Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system,[1] and, therefore, the ability of a body to sense potential harm. It is the afferent activity in the peripheral and central nervous systems produced by stimulation of specialized free nerve endings called nociceptors or "pain receptors" that only respond to tissue damage caused by intense chemical (e.g., chilli powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat and cold) stimulation.[2][3] Once stimulated, a nociceptor sends a signal along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of autonomic responses and may also result in a subjective experience of pain in sentient beings.[3] Nociceptive neurons generate trains of action potentials in response to intense stimuli, and the frequency of firing determines the intensity of the pain.[4]
The three types of pain receptors are cutaneous (skin), somatic (joints and bones), and visceral (body organs). It was previously believed that pain was simply the overloading of sensory receptors, but research in the first half of the 20th century indicated that pain is a distinct phenomenon that intertwines with all of the other senses, including touch. Pain was once considered a non-material experience, but recent studies show that pain is registered in specific parts of the brain. The main function of pain is to attract our attention to dangers and motivate us to avoid them.
Contents
- 1 Detection of noxious stimuli
- 2 Transmission through the central nervous system
- 2.1 Spinothalamic tract
- 2.1.1 Neospinothalamic tract
- 2.1.2 Paleospinothalamic tract
- 3 Regulation
- 3.1 Central
- 3.2 Peripheral
- 3.3 Factors
- 4 Nociception response
- 5 Nociception in non-mammalian animals
- 6 History of term
- 7 References
Detection of noxious stimuli
Potentially damaging mechanical, thermal, and chemical stimuli are detected by nerve endings called nociceptors, which are found in the skin, on internal surfaces such as the periosteum, joint surfaces, and in some internal organs. The concentration of nociceptors varies throughout the body; they are found in greater numbers in the skin than in deep internal surfaces. The nociceptors are unspecialized free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglia.[5] Nociceptors are categorized according to the axons which travel from the receptors to the spinal cord or brain.
Nociceptors have a certain threshold; that is, they require a minimum intensity of stimulation before they trigger a signal. Once this threshold is reached a signal is passed along the axon of the neuron into the spinal cord.
Nociceptive threshold testing deliberately applies a noxious stimulus to a human or animal subject in order to study pain. In animals, the technique is often used to study the efficacy of analgesic drugs and to establish dosing levels and period of effect. After establishing a baseline, the drug under test is given and the elevation in threshold recorded at specified time points. When the drug wears off, the threshold should return to the baseline (pre-treatment) value.
In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.
Transmission through the central nervous system
Spinothalamic tract
Before reaching the brain, the spinothalamic tract splits into the lateral, "neospinothalamic" tract and the medial, "paleospinothalamic" tract.[6]
Neospinothalamic tract
Fast pain travels via type Aδ fibers to terminate in the dorsal horn of the spinal cord where they synapse on dendrites of the neospinothalamic tract. The axons of these neurons cross the midline (decussate) through the anterior white commissure and ascend contralaterally along the anterolateral system. These fibres terminate on the ventrobasal complex of the thalamus and synapse with the dendrites of the somatosensory cortex. Fast pain is felt within a tenth of a second of application of the pain stimulus and is a sharp, acute, prickling pain felt in response to mechanical and thermal stimulation. It can be localised easily if Aδ fibres are stimulated together with tactile receptors.[citation needed]
Paleospinothalamic tract
Slow pain is transmitted via slower type C fibers to laminae II and III of the dorsal horns, together known as the substantia gelatinosa. Impulses are then transmitted to nerve fibers that terminate in lamina V, also in the dorsal horn, synapsing with neurons that join fibers from the fast pathway, crossing to the opposite side via the anterior white commissure, and traveling upwards through the anterolateral pathway. These neurons terminate throughout the brain stem, with one tenth of fibres stopping in the thalamus and the rest stopping in the medulla, pons and periaqueductal grey of the midbrain tectum.
Regulation
The body possesses an endogenous analgesia system, which can be supplemented with analgesic drugs to regulate nociception and pain. There is both an analgesia system in the central nervous system and peripheral receptors that decreases the grade in which nociception reaches the higher brain areas. The degree of pain can be modified by the periaqueductal gray before it reaches the thalamus and consciousness. According to gate control theory of pain, this area can also reduce pain when non-painful stimuli are received in conjunction with nociception.
Central
The central analgesia system is mediated by three major components: the periaqueductal grey matter, the nucleus raphes magnus and the nociception inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit nociception-transmitting neurons also located in the spinal dorsal horn.
Peripheral
The peripheral regulation consists of several different types of opioid receptors that are activated in response to the binding of the body's endorphins. These receptors, which exist in a variety of areas in the body, inhibit firing of neurons that would otherwise be stimulated to do so by nociceptors.
Factors
Main article: Pain § Theory
The gate control theory of pain, proposed by Patrick David Wall and Ronald Melzack, postulates that nociception (pain) is "gated" by non-nociception stimuli such as vibration. Thus, rubbing a bumped knee seems to relieve pain by preventing its transmission to the brain. Pain is also "gated" by signals that descend from the brain to the spinal cord to suppress (and in other cases enhance) incoming nociception (pain) information.
Nociception response
When nociceptors are stimulated they transmit signals through sensory neurons in the spinal cord. These neurons release the excitatory neurotransmitter glutamate at their synapses.
If the signals are sent to the reticular formation and thalamus, the sensation of pain enters consciousness in a dull poorly localized manner. From the thalamus, the signal can travel to the somatosensory cortex in the cerebrum, when the pain is experienced as localized and having more specific qualities.
Nociception can also cause generalized autonomic responses before or without reaching consciousness to cause pallor, diaphoresis, tachycardia, hypertension, lightheadedness, nausea and fainting.[7]
Nociception in non-mammalian animals
Nociception has been documented in non-mammalian animals, including fish[8] and a wide range of invertebrates,[9] including leeches,[10] nematode worms,[11] sea slugs,[12] and fruit flies.[13] As in mammals, nociceptive neurons in these species are typically characterized by responding preferentially to high temperature (40º Celsius or more), low pH, capsaicin, and tissue damage.
History of term
The term "nociception" was coined by Charles Scott Sherrington to distinguish the physiological process (nervous activity) from pain (a subjective experience).[14] It is derived from the Latin verb "nocēre", which means "to harm".
References
- ^ Loeser, J. D.; Treede, R. D. (2008). "The Kyoto protocol of IASP Basic Pain Terminology". Pain 137 (3): 473–7. doi:10.1016/j.pain.2008.04.025. PMID 18583048.
- ^ Portenoy, Russell K.; Brennan, Michael J. (1994). "Chronic Pain Management". In Good, David C.; Couch, James R. Handbook of Neurorehabilitation. Informa Healthcare. ISBN 0-8247-8822-2.
- ^ a b "Assessing Pain and Distress: A Veterinary Behaviorist's Perspective by Kathryn Bayne". Definition of Pain and Distress and Reporting Requirements for Laboratory Animals (Proceedings of the Workshop Held June 22, 2000). 2000.
- ^ Momin, A.; McNaughton, PA. (2009). "Regulation of firing frequency in nociceptive neurons by pro-inflammatory mediators.". Exp Brain Res 196 (1): 45–52. doi:10.1007/s00221-009-1744-2. PMID 19350231.
- ^ Purves, D. (2001). "Nociceptors". In Sunderland, MA. Neuroscience. Sinauer Associates.
- ^ Skevington, S. M. (1995). Psychology of pain. Chichester, UK: Wiley. p. 18. ISBN 0-471-95771-2.
- ^ Feinstein, B.; Langton, J.; Jameson, R.; Schiller, F. (1954). "Experiments on pain referred from deep somatic tissues". J Bone Joint Surg 36–A (5): 981–97. PMID 13211692. Retrieved 2007-01-06.
- ^ Sneddon, L. U.; Braithwaite, V. A.; Gentle, M. J. (2003). "Do fishes have nociceptors? Evidence for the evolution of a vertebrate sensory system". Proceedings of the Royal Society B 270 (1520): 1115–1121. doi:10.1098/rspb.2003.2349.
- ^ Jane A. Smith (1991). "A Question of Pain in Invertebrates". Institute for Laboratory Animals Journal 33 (1–2).
- ^ Pastor, J.; Soria, B.; Belmonte, C. (1996). "Properties of the nociceptive neurons of the leech segmental ganglion". Journal of Neurophysiology 75 (6): 2268–2279. PMID 8793740.
- ^ Wittenburg, N.; Baumeister, R. (1999). "Thermal avoidance in Caenorhabditis elegans: an approach to the study of nociception". PNAS 96 (18): 10477–10482. doi:10.1073/pnas.96.18.10477.
- ^ Illich, P. A.; Walters, E. T. (1997). "Mechanosensory neurons innervating Aplysia siphon encode noxious stimuli and display nociceptive sensitization". Journal of Neuroscience 17 (1): 459–469. PMID 8987770.
- ^ Tracey, J.; Daniel, W.; Wilson, R. I.; Laurent, G.; Benzer, S. (2003). "painless, a Drosophila gene essential for nociception". Cell 113 (2): 261–273. doi:10.1016/S0092-8674(03)00272-1. PMID 12705873.
- ^ Sherrington, C. (1906). The Integrative Action of the Nervous System. Oxford: Oxford University Press.
