Sensory Receptors

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This is due to the light or non-myelination of the axon. As airborne molecules are inhaled through the nose, they pass over the olfactory epithelial region and dissolve into the mucus. This molecule is referred to as 11- cis-retinal.

Based on the animation, where do frequencies—from high to low pitches—cause activity in the hair cells within the cochlear duct? Within the realm of physiology, senses can be classified as either general or specific.

Sensory Receptors

If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called. Nociceptor Nociceptors were discovered by in 1906. In earlier centuries, scientists believed that animals were like mechanical devices that transformed the energy of sensory stimuli into motor responses. Sherrington used many different experiments to demonstrate that different types of stimulation to an 's led to different responses. Some intense stimuli trigger reflex , certain , and. The specific receptors for these intense stimuli were called nociceptors. In mammals, nociceptors are found in any area of the body that can sense noxious stimuli. External nociceptors are found in such as the , the , and the. Internal nociceptors are found in a variety of organs, such as the , the , the , the , and the digestive tract. The cell bodies of these neurons are located in either the or the ganglia. The trigeminal ganglia are specialized nerves for the face, whereas the dorsal root ganglia are associated with the rest of the body. The axons extend into the peripheral nervous system and terminate in branches to form receptive fields. Nociceptors develop from stem cells. The neural crest is responsible for a large part of early development in vertebrates. It is specifically responsible for development of the peripheral nervous system PNS. The neural-crest stem cells split from the neural tube as it closes, and nociceptors grow from the dorsal part of this neural-crest tissue. They form late during neurogenesis. Earlier forming cells from this region can become non-pain sensing receptors, either or low-threshold. All neurons derived from the neural crest, including embryonic nociceptors, express the TrkA, which is a receptor to nerve-growth factor NGF. However, transcription factors that determine the type of nociceptor remain unclear. Following sensory neurogenesis, differentiation occurs, and two types of nociceptors are formed. They are classified as either peptidergic or nonpeptidergic nociceptors, each of which express a distinct repertoire of ion channels and receptors. Their specializations allow the receptors to innervate different central and peripheral targets. This differentiation occurs in both perinatal and postnatal periods. The nonpeptidergic nociceptors switch off the TrkA and begin expressing Ret, which is a transmembrane signaling component that allows the expression of glial-cell-derived growth factor GDNF. This transition is assisted by Runx1 which is vital in the development of nonpeptidergic nociceptors. On the contrary, the peptidergic nociceptors continue to use TrkA, and they express a completely different type of growth factor. There currently is a lot of research about the differences between nociceptors. The peripheral terminal of the mature nociceptor is where the are detected and transduced into electrical energy. When the electrical energy reaches a threshold value, an is induced and driven towards the CNS. This leads to the train of events that allows for the conscious awareness of pain. The sensory specificity of nociceptors is established by the high threshold only to particular features of stimuli. Only when the high threshold has been reached by either chemical, thermal, or mechanical environments are the nociceptors triggered. The majority of nociceptors are classified by which of the environmental modalities they respond to. Some nociceptors respond to more than one of these modalities and are consequently designated polymodal. Other nociceptors respond to none of these modalities although they may respond to stimulation under conditions of inflammation and are referred to as sleeping or silent. Nociceptors have two different types of axons. The first are the axons. The other type is the more slowly conducting axons. This is due to the light or non-myelination of the axon. As a result, pain comes in two phases. The first phase is mediated by the fast-conducting Aδ fibers and the second part due to Polymodal C fibers. The pain associated with the Aδ fibers can be associated to an initial extremely sharp pain. The second phase is a more prolonged and slightly less intense feeling of pain as a result of the acute damage. If there is massive or prolonged input to a C fiber, there is a progressive build up in the spinal cord dorsal horn; this phenomenon is similar to in muscles but is called. If wind-up occurs there is a probability of increased sensitivity to pain. Thermal Thermal nociceptors are activated by noxious heat or cold at various temperatures. There are specific nociceptor transducers that are responsible for how and if the specific nerve ending responds to the thermal stimulus. The first to be discovered was , and it has a threshold that coincides with the heat pain temperature of 42 °C. Other temperature in the warm—hot range is mediated by more than one. Each of these channels express a particular C-terminal domain that corresponds to the warm—hot sensitivity. The interactions between all these channels and how the temperature level is determined to be above the pain threshold are unknown at this time. The cool stimuli are sensed by channels. Its C-terminal domain differs from the heat sensitive TRPs. Although this channel corresponds to cool stimuli, it is still unknown whether it also contributes in the detection of intense cold. An interesting finding related to cold stimuli is that tactile sensibility and motor function deteriorate while pain perception persists. Mechanical Mechanical nociceptors respond to excess pressure or mechanical deformation. They also respond to incisions that break the skin surface. The reaction to the stimulus is processed as pain by the cortex, just like chemical and thermal responses. These mechanical nociceptors frequently have polymodal characteristics. So it is possible that some of the transducers for thermal stimuli are the same for mechanical stimuli. The same is true for chemical stimuli, since TRPA1 appears to detect both mechanical and chemical changes. Chemical Chemical nociceptors have TRP channels that respond to a wide variety of spices. The one that sees the most response and is very widely tested is. Other chemical stimulants are environmental irritants like , a and a component of cigarette smoke. Apart from these external stimulants, chemical nociceptors have the capacity to detect endogenous ligands, and certain fatty acid amines that arise from changes in internal tissues. Like in thermal nociceptors, TRPV1 can detect chemicals like capsaicin and spider toxins. These are typically referred to as silent or sleeping nociceptors since their response comes only on the onset of inflammation to the surrounding tissue. This nociceptive fiber located in the periphery is a first order neuron. The in the dorsal horn are divided into physiologically distinct layers called laminae. Different fiber types form in different layers, and use either or as the neurotransmitter. After reaching the specific lamina within the spinal cord, the first order nociceptive project to second order neurons that cross the midline at the anterior white commissure. The second order neurons then send their information via two pathways to the : the and the. The first is reserved more for regular non-painful sensation, while the lateral is reserved for pain sensation. Upon reaching the thalamus, the information is processed in the ventral posterior nucleus and sent to the in the brain via fibers in the posterior limb of the internal capsule. As there is an ascending pathway to the brain that initiates the conscious realization of pain, there also is a descending pathway which modulates pain sensation. The brain can request the release of specific or chemicals that can have analgesic effects which can reduce or inhibit pain sensation. The area of the brain that stimulates the release of these hormones is the. This effect of descending inhibition can be shown by electrically stimulating the area of the midbrain. The periaqueductal grey in turn projects to other areas involved in pain regulation, such as the which also receives similar afferents from the NPG. In turn the projects to the region of the dorsal horn and mediates the sensation of spinothalamic inputs. The periaqueductal grey also contains which explains one of the mechanisms by which opioids such as and exhibit an analgesic effect. Nociceptor neuron sensitivity is modulated by a large variety of mediators in the extracellular space. Peripheral sensitization represents a form of functional plasticity of the nociceptor. The nociceptor can change from being simply a noxious stimulus detector to a detector of non-noxious stimuli. The result is that low intensity stimuli from regular activity, initiates a painful sensation. This is commonly known as. Inflammation is one common cause that results in the sensitization of nociceptors. Allodynia can also be caused when a nociceptor is damaged in the peripheral nerves. This can result in deafferentation, which means the development of different central processes from the surviving afferent nerve. With this situation, surviving dorsal root axons of the nociceptors can make contact with the spinal cord, thus changing the normal input. Nociception has been documented in non-mammalian animals, including fish and a wide range of invertebrates, including leeches, nematode worms, sea slugs, and fruit flies. Although these neurons may have different pathways and relationships to the central nervous system than mammalian nociceptors, nociceptive neurons in non-mammals often fire in response to similar stimuli as mammals, such as high temperature 40 degrees C or more , low pH, capsaicin, and tissue damage. National Academies Press US — via www. The Integrative Action of the Nervous System. Oxford: Oxford University Press; 1906. Principles of neural science. Sunderland, Mass: Sinauer Associates. Proceedings of the Royal Society of London B: Biological Sciences. Proceedings of the National Academy of Sciences of the United States of America. The Journal of Neuroscience.

The wavelength of visible light determines its color. This vibration is amplified as it moves across the malleus, incus, and stapes. Somatosensation is the group of sensory modalities that are associated with touch, proprioception, and interoception. Head position is sensed by the utricle and saccule, whereas head movement is sensed by the semicircular canals. Interactive Link Questions Watch this to learn about Dr. The brain can request the release of specific or chemicals that can have analgesic effects which can reduce or inhibit pain sensation. So it is possible that some of the transducers for thermal stimuli are the same for mechanical stimuli. Stretch receptors monitor the stretching of tendons, muscles, and the components of joints. Other transmembrane proteins, which are not accurately called receptors, are sensitive to mechanical or thermal changes. Other somatosensory receptors are found in the joints and muscles. As stated above, a given region of the basilar membrane will only move if the incoming sound is at a specific frequency. Absolute Threshold and Differential Threshold Our five physiological senses have unknowingly fooled us — on a regular basis, no less — to the benefit of marketers and manufacturers.