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Sensory neurons are typically classified as the neurons responsible for converting external stimuli from the environment into internal stimuli. They are activated by sensory input (vision, touch, hearing, etc.), and send projections into the central nervous system that convey sensory information to the brain or spinal cord. Unlike neurons of the central nervous system, whose inputs come from other neurons, sensory neurons are activated by physical modalities such as light, sound, and temperature.
In complex organisms, sensory neurons relay their information to the central nervous system or in less complex organisms, such as the hydra, directly to motor neurons and sensory neurons also transmit information (electrical impulses) to the brain, where it can be further processed and acted upon. For example, olfactory sensory neurons make synapses with neurons of the olfactory bulb, where the sense of olfaction (smell) is processed.
At the molecular level, sensory receptors located on the cell membrane of sensory neurons are responsible for the conversion of stimuli into electrical impulses. The type of receptor employed by a given sensory neuron determines the type of stimulus it will be sensitive to. For example, neurons containing mechanoreceptors are sensitive to tactile stimuli, while olfactory receptors make a cell sensitive to odors. [1]
Types and Function
[edit]Somatic sensory system
[edit]The somatic sensory system includes the sensations of touch, pressure, vibration, limb position, heat, cold, and pain.
The cell bodies of somatic sensory afferent fibers lying in the ganglia are responsible for relaying information about the body to the central nervous system. Neurons residing in ganglia of the head and body supply the central nervous system with information about the aforementioned external stimuli occurring to the body. Pseudounipolar neurons are the ones located in the dorsal root ganglia (the head).
Mechanoreceptors
[edit]Specialized receptor cells called mechanoreceptors often encapsulate afferent fibers to help tune the afferent fibers to the different types of somatic stimulation. Mechanoreceptors also help lower thresholds for action potential generation in afferent fibers and thus make them more likely to fire in the presence of sensory stimulation. [2]
Proprioceptors are another type of mechanoreceptors which literally means "receptors for self." These receptors provide spatial information about limbs and other body parts. [3]
Nociceptors are responsible for processing pain and temperature changes. The burning pain and irritation experienced after eating a chili pepper (due to its main ingredient, capsaicin), the cold sensation experienced after ingesting a chemical such as menthol or icillin, as well as the common sensation of pain are all a result of neurons with these receptors. [4]
Problems with mechanoreceptors lead to disorders such as:
- Neuropathic pain - a severe pain condition resulting from a damaged sensory nerve [5]
- Hyperalgesia - an increased sensitivity to pain caused by sensory ion channel, TRPM8, which is typically responds to temperatures between 23 and 26 degrees, and provides the cooling sensation associated with menthol and icillin [6]
- Phantom limb syndrome - a sensory system disorder where pain or movement is experienced in a limb that does not exist [7]
Vision
[edit]Vision is one of the most complex sensory systems. The eye has to first "see" via refraction of light. Then, light energy has to be converted to electrical signals by photoreceptors and finally these signals have to be refined and controlled by the synaptic interactions within the neurons of the retina. The five basic classes of neurons within the retina are photoreceptors, bipolar cells, ganglion cells, horizontal cells, and amacrine cells. The basic circuitry of the retina incorporates a three-neuron chain consisting of the photoreceptor (either a rod or cone), bipolar cell, and the ganglion cell. As the picture shows, the first action potential occurs in the retinal ganglion cell. This pathway is the most direct way for transmitting visual information to the brain. Problems and decay of sensory neurons associated with vision lead to disorders such as:
- Macular degeneration – degeneration of the central visual field due to either cellular debris or blood vessels accumulating between the retina and the choroid, thereby disturbing and/or destroying the complex interplay of neurons that are present there.[9]
- Glaucoma – loss of retinal ganglion cells which causes some loss of vision to blindness. [10]
- Diabetic retinopathy – poor blood sugar control due to diabetes damages the tiny blood vessels in the retina. [11]
Auditory
[edit]The auditory system is responsible for converting pressure waves generated by vibrating air molecules or sound into signals that can be interpreted by the brain. This mechanoelectrical transduction is mediated with hair cells within the ear. As the picture shows, depending on the movement, the hair cell can either hyperpolarize or depolarize. When the movement is towards the tallest stereocilia, the K+ cation channels open allowing K+ to flow into cell and the resulting depolarization causes the Ca2+ channels to open, thus releasing its neurotransmitter into the afferent auditory nerve. There are two types of hair cells: inner and outer. The inner hair cells are the sensory receptors while the outer hair cells are usually from efferent axons originating from cells in the superior olivary complex[12] Problems with sensory neurons associated with the auditory system leads to disorders such as:
- Auditory Processing Disorder – auditory information in the brain is processed in an abnormal way. Patients with auditory processing disorder can usually gain the information normally, but their brain cannot process it properly, leading to hearing disability. [13]
- Pure word deafness – comprehension of speech is lost but hearing, speaking, reading, and writing ability is retained. This is caused by damage to the posterior superior temporal lobes, again not allowing the brain to process auditory input correctly. [14]
Drugs
[edit]There are many drugs currently on the market that are used to manipulate or treat sensory system disorders. For instance, Gabapentin is a drug that is used to treat neuropathic pain by interacting with one of the voltage-dependent calcium channels present on nociceptive neurons. [15] Some drugs may be used to combat other health problems, but can have unintended side effects on the sensory system. Ototoxic drugs are drugs which affect the cochlea through the use of a toxin like aminoglycoside antibiotics, which poison hair cells. Through the use of these toxins, the K+ pumping hair cells cease their function. Thus, the energy generated by the endocochlear potential which drives the auditory signal transduction process is lost, leading to hearing loss. [16]
Plasticity (Neuroplasticity)
[edit]Ever since scientists observed cortical remapping in the brain of Taub’s Silver Spring monkeys, there has been a lot of research into sensory system plasticity. Huge strides have been made in treating disorders of the sensory system. Techniques such as constraint-induced movement therapy developed by Taub have helped patients with paralyzed limbs regain use of their limbs by forcing the sensory system to grow new neural pathways [17]. The mirror box developed by V.S. Ramachandran has enabled patients with phantom limb syndrome realign their body map, the somatosensory system’s perception of where the body is in space with physical reality [18]
Fiber types
[edit]Peripheral nerve fibers can be classified based on axonal conduction velocity, mylenation, fiber size etc. For example, there are slow-conducting unmyelinated C fibers and faster-conducting myelinated Aδ fibers.
See also
[edit]Footnotes
[edit]- ^ Purves et al., 207-392
- ^ Purves et al., 209
- ^ Purves et al., 215-216
- ^ Lee 2005
- ^ Lee 2005
- ^ Lee 2005
- ^ Halligan 1999
- ^ Purves et al., 262
- ^ de Jong 2006
- ^ Alguire 1990
- ^ Diabetic retinopathy 2005
- ^ Purves et al., pg 327-330
- ^ Auditory processing disorder, 2004
- ^ Stefanatos et al., 2005
- ^ Lee 2005
- ^ Priuska and Schact 1997
- ^ Schwartz and Begley 2002
- ^ Ramachandran 1998
References
[edit]- Alguire P (1990). "The Eye Chapter 118 Tonometry>Basic Science". in Walker HK, Hall WD, Hurst JW. Clinical methods: the history, physical, and laboratory examinations (3rd ed.). London: Butterworths. ISBN 0-409-90077-X. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&partid=222#A3607.
- "Auditory Processing Disorder (APD). Pamphlet, (2004).". British Society of Audiology APD Special Interest Group. MRC Institute of Hearing Research. http://www.ihr.mrc.ac.uk/research/apd.php/apd.php?page=apd_docs.
- de Jong, Ptvm. "Mechanisms of Disease: Age-Related Macular Degeneration." New England Journal of Medicine 355 14 (2006): 1474-85. Print.
- Halligan, P. W., A. Zeman, and A. Berger. "Phantoms in the Brain - Question the Assumption That the Adult Brain Is "Hard Wired"." British Medical Journal 319 7210 (1999): 587-88. Print.
- Lee, Y., Lee, C. H., & Oh, U. (2005). Painful channels in sensory neurons. [Review]. Molecules and Cells, 20(3), 315-324. Print.
- "NIHSeniorHealth: Diabetic Retinopathy - Causes and Risk Factors". Diabetic Retinopathy. NIHSenior Health. 2005. http://nihseniorhealth.gov/diabeticretinopathy/causesandriskfactors/02.html.
- Priuska, E.M. and J. Schact (1997) Mechanism and prevention of aminoglycoside ototoxicity: Outer hair cells as targets and tools. Ear, Nose, Throat J. 76: 164-171.
- Purves, D., Augustine, G.J., Fitzpatrick, D., Hall, W.C., LaMantia, A., McNamara, J.O., White, L.E. Neuroscience. Fourth edition. (2008). Sinauer Associates, Sunderland, Mass. Print.
- Ramachandran, V. S. and S. Blakeslee (1998), Phantoms in the brain: Probing the mysteries of the human mind., William Morrow & Company, ISBN 0-688-15247-3. Print.
- Schwartz and Begley 2002, p. 160; "Constraint-Induced Movement Therapy", excerpted from "A Rehab Revolution," Stroke Connection Magazine, September/October 2004. Print.
- Stefanatos GA, Gershkoff A, Madigan S (2005). "On pure word deafness, temporal processing, and the left hemisphere". Journal of the International Neuropsychological Society : JINS 11 (4): 456–70; discussion 455.