Sökning: onr:"swepub:oai:DiVA.org:kth-93681" > Modeling activity-d...
Fältnamn | Indikatorer | Metadata |
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000 | 04377naa a2200445 4500 | |
001 | oai:DiVA.org:kth-93681 | |
003 | SwePub | |
008 | 120423s2014 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-936812 URI |
024 | 7 | a https://doi.org/10.1152/jn.00777.20122 DOI |
040 | a (SwePub)kth | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Tigerholm, Jennyu KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u1k1jm7d |
245 | 1 0 | a Modeling activity-dependent changes of axonal spike conduction in primary afferent C-nociceptors |
264 | 1 | b American Physiological Society,c 2014 |
338 | a print2 rdacarrier | |
500 | a QC 20140602. Updated from manuscript to article in journal. | |
520 | a Action potential initiation and conduction along peripheral axons is a dynamic process that displays pronounced activity dependence. In patients with neuropathic pain, differences in the modulation of axonal conduction velocity by activity suggest that this property may provide insight into some of the pathomechanisms. To date, direct recordings of axonal membrane potential have been hampered by the small diameter of the fibers. We have therefore adopted an alternative approach to examine the basis of activity-dependent changes in axonal conduction by constructing a comprehensive mathematical model of human cutaneous C-fibers. Our model reproduced axonal spike propagation at a velocity of 0.69 m/s commensurate with recordings from human C-nociceptors. Activity-dependent slowing (ADS) of axonal propagation velocity was adequately simulated by the model. Interestingly, the property most readily associated with ADS was an increase in the concentration of intra-axonal sodium. This affected the driving potential of sodium currents, thereby producing latency changes comparable to those observed for experimental ADS. The model also adequately reproduced post-action potential excitability changes (i.e., recovery cycles) observed in vivo. We performed a series of control experiments replicating blockade of particular ion channels as well as changing temperature and extracellular ion concentrations. In the absence of direct experimental approaches, the model allows specific hypotheses to be formulated regarding the mechanisms underlying activity-dependent changes in C-fiber conduction. Because ADS might functionally act as a negative feedback to limit trains of nociceptor activity, we envisage that identifying its mechanisms may also direct efforts aimed at alleviating neuronal hyperexcitability in pain patients. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng |
650 | 7 | a NATURVETENSKAPx Data- och informationsvetenskapx Bioinformatik0 (SwePub)102032 hsv//swe |
650 | 7 | a NATURAL SCIENCESx Computer and Information Sciencesx Bioinformatics0 (SwePub)102032 hsv//eng |
653 | a activity-dependent slowing | |
653 | a recovery cycles | |
653 | a mechano-insensitive nociceptor | |
653 | a computer modeling | |
700 | 1 | a Petersson, Marcusu KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u14bsy5t |
700 | 1 | a Obreja, Otiliau Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg4 aut |
700 | 1 | a Lampert, Angelikau Inst. of Physiol. and Pathophysiology, Friedrich-Alexander-Uni versität Erlangen-Nürnberg4 aut |
700 | 1 | a Carr, Richardu Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg4 aut |
700 | 1 | a Schmelz, Martinu Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg,4 aut |
700 | 1 | a Fransén, Eriku KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u14yg0os |
710 | 2 | a KTHb Beräkningsbiologi, CB4 org |
773 | 0 | t Journal of Neurophysiologyd : American Physiological Societyg 111:9, s. 1721-1735q 111:9<1721-1735x 0022-3077x 1522-1598 |
856 | 4 | u https://europepmc.org/articles/pmc4044369 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-93681 |
856 | 4 8 | u https://doi.org/10.1152/jn.00777.2012 |
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