nociceptive impulse

nociceptive impulse

(nō″sĭ-sĕp′tĭv)
Impulse giving rise to sensations of pain.
References in periodicals archive ?
According to the gate control theory, interneurons in the dorsal horn release gamma-aminobutyric acid (GABA) and glycine, which mediate inhibitory postsynaptic potential to reduce nociceptive impulse [1, 2].
Dexamethasone, a steroid with anti-inflammatory properties block the nociceptive impulse transmission along the unmyelinated C fibres (11) and suppressing ectopic neuronal discharge.
NO might also promote the release of serotonin, an important neurotransmitter involved in the inhibition of nociceptive impulses in the dorsal horn of the spinal cord (37).
It likely stems from a prolonged, intense, and persistent generation of afferent nociceptive impulses. When this occurs, CNS pathways are well established and sensations of pain can remain even after careful surgery to remove sources of inflammation and anatomic deformity (visceral scarring).
So the early phase of the formalin test represents the transmission of nociceptive impulses, while late phase is associated with the development of a delayed inflammatory response.
Thus, if nociceptive input from C-and A-delta fibres exceeds A-beta fibre input, then the gate is open and nociceptive impulses ascend to the spinal cord.
Modulation, which takes place primarily in the dorsal horn, is the stage in which nociceptive impulses are amplified or inhibited.
* Transduction: This is the phase at which afferent nerve endings translate the energy from noxious stimuli into nociceptive impulses.
* Transmission: During this stage, the nociceptive impulses are conveyed from the peripheral site of injury to the dorsal horn of the spinal cord and from there to the brain.
* Modulation: This is the process by which the nociceptive impulses are either inhibited or amplified, with input from both the ascending and descending pathways.
In humans, the mechanism of the latter was suggested to be the result of alpha-2 adrenoreceptor proliferation at the site of nerve damage and reduced transmission of nociceptive impulses and prevention or lessening of spinal cord sensitization when these receptors are activated.