Shaker Mutants Lack Post‐tetanic Potentiation at Motor End‐plates
Author
dc.contributor.author
Delgado, Ricardo
Author
dc.contributor.author
Latorre, Ramón
Author
dc.contributor.author
Labarca, Pedro
Admission date
dc.date.accessioned
2019-01-29T15:49:54Z
Available date
dc.date.available
2019-01-29T15:49:54Z
Publication date
dc.date.issued
1994
Cita de ítem
dc.identifier.citation
European Journal of Neuroscience, Volumen 6, Issue 7, 2018, Pages 1160-1166
Identifier
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14609568
Identifier
dc.identifier.issn
0953816X
Identifier
dc.identifier.other
10.1111/j.1460-9568.1994.tb00614.x
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/162482
Abstract
dc.description.abstract
The two‐electrode voltage clamp technique was employed to measure end‐plate currents in larval neuromuscular junctions of wild‐type (Canton‐S) and of three different Drosophila Shaker mutants: ShakerKS133, Shaker102 and f5Shaker5. In the Shaker mutants, nerve‐evoked end‐plate currents (neepc) were 4–5‐fold larger than those measured in Canton‐S. Shaker motor end‐plates were found to lack post‐tetanic potentiation (PTP), but could undergo facilitation. Moreover, PTP but not facilitation was lost in wild‐type larvae if the neuromuscular junction was exposed to 4‐aminopyridine (4‐AP), a blocker of Shaker A‐type K+ currents. End‐plate currents were depressed by Ca2+ channel blockers like Mg2+, at millimolar concentrations, and Co2+ and Cd2+, at micromolar concentrations, but not by nifedipine (100 nM) and verapamil (100 nM). After exposure to Ca2+ channel blockers, Shaker end‐plates exhibited PTP. In particular, Cd2+ was most effective in depressing neepes and in restoring PTP in all Shake