Faculty Opinions recommendation of TMEM16C facilitates Na(+)-activated K+ currents in rat sensory neurons and regulates pain processing.

Author(s):  
Gerald Zamponi
2013 ◽  
Vol 16 (9) ◽  
pp. 1284-1290 ◽  
Author(s):  
Fen Huang ◽  
Xidao Wang ◽  
Eric M Ostertag ◽  
Tulip Nuwal ◽  
Bo Huang ◽  
...  

1990 ◽  
Vol 64 (5) ◽  
pp. 1474-1483 ◽  
Author(s):  
D. A. Baxter ◽  
J. H. Byrne

1. Forskolin is often used to activate adenylate cyclase in studies relating adenosine 3',5'-cyclic monophosphate (cAMP) to the modulation of membrane current. There is growing concern, however, that some actions of forskolin are independent of cAMP. With the use of two-electrode voltage-clamp techniques, we compared the effects of analogues of cAMP to the effects of forskolin on K+ currents in somata of sensory neurons that were isolated from pleural ganglia of Aplysia californica. 2. Analogues of cAMP did not reduce the peak amplitude of either the transient K+ current (IA) or the voltage-dependent K+ current (IK.V). Analogues of cAMP did reduce the previously described cAMP-sensitive S K+ current (IK.S). In contrast, forskolin reduced the peak amplitude of both IA and IK.V. Furthermore, both IA and IK.V were reduced by 1,9-dideoxy-forskolin, a derivative of forskolin that does not activate adenylate cyclase. These results indicate that the effects of forskolin and 1,9-dideoxy-forskolin on IA and IK.V were not mediated via cAMP. 3. Bath application of a modified form of forskolin (7-deacetyl-6-[N-acetylglycyl]-forskolin), which has enhanced water solubility and activates adenylate cyclase, reduced IK.S, but did not alter either IA or IK.V. Thus it appears that certain derivatives of forskolin can be used to activate adenylate cyclase and avoid some of the nonspecific actions on membrane current that are associated with forskolin.


2002 ◽  
Vol 64 (4) ◽  
pp. 1833-1840 ◽  
Author(s):  
Shogo Endo ◽  
Stuart D. Critz ◽  
John H. Byrne ◽  
Shirish Shenolikar

1996 ◽  
Vol 75 (6) ◽  
pp. 2629-2646 ◽  
Author(s):  
M. S. Gold ◽  
M. J. Shuster ◽  
J. D. Levine

1. Previously three voltage-gated K+ currents were described in neurons from mammalian sensory ganglia: two transient and one sustained. Because there is considerable variability in the gating properties of these three currents, we have investigated the possibility that this variability reflects the presence of additional currents in sensory neurons. 2. Using whole cell patch-clamp techniques, we provide evidence for the existence of six voltage-gated K+ currents in cultured dorsal root ganglion (DRG) neurons from the adult rat. The six currents were identified on the basis of distinct biophysical and pharmacological properties; three currents are transient (IAf, IAht, and IAs), and three are sustained (IKi, IKlt, and IKn). 3. In addition to possessing distinct biophysical and pharmacological properties, four of the six currents are differentially expressed among subpopulations of DRG neurons. IAht is selectively expressed in small-diameter neurons. IKi is expressed more frequently in neurons with an action-potential shoulder, and both IAht and IAs are selectively coexpressed in neurons that respond to the algogenic agent capsaicin. IAf is selectively expressed in large-diameter neurons and is the only current expressed more frequently in neurons without an action-potential shoulder. 4. It is likely that much of apparent variability in the properties of the three voltage-gated K+ currents reported previously in vertebrate sensory neurons can be accounted for by the existence of at least three additional voltage-gated K+ currents described in this report.


Author(s):  
Paul Farquhar-Smith

This paper was one of several that cemented the key role of nerve growth factor (NGF) in sensory neurons in inflammatory pain processing. It used a novel way of biologically ‘removing’ NGF using a sequestration molecule that could then investigate the effect of the absence of NGF in pain paradigms. These data contributed to the robust evidence base indicating the importance of NGF and, although there had been issues in developing usable anti-NGF moieties in human pain conditions, this study could be considered part of the journey that has led to the introduction of antagonists to NGF actions for the treatment of pain in bone.


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