive processes at the spinal and supraspinal levels.

The physiological aspects of the aetiology of pain comprise reception of any physical/chemical stimulus of a potentially tissue-threatening intensity by activation of the so-called nociceptors, specific uni- or polymodal nocisensors of high-threshold primary ascending neural pathways.

The nociceptors which are primarily generating pain, the morphologically least differentiated receptors, are mainly of importance to the treatment with physiological liposomes of the invention.

The formation of prostaglandin E2 which sensibilizes the nociceptors for the algogenic substances is very important in this acute process.

At least part of the mediators which are released by virally caused tissue lesions or allergic reactions are algogenic substances which alarm the nociceptors of the corresponding tissue.

In contrast to the above-described therapeutical approaches to reduce pain, the model which is here presented starts from the assumption that the mediator release has an inhibiting effect and also that the membranes of the nociceptors are "stabilized" by fusion with physiological liposomes and/or that their resting potential is shifted towards "firing level".

Chemical noxae as well as temperature differences pass through the porous dentine in hardly attenuated form to the nociceptors, thereby producing pain.

With nociceptors, there might be an increase in the stimulus threshold or decrease in the action potential after fusion and/or an influencing of receptors (for instance of the opioid receptors) or, accordingly, of associated membrane proteins.