Translation of "Nozizeptoren" in English

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

Another criterion is the possession of drivers like nociceptors.

The Nozizeptoren own Nervenendigungen of the classes C and A-delta:

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

Nozizeptoren can react to different stimuli:

Another criterion is the possession of drivers like nociceptors.

Nerve receptors called nociceptors transmit signals to the spinal cord.

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.

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.

The first application of physiological liposomes (rinsing or spraying) often causes a short piercing pain which possibly points to a change in membrane potential of the nociceptors due to fusion with liposomes.

There is actually a group of specialized nerve cells in your body called nociceptors that react to pain.

And well some internal organs such as the liver feel no pain, others like the testicles are covered with many nociceptors making them extremely sensitive.

But not so fast gentlemen, even though childbirth may not be facing a direct blow to any internal organs, the mechanical distension of the uterine area also triggers nociceptors and causes the same kind of visceral pain.

Unlike other nerves which readily fire in response to normal touch or temperature, nociceptors will only fire once a certain pain threshold has been passed.

Some of these nociceptors respond quickly sending signals to the spinal cord and brain which produce sharp and sudden pain, allowing you to react quickly while others transmit more slowly and are responsible for the prolonged dull ache you feel.