TY - JOUR
T1 - SLO-1 potassium channels control quantal content of neurotransmitter release at the C. elegans neuromuscular junction
AU - Wang, Zhao Wen
AU - Saifee, Owais
AU - Nonet, Michael L.
AU - Salkoff, Lawrence
N1 - Funding Information:
The authors thank Janet Richmond for her kind help with setting up the technique for making the C. elegans NMJ prep in our labs. We also thank Kenneth Miller and James Rand for providing us with two slo-1 alleles, Maria Garcia for the BK channel antibody, Pam Hoppe for p rol-6 ::GFP, Yuji Kohara for an EST clone, and Andy Fire for pPD95.67 and pPD96.52 vectors. Gratitude also goes to Gonzalo Ferreira and members of the Salkoff and Nonet labs (in particular Aguan Wei, Maya T. Kunkel, Alex Yuan, and Nina Walton) for their intellectual contributions and/or technical assistance. We thank Jeanne M. Nerbonne for her critical comments about the manuscript. This work was supported by NIH grants to L.S. and M.L.N.
PY - 2001/12/6
Y1 - 2001/12/6
N2 - Six mutants of SLO-1, a large-conductance, Ca2+-activated K+ channel of C. elegans, were obtained in a genetic screen for regulators of neurotransmitter release. Mutants were isolated by their ability to suppress lethargy of an unc-64 syntaxin mutant that restricts neurotransmitter release. We measured evoked postsynaptic currents at the neuromuscular junction in both wild-type and mutants and observed that the removal of SLO-1 greatly increased quantal content primarily by increasing duration of release. The selective isolation of slo-1 as the only ion channel mutant derived from a whole genomic screen to detect regulators of neurotransmitter release suggests that SLO-1 plays an important, if not unique, role in regulating neurotransmitter release.
AB - Six mutants of SLO-1, a large-conductance, Ca2+-activated K+ channel of C. elegans, were obtained in a genetic screen for regulators of neurotransmitter release. Mutants were isolated by their ability to suppress lethargy of an unc-64 syntaxin mutant that restricts neurotransmitter release. We measured evoked postsynaptic currents at the neuromuscular junction in both wild-type and mutants and observed that the removal of SLO-1 greatly increased quantal content primarily by increasing duration of release. The selective isolation of slo-1 as the only ion channel mutant derived from a whole genomic screen to detect regulators of neurotransmitter release suggests that SLO-1 plays an important, if not unique, role in regulating neurotransmitter release.
UR - http://www.scopus.com/inward/record.url?scp=0035819056&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(01)00522-0
DO - 10.1016/S0896-6273(01)00522-0
M3 - Article
C2 - 11738032
AN - SCOPUS:0035819056
SN - 0896-6273
VL - 32
SP - 867
EP - 881
JO - Neuron
JF - Neuron
IS - 5
ER -