The most widely accepted hypothesis of migraine suggests that a migraine attack is precipitated when pain-sensing nerve cells in the brain (called nociceptors) release chemicals called neuropeptides. ❋ Unknown (2008)
The sensation starts in cells called nociceptors, which respond to injury by sending electrical messages to an area in the spinal cord called the dorsal horn. ❋ Unknown (2007)
Sensory nerves, called nociceptors i.e. danger receptors detect elements capable of body-tissue damage, such as pressure or extreme heat. ❋ MARK FENSKE (2011)
Researchers from the California Institute of Technology (Caltech) and the University of California, San Francisco (UCSF) have found that this sensory discrimination begins in the skin at the very earliest stages of neuronal information processing, with different populations of sensory neurons-called nociceptors-responding to different kinds of painful stimuli. ❋ Unknown (2009)
These receptors are called "nociceptors" and are free nerve endings connected to small diameter myelinated A and unmyelinated C nerve fibers - these are the nerve fibers that are LACKING in people with congenital insensitivity to pain (here is more information about nerve fibers). ❋ Mayasark (2009)
It is also possible to identify the object of perception in pain with the activation of nociceptors innervating the damaged or irritated tissue. ❋ Aydede, Murat (2009)
At least one of the neurotransmitters, substance P, increases the pain sensitivity of other nearby nociceptors. ❋ Unknown (2008)
Constant strain can also activate nociceptors -- cells in the junctures between tendons, muscles and bones that become chemically sensitized and make even normal activity uncomfortable. ❋ Unknown (2008)
The skin, muscles, bones and other tissues have nerve cells, with endings that are called nociceptors. ❋ Unknown (2008)
Calming Lotion contains the breakthrough COSMEDERM-7™, a strontium compound proven to block irritation-producing nerve endings type C nociceptors that cause itching, burning, and stinging. ❋ Kat James (2007)
It works in the periphery, on nociceptors themselves, in the spinal cord at the first synapse on the way to the brain, in the brainstem where it probably has its biggest action and in subcortical and likely even cortical areas. ❋ Unknown (2005)
Quite a bit of work has been done on when nociceptors develop their formal synapses in the dorsal horn and this might actually come along later than thalamo-cortical connections making that whole point mute. ❋ Unknown (2005)
Although they do that indirectly, all nociceptors synapse first in the dorsal horn and then the second order neurons cross and go to the thalamus different from low threshold mechano-sensitive neurons which go on up to the gracile or cuneate nuclei, but still not directly to the thalamus. ❋ Unknown (2005)
Just as the larynx, the ear, the nose, the sole of the foot, and the skin have all developed the specific type of nociceptors which are adapted for their specific protective purposes, and which, when adequately stimulated, respond in a specific manner in accordance with the law of phylogenetic association, so, the abdominal viscera have developed equally specific nociceptors as a protection against specific nocuous influences. ❋ Unknown (1915)
Under such conditions the nervous system is protected against noci-association, resulting from noci-perception or from an adequate stimulation of nociceptors. ❋ Unknown (1915)
In the abdominal viscera, as in the superficial parts, nociceptors have presumably been developed by specific harmful influences and each nociceptor is open to stimulation only by a stimulus of the particular type that produced it. ❋ Unknown (1915)
This law explains why there are no nociceptors for cancer, while there are active nociceptors for the acute infections. ❋ Unknown (1915)
The receptors for pain have been designated nociceptors (nocuous or harmful) by Sherrington. ❋ Unknown (1915)
The most numerous receptors are those for harmful contact; these are the nociceptors. ❋ Unknown (1915)
