Axonal flow in the afferent fiber maintains the electroreceptor in the skin of fish

1985 ◽  
Vol 72 (7) ◽  
pp. 380-381 ◽  
Author(s):  
A. Roth
Keyword(s):  
2001 ◽  
Vol 21 (12) ◽  
pp. 4469-4477 ◽  
Author(s):  
Isobel J. Lever ◽  
Elizabeth J. Bradbury ◽  
Joanna R. Cunningham ◽  
David W. Adelson ◽  
Martyn G. Jones ◽  
...  

Neuron ◽  
2011 ◽  
Vol 70 (2) ◽  
pp. 326-338 ◽  
Author(s):  
Michael E. Schnee ◽  
Joseph Santos-Sacchi ◽  
Manuel Castellano-Muñoz ◽  
Jee-Hyun Kong ◽  
Anthony J. Ricci

2009 ◽  
Vol 107 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Jérôme Laurin ◽  
Erick Dousset ◽  
Serge Mesure ◽  
Patrick Decherchi

The medial collateral ligament (MCL) is one of the most injured ligaments during sport activities. The resulting joint damage effects on neuromuscular system remain unclear. Thus this study was designed to assess the changes in neuromuscular properties of vastus medialis muscle after MCL transection. Complete rupture of MCL was performed on rats, and dynamic functional assessment during locomotion was achieved before and once a week from 1–5 wk postlesion. Twitch properties and metabo- and mechanosensitive afferent fiber responses to specific stimuli were measured 1, 3, and 5 wk after MCL transection. Results indicated that maximum knee angle measured during the stance phase of the gait cycle was decreased during 3 wk after MCL injury and then recovered. Minimum knee angle measured during the stance phase was decreased during 2 wk and showed compensatory effects at week 5. A stepwise decrease in maximum relaxation rate-to-amplitude ratio concomitant with a stepwise increase in half-relaxation time were observed following MCL injury. Variations in metabosensitive afferent response to chemical (KCl and lactic acid) injections were decreased at week 1 and recovered progressively from week 3 to week 5 postlesion. Recovery of the mechanosensitive afferent response to vibrations was not totally complete after 5 wk. Our data indicate that alteration of the sensory pathways from the vastus medialis muscle could be considered as a source of neuromuscular deficits following MCL transection. Our results should be helpful in clinical purpose to improve the knowledge of the influence exerted by ligament rupture on the motor system and permit development of rehabilitation protocols and exercises more appropriate for recovery of functional stability.


1973 ◽  
Vol 21 (4) ◽  
pp. 1003-1007 ◽  
Author(s):  
J. J. Brink ◽  
M. L. Karnovsky

2013 ◽  
Vol 305 (9) ◽  
pp. G638-G648 ◽  
Author(s):  
Michael E. Kiyatkin ◽  
Bin Feng ◽  
Erica S. Schwartz ◽  
G. F. Gebhart

The ligand-gated channels transient receptor potential vanilloid 1 (TRPV1) and P2X3 have been reported to facilitate colorectal afferent neuron sensitization, thus contributing to organ hypersensitivity and pain. In the present study, we hypothesized that TRPV1 and P2X3 cooperate to modulate colorectal nociception and afferent sensitivity. To test this hypothesis, we employed TRPV1-P2X3 double knockout (TPDKO) mice and channel-selective pharmacological antagonists and evaluated combined channel contributions to behavioral responses to colorectal distension (CRD) and afferent fiber responses to colorectal stretch. Baseline responses to CRD were unexpectedly greater in TPDKO compared with control mice, but zymosan-produced CRD hypersensitivity was absent in TPDKO mice. Relative to control mice, proportions of mechanosensitive and -insensitive pelvic nerve afferent classes were not different in TPDKO mice. Responses of mucosal and serosal class afferents to mechanical probing were unaffected, whereas responses of muscular (but not muscular/mucosal) afferents to stretch were significantly attenuated in TPDKO mice; sensitization of both muscular and muscular/mucosal afferents by inflammatory soup was also significantly attenuated. In pharmacological studies, the TRPV1 antagonist A889425 and P2X3 antagonist TNP-ATP, alone and in combination, applied onto stretch-sensitive afferent endings attenuated responses to stretch; combined antagonism produced greater attenuation. In the aggregate, these observations suggest that 1) genetic manipulation of TRPV1 and P2X3 leads to reduction in colorectal mechanosensation peripherally and compensatory changes and/or disinhibition of other channels centrally, 2) combined pharmacological antagonism produces more robust attenuation of mechanosensation peripherally than does antagonism of either channel alone, and 3) the relative importance of these channels appears to be enhanced in colorectal hypersensitivity.


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