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- 2019
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Tidskriftsartikel (refereegranskat)
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- Hess, D, et al.
(författare)
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Characterization of Na+-activated K+ currents in larval lamprey spinal cord neurons
- 2007
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Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 97:5, s. 3484-3493
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Tidskriftsartikel (refereegranskat)abstract
- Potassium channels play an important role in controlling neuronal firing and synaptic interactions. Na+-activated K+ ( KNa) channels have been shown to exist in neurons in different regions of the CNS, but their physiological function has been difficult to assess. In this study, we have examined if neurons in the spinal cord possess KNa currents. We used whole cell recordings from isolated spinal cord neurons in lamprey. These neurons display two different KNa currents. The first was transient and activated by the Na+ influx during the action potentials, and it was abolished when Na+ channels were blocked by tetrodotoxin. The second KNa current was sustained and persisted in tetrodotoxin. Both KNa currents were abolished when Na+ was substituted with choline or N-methyl-d-glucamine, indicating that they are indeed dependent on Na+ influx into neurons. When Na+ was substituted with Li+, the amplitude of the inward current was unchanged, whereas the transient KNa current was reduced but not abolished. This suggests that the transient KNa current is partially activated by Li+. These two KNa currents have different roles in controlling the action potential waveform. The transient KNa appears to act as a negative feedback mechanism sensing the Na+ influx underlying the action potential and may thus be critical for setting the amplitude and duration of the action potential. The sustained KNa current has a slow kinetic of activation and may underlie the slow Ca2+-independent afterhyperpolarization mediated by repetitive firing in lamprey spinal cord neurons.
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- Nanou, E, et al.
(författare)
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Differential regulation of synaptic transmission by pre- and postsynaptic SK channels in the spinal locomotor network
- 2013
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Ingår i: Journal of neurophysiology. - : American Physiological Society. - 1522-1598 .- 0022-3077. ; 109:12, s. 3051-3059
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Tidskriftsartikel (refereegranskat)abstract
- The generation of activity in the central nervous system requires precise tuning of cellular properties and synaptic transmission. Neural networks in the spinal cord produce coordinated locomotor movements. Synapses in these networks need to be equipped with multiple mechanisms that regulate their operation over varying regimes to produce locomotor activity at different frequencies. Using the in vitro lamprey spinal cord, we explored whether Ca2+ influx via different routes in postsynaptic soma and dendrites and in presynaptic terminals can activate apamin-sensitive Ca2+-activated K+ (SK) channels and thereby shape synaptic transmission. We show that postsynaptic SK channels are tightly coupled to Ca2+ influx via NMDA receptors. Activation of these channels by synaptically induced NMDA-dependent Ca2+ transients restrains the time course of the synaptic current and the amplitude of the synaptic potential. In addition, presynaptic SK channels are activated by Ca2+ influx via voltage-gated channels and control the waveform of the action potential and the resulting Ca2+ dynamics in the axon terminals. The coupling of SK channels to different Ca2+ sources, pre- and postsynaptically, acts as a negative feedback mechanism to shape synaptic transmission. Thus SK channels can play a pivotal role in setting the dynamic range of synapses and enabling short-term plasticity in the spinal locomotor network.
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- Nanou, E, et al.
(författare)
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Mechanisms of modulation of AMPA-induced Na+-activated K+ current by mGluR1
- 2010
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Ingår i: Journal of neurophysiology. - : American Physiological Society. - 1522-1598 .- 0022-3077. ; 103:1, s. 441-445
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Tidskriftsartikel (refereegranskat)abstract
- Na+-activated K+ (KNa) channels can be activated by Na+ influx via ionotropic receptors and play a role in shaping synaptic transmission. In expression systems, KNa channels are modulated by G protein–coupled receptors, but such a modulation has not been shown for the native channels. In this study, we examined whether KNa channels coupled to AMPA receptors are modulated by metabotropic glutamate receptors (mGluRs) in lamprey spinal cord neurons. Activation of mGluR1 strongly inhibited the AMPA-induced KNa current. However, when intracellular Ca2+ was chelated with 1,2-bis(2-aminophenoxy)ethane- N,N,N′, N′-tetraacetic acid (BAPTA), the KNa current was enhanced by mGluR1. Activation of protein kinase C (PKC) mimicked the inhibitory effect of mGluR1 on the KNa current. Blockade of PKC prevented the mGluR1-induced inhibition of the KNa current, but did not affect the enhancement of the current seen in BAPTA. Together these results suggest that mGluR1 can differentially modulate AMPA-induced KNa current in a Ca2+- and PKC-dependent manner.
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