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dc.contributor.authorO'Mara, M.
dc.contributor.authorDeplazes, Evelyne
dc.date.accessioned2017-01-30T12:21:05Z
dc.date.available2017-01-30T12:21:05Z
dc.date.created2016-04-03T19:30:34Z
dc.date.issued2014
dc.identifier.citationO'Mara, M. and Deplazes, E. 2014. Polypeptide and Protein Modeling for Drug Design, in Jaeger, D. and Jung, Ranu (ed), Encyclopedia of Computational Neuroscience, pp. 2439-2447. New York: Springer.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/20769
dc.identifier.doi10.1007/978-1-4614-7320-6
dc.description.abstract

The main pathways involved in pain processing have been known for some time, but the precise microcircuitry remains surprisingly unclear. This has allowed very different theories of pain processing to persist. Specificity theory holds that pain is qualitatively distinct from other somatosensory percepts and that the underlying circuitry is arranged as labeled lines. Gate control theory holds that all inputs converge and that it is the level of activation in unspecialized neurons that code for pain. The truth lies somewhere in between. The dorsal horn of the spinal cord, which corresponds to the first synaptic relay point, comprises a diverse set of interneurons whose connectivity is only partially worked out. This lack of data has hindered network-level modeling, but this also presents an opportunity for modeling to help guide future experiments.

dc.titlePolypeptide and Protein Modeling for Drug Design
dc.typeBook Chapter
dcterms.source.titleEncyclopedia of Computational Neuroscience
dcterms.source.isbn978-1-4614-7320-6
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available


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