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Sensory neuron

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Sensory neurons are nerves that transmit sensory information (sight, sound, feeling, etc.). They are activated by sensory input, and send projections to other elements of the nervous system, ultimately conveying sensory information to the brain or spinal cord. In complex organisms, when stimulation of a peripheral sensory neuron (a first-order sensory neuron) sensory receptor exceeds a set level of intensity, an electrical impulse travels down the nerve fiber to the central nervous system, where it may activate a motor neuron or another sensory neuron (a second- or third-order neuron), or both. In less complex organisms, such as the hydra, sensory neurons transmit data to motor neurons or ganglia. Different types of receptor respond to different kinds of stimulus.

Types and function

Somatosensory system

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 lie in ganglia throughout the spine. These neurons 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 cell bodies are located in the dorsal root ganglia.[1]

Mechanoreceptors

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

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 photoreceptor cells 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 photoreceptor cells, 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.

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.[8]
  • Glaucoma – loss of retinal ganglion cells which causes some loss of vision to blindness.[9]
  • Diabetic retinopathy – poor blood sugar control due to diabetes damages the tiny blood vessels in the retina.[10]

Auditory

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. 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 Ca++ 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.[11]

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.[12]
  • Auditory verbal agnosia – 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.[13]

Drugs

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 non-receptive neurons.[14] 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.[15]

Plasticity (Neuroplasticity)

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.[16] Phantom limb syndrome is a sensory system disorder in which amputees perceive that their amputated limb still exists and they may still be experiencing pain in it. The mirror box developed by V.S. Ramachandran, has enabled patients with phantom limb syndrome to relieve the perception of paralyzed or painful phantom limbs. It is a simple device which uses a mirror in a box to create an illusion in which the sensory system perceives that it is seeing two hands instead of one, therefore allowing the sensory system to control the "phantom limb". By doing this, the sensory system can gradually get acclimated to the amputated limb, and thus alleviate this syndrome.[17]

Fiber types

Main article: Sensory fiber types

Peripheral nerve fibers can be classified based on axonal conduction velocity, myelination, fiber size etc. For example, there are slow-conducting unmyelinated C fibers and faster-conducting myelinated Aδ fibers. These nerve fibers work with neurons to form the nervous system

See also

Footnotes

  1. ^ Purves et al., p 207
  2. ^ Purves et al., 209
  3. ^ Purves et al., 215-216
  4. ^ Lee 2005
  5. ^ Lee 2005
  6. ^ Lee 2005
  7. ^ Halligan 1999
  8. ^ de Jong 2006
  9. ^ Alguire 1990
  10. ^ Diabetic retinopathy 2005
  11. ^ Purves et al., p 327-330
  12. ^ Auditory processing disorder, 2004
  13. ^ Stefanatos et al., 2005
  14. ^ Lee 2005
  15. ^ Priuska and Schact 1997
  16. ^ Schwartz and Begley 2002
  17. ^ Ramachandran 1998

References

  • 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.
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