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SLO-2 potassium channel is an important regulator of neurotransmitter release in Caenorhabditis elegans.

Liu P, Chen B, Wang ZW - Nat Commun (2014)

Bottom Line: Loss-of-function mutation of slo-2 increases the duration and charge transfer rate of spontaneous postsynaptic current bursts at the neuromuscular junction, which are physiological signals used by motor neurons to control muscle cells, without altering postsynaptic receptor sensitivity.SLO-2 activity in motor neurons depends on Ca(2+) entry through EGL-19, an L-type voltage-gated Ca(2+) channel (CaV1), but not on other proteins implicated in either Ca(2+) entry or intracellular Ca(2+) release.Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030, USA.

ABSTRACT
Slo2 channels are prominent K(+) channels in mammalian neurons but their physiological functions are not well understood. Here we investigate physiological functions and regulation of the Caenorhabditis elegans homologue SLO-2 in motor neurons through electrophysiological analyses of wild-type and mutant worms. We find that SLO-2 is the primary K(+) channel conducting delayed outward current in cholinergic motor neurons, and one of two K(+) channels with this function in GABAergic motor neurons. Loss-of-function mutation of slo-2 increases the duration and charge transfer rate of spontaneous postsynaptic current bursts at the neuromuscular junction, which are physiological signals used by motor neurons to control muscle cells, without altering postsynaptic receptor sensitivity. SLO-2 activity in motor neurons depends on Ca(2+) entry through EGL-19, an L-type voltage-gated Ca(2+) channel (CaV1), but not on other proteins implicated in either Ca(2+) entry or intracellular Ca(2+) release. Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

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Postsynaptic receptor sensitivities and ePSCs were normal inslo-2(nf101). A. Comparison of muscle cell response topressure-ejected acetylcholine (ACh, 100 μM) or GABA (100 μM) between wildtype (WT) and slo-2(nf101). B. Comparison of ePSC between WTand slo-2(nf101) in the presence of two different extracellularCa2+ concentrations (5 mM and 0.5 mM). Data are shown as mean± SE. No significant difference was detected (unpaired t-test).The holding voltage was −60 mV in all the experiments. The numbers inside thecolumns indicate the sample sizes (n). All the recordings were performedwith pipette solution I. The recordings of ePSC at 0.5 mM[Ca2+]o were performed with extracellularsolution II whereas the remaining recordings were recorded with extracellular solutionI.
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Figure 4: Postsynaptic receptor sensitivities and ePSCs were normal inslo-2(nf101). A. Comparison of muscle cell response topressure-ejected acetylcholine (ACh, 100 μM) or GABA (100 μM) between wildtype (WT) and slo-2(nf101). B. Comparison of ePSC between WTand slo-2(nf101) in the presence of two different extracellularCa2+ concentrations (5 mM and 0.5 mM). Data are shown as mean± SE. No significant difference was detected (unpaired t-test).The holding voltage was −60 mV in all the experiments. The numbers inside thecolumns indicate the sample sizes (n). All the recordings were performedwith pipette solution I. The recordings of ePSC at 0.5 mM[Ca2+]o were performed with extracellularsolution II whereas the remaining recordings were recorded with extracellular solutionI.

Mentions: The larger persistent current of cholinergic PSC bursts observed inslo-2(nf101) could have resulted from either increased neurotransmitterrelease or increased postsynaptic receptor sensitivity to ACh. To examine the secondpossibility, we compared the amplitude of inward current caused by pressure-ejectingexogenous ACh (100 μM) to body-wall muscle cells between wild type andslo-2(nf101). A similar experiment with exogenous GABA (100 μM)was also performed although GABA did not contribute to the PSC bursts under theexperimental conditions27. We found thatamplitudes of ACh- and GABA-induced inward current were similar between wild type andslo-2(nf101) (Figure 4A). Thus,the larger persistent current of PSC bursts in slo-2(nf101) did notresult from an increased postsynaptic receptor function or expression.


SLO-2 potassium channel is an important regulator of neurotransmitter release in Caenorhabditis elegans.

Liu P, Chen B, Wang ZW - Nat Commun (2014)

Postsynaptic receptor sensitivities and ePSCs were normal inslo-2(nf101). A. Comparison of muscle cell response topressure-ejected acetylcholine (ACh, 100 μM) or GABA (100 μM) between wildtype (WT) and slo-2(nf101). B. Comparison of ePSC between WTand slo-2(nf101) in the presence of two different extracellularCa2+ concentrations (5 mM and 0.5 mM). Data are shown as mean± SE. No significant difference was detected (unpaired t-test).The holding voltage was −60 mV in all the experiments. The numbers inside thecolumns indicate the sample sizes (n). All the recordings were performedwith pipette solution I. The recordings of ePSC at 0.5 mM[Ca2+]o were performed with extracellularsolution II whereas the remaining recordings were recorded with extracellular solutionI.
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Related In: Results  -  Collection

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Figure 4: Postsynaptic receptor sensitivities and ePSCs were normal inslo-2(nf101). A. Comparison of muscle cell response topressure-ejected acetylcholine (ACh, 100 μM) or GABA (100 μM) between wildtype (WT) and slo-2(nf101). B. Comparison of ePSC between WTand slo-2(nf101) in the presence of two different extracellularCa2+ concentrations (5 mM and 0.5 mM). Data are shown as mean± SE. No significant difference was detected (unpaired t-test).The holding voltage was −60 mV in all the experiments. The numbers inside thecolumns indicate the sample sizes (n). All the recordings were performedwith pipette solution I. The recordings of ePSC at 0.5 mM[Ca2+]o were performed with extracellularsolution II whereas the remaining recordings were recorded with extracellular solutionI.
Mentions: The larger persistent current of cholinergic PSC bursts observed inslo-2(nf101) could have resulted from either increased neurotransmitterrelease or increased postsynaptic receptor sensitivity to ACh. To examine the secondpossibility, we compared the amplitude of inward current caused by pressure-ejectingexogenous ACh (100 μM) to body-wall muscle cells between wild type andslo-2(nf101). A similar experiment with exogenous GABA (100 μM)was also performed although GABA did not contribute to the PSC bursts under theexperimental conditions27. We found thatamplitudes of ACh- and GABA-induced inward current were similar between wild type andslo-2(nf101) (Figure 4A). Thus,the larger persistent current of PSC bursts in slo-2(nf101) did notresult from an increased postsynaptic receptor function or expression.

Bottom Line: Loss-of-function mutation of slo-2 increases the duration and charge transfer rate of spontaneous postsynaptic current bursts at the neuromuscular junction, which are physiological signals used by motor neurons to control muscle cells, without altering postsynaptic receptor sensitivity.SLO-2 activity in motor neurons depends on Ca(2+) entry through EGL-19, an L-type voltage-gated Ca(2+) channel (CaV1), but not on other proteins implicated in either Ca(2+) entry or intracellular Ca(2+) release.Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030, USA.

ABSTRACT
Slo2 channels are prominent K(+) channels in mammalian neurons but their physiological functions are not well understood. Here we investigate physiological functions and regulation of the Caenorhabditis elegans homologue SLO-2 in motor neurons through electrophysiological analyses of wild-type and mutant worms. We find that SLO-2 is the primary K(+) channel conducting delayed outward current in cholinergic motor neurons, and one of two K(+) channels with this function in GABAergic motor neurons. Loss-of-function mutation of slo-2 increases the duration and charge transfer rate of spontaneous postsynaptic current bursts at the neuromuscular junction, which are physiological signals used by motor neurons to control muscle cells, without altering postsynaptic receptor sensitivity. SLO-2 activity in motor neurons depends on Ca(2+) entry through EGL-19, an L-type voltage-gated Ca(2+) channel (CaV1), but not on other proteins implicated in either Ca(2+) entry or intracellular Ca(2+) release. Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

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