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Molecular and cellular limits to somatosensory specificity

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dc.creator Belmonte, Carlos
dc.creator Viana, Félix
dc.date 2008-04-28T06:43:40Z
dc.date 2008-04-28T06:43:40Z
dc.date 2008
dc.date.accessioned 2017-01-31T01:04:21Z
dc.date.available 2017-01-31T01:04:21Z
dc.identifier Molecular Pain 2008, 4:14
dc.identifier 1744-8069
dc.identifier http://hdl.handle.net/10261/3774
dc.identifier 10.1186/1744-8069-4-14
dc.identifier.uri http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3774
dc.description Animals detect environmental changes through sensory neural mechanisms that enable them to differentiate the quality, intensity and temporal characteristics of stimuli. The 'doctrine of specific nervous energies' postulates that the different sensory modalities experienced by humans result of the activation of specific nervous pathways. Identification of functional classes of sensory receptors provided scientific support to the concept that somatosensory modalities (touch, pain, temperature, kinesthesis) are subserved by separate populations of sensory receptor neurons specialized in detecting innocuous and injurious stimuli of different quality (mechanical forces, temperature, chemical compounds). The identification of receptor proteins activated by different physicochemical stimuli, in particular ion channels of the Transient Receptor Potential (TRP) superfamily, has put forward the concept that specificity of peripheral sensory receptor neurons is determined by their expression of a particular "molecular sensor" that confers to each functional type its selectivity to respond with a discharge of nerve impulses to stimuli of a given quality. Nonetheless, recent experimental data suggest that the various molecular sensors proposed as specific transducer molecules for stimuli of different quality are not as neatly associated with the distinct functional types of sensory receptors as originally proposed. First, many ion channel molecules initially associated to the transduction of only one particular form of energy are also activated by stimuli of different quality, implying a limited degree of specificity in their transducing capacities. Second, molecular sensors associated with a stimulus quality and hence to a sensory receptor type and ultimately to a sensory modality may be concomitantly expressed in sensory receptor neurons functionally defined as specific for another stimulus quality. Finally, activation of voltage gated channels involved primarily in nerve impulse generation can also influence the gating of transducing channels, dramatically modifying their activation profile. Thus, we propose that the capacity exhibited by the different functional types of somatosensory receptor neurons to preferentially detect and encode specific stimuli into a discharge of nerve impulses, appears to result of a characteristic combinatorial expression of different ion channels in each neuronal type that finally determines their transduction and impulse firing properties. Transduction channels don't operate in isolation and their cellular context should also be taken into consideration to fully understand their function. Moreover, the inhomogeneous distribution of transduction and voltage-gated channels at soma, axonal branches and peripheral endings of primary sensory neurons influences the characteristics of the propagated impulse discharge that encodes the properties of the stimulus. Alteration of this concerted operation of ion channels in pathological conditions may underlie the changes in excitability accompanying peripheral sensory neuron injuries.
dc.description This work was supported by grants from the Spanish Ministry of Education and Science: project BFU2007-61855 to F.V and projects CONSOLIDER-INGENIO 2010 CSD2007-00023 and BFI2002-03788 to C.B.
dc.description Peer reviewed
dc.format 1572224 bytes
dc.format application/pdf
dc.language eng
dc.publisher BioMed Central
dc.relation Publisher’s version
dc.rights openAccess
dc.title Molecular and cellular limits to somatosensory specificity
dc.type Artículo


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