Properties and functions of Na(+)‐activated K+ channels in the soma of rat motoneurones.

Safronov, Boris V.; Vogel, Werner

doi:10.1113/jphysiol.1996.sp021803

Cited by 67 publications

(52 citation statements)

References 22 publications

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“…In mouse motoneurons in culture, unitary currents from SK channels have a ~18-pS conductance, a 3.5-ms mean open time, and show no voltage dependency (825). Na + -activated K + channels (I K Na ) are found in membrane patches from spinal motoneurons (1069). I K Na does not appear to contribute to single action potentials but gives rise to the postdischarge hyperpolarization that follows trains of action potentials, due to accumulation of internal Na + .…”

Section: Active Membrane Properties Of Motoneuronsmentioning

confidence: 99%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

528

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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Section: Active Membrane Properties Of Motoneuronsmentioning

confidence: 99%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

528

482

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“…Na ϩ -activated K ϩ channels (K Na ) have been shown to exist in many types of neurons (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). They are encoded for by two genes, Slick (Slo 2.1) and Slack (Slo 2.2) (11)(12)(13), and display a wide distribution in many regions in the brain (12,14,15).…”

mentioning

confidence: 99%

Na ⁺ -mediated coupling between AMPA receptors and K _Na channels shapes synaptic transmission

Nanou

Kyriakatos²,

Bhattacharjee³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Na ؉ -activated K ؉ (KNa) channels are expressed in neurons and are activated by Na ؉ influx through voltage-dependent channels or ionotropic receptors, yet their function remains unclear. Here we show that KNa channels are associated with AMPA receptors and that their activation depresses synaptic responses. Synaptic activation of KNa channels by Na ؉ transients via AMPA receptors shapes the decay of AMPA-mediated current as well as the amplitude of the synaptic potential. Thus, the coupling between KNa channels and AMPA receptors by synaptically induced Na ؉ transients represents an inherent negative feedback mechanism that scales down the magnitude of excitatory synaptic responses.ionotropic receptors ͉ Li ϩ ͉ Slack channels ͉ dendritic integration ͉ synaptic plasticity

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“…The two preferred amplitudes of the KNa channel in our recordings were 1·3 and 3·3 pA at 0 mV, equivalent to about 15 and 39 pS in the presence of 5·4 mÒ Ké and 145 mÒ Kï, respectively. These conductances are considerably smaller than those recorded in heart myocytes (130-207 pS; Kameyama et al 1984;Luk & Carmeliet, 1990) but close to those recorded under similar, and more physiological conditions in the nodal region of myelinated axons of Xenopus (34 pS; Koh et al 1994), rat motoneurones (44·8 pS; Safronov & Vogel, 1996), quail trigeminal ganglion neurones (50 pS; Haimann et al 1990) and chick brainstem neurones (50 pS; Dryer et al 1989). …”

Section: Discussionmentioning

confidence: 91%

“…Low densities have also been reported in other preparations. For example, only nine of about 100 membrane patches from the soma of rat motoneurones contained KNa channels (Safronov & Vogel, 1996). The conductance of KNa channels has been reported to vary almost 10-fold, from about 30 pS (Koh et al 1994) to more than 200 pS (Kameyama et al 1984).…”

Section: Discussionmentioning

confidence: 99%

“…However, spontaneous [Na¤]é transients could be as high as •20 mÒ (Rose & Ransom, 1997), a level high enough to activate KNa channels in some cell types (Dryer et al 1989;Haimann et al 1990;Dale, 1993;Koh et al 1994;Safronov & Vogel, 1996). Moreover, exposing cultured neurones to 50 ìÒ glutamate could induce, through activation of both NMDA and non-NMDA receptors, an increase in intracellular Na¤ to •60 mÒ that could last for more than 10 min after removal of glutamate (Kiedrowski et al 1994;Pinelis et al 1994).…”

Section: Kainate Evokes Na¤ Influx That Activates Kna Channelsmentioning

confidence: 99%

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Kainate induces an intracellular Na⁺‐activated K⁺ current in cultured embryonic rat hippocampal neurones

Liu

Schaffner

Barker

1998

The Journal of Physiology

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In embryonic rat hippocampal neurones cultured for < 3 days, kainate induced an inward current at negative potentials that recovered to baseline levels immediately upon termination of agonist application. However, in neurones cultured for longer, the kainate‐induced current was often followed by a long‐lasting inward current that slowly recovered to baseline levels. The amplitude of the delayed current (Idelay) triggered by kainate was positively related both to the duration of application at constant agonist concentration and to concentration at constant application duration. I delay could last for several minutes and was accompanied by a conductance increase, which closely paralleled current amplitude. Depression of the kainate‐induced current response at receptor level with CNQX or at ionic level with Na+‐free solution eliminated Idelay. However, when applied during Idelay neither CNQX nor Na+‐free solution had any effect on Idelay. Li+ effected the same response as Na+ in mediating kainate‐induced Idelay. GABA‐activated Cl− current, which was associated with the same amount of inwardly directed charge flow at the same potential as that induced by kainate, did not trigger a long‐lasting delayed current. I delay depended on the existence of extracellular K+ and its amplitude increased with the increase in K+ concentration. Neither applying Cl−‐ or Ca2+‐free solutions nor increasing intracellular Ca2+ buffering speed and capacity altered Idelay. Exposure to the specific KCa channel blockers apamin and charybdotoxin also failed to alter Idelay. However, Idelay could be blocked by Cs+, Ba2+ and high concentrations of 4‐aminopyridine (4‐AP) and TEA. Inside‐out excised patch‐clamp recordings revealed that low density or highly clustered Na+‐activated K+ channels were expressed in the cell bodies of cultured embryonic rat hippocampal neurones. These could be the elementary channels underlying Idelay.

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Properties and functions of Na(+)‐activated K+ channels in the soma of rat motoneurones.

Cited by 67 publications

References 22 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

Na ⁺ -mediated coupling between AMPA receptors and K _Na channels shapes synaptic transmission

Kainate induces an intracellular Na⁺‐activated K⁺ current in cultured embryonic rat hippocampal neurones

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Properties and functions of Na(+)‐activated K+ channels in the soma of rat motoneurones.

Cited by 67 publications

References 22 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

Na + -mediated coupling between AMPA receptors and K Na channels shapes synaptic transmission

Kainate induces an intracellular Na+‐activated K+ current in cultured embryonic rat hippocampal neurones

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Na ⁺ -mediated coupling between AMPA receptors and K _Na channels shapes synaptic transmission

Kainate induces an intracellular Na⁺‐activated K⁺ current in cultured embryonic rat hippocampal neurones