The electrical properties of the motoneurone membrane

Coombs, J. S.; Eccles, John C.; Fatt, P.

doi:10.1113/jphysiol.1955.sp005411

Cited by 417 publications

(237 citation statements)

References 18 publications

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“…For some time it has been known that the axon exhibits a high degree of regional specialization in its electrical properties linked to the diverse physiology of the neuron (15). Hence, to understand neuronal development it is important to learn how the regional differentiation of its surface arises and is maintained.…”

Section: Discussionmentioning

confidence: 99%

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Distribution and lateral mobility of voltage-dependent sodium channels in neurons [published erratum appears in J Cell Biol 1989 May;108(5):preceding 2001]

Angelides

Elmer

Loftus

et al. 1988

The Journal of Cell Biology

146

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Abstract. Voltage-dependent sodium channels are distributed nonuniformly over the surface of nerve cells and are localized to morphologically distinct regions. Fluorescent neurotoxin probes specific for the voltagedependent sodium channel stain the axon hillock 5-10 times more intensely than the cell body and show punctate fluorescence confined to the axon hillock which can be compared with the more diffuse and uniform labeling in the cell body. Using fluorescence photobleaching recovery (FPR) we measured the lateral mobility of voltage-dependent sodium channels over specific regions of the neuron. Nearly all sodium channels labeled with specific neurotoxins are free to diffuse within the cell body with lateral diffusion coefficients on the order of 10 -9 cm2/s. In contrast, lateral diffusion of sodium channels in the axon hillock is restricted, apparently in two different ways. Not only do sodium channels in these regions diffuse more slowly (10-1°-10 -H cm2/s), but also they are prevented from diffusing between axon hillock and cell body. No regionalization or differential mobilities were observed, however, for either tetramethylrhodaminephosphatidylethanolamine, a probe of lipid diffusion, or FITC-succinyl concanavalin A, a probe for glycoproteins. During the maturation of the neuron, the plasma membrane differentiates and segregates voltagedependent sodium channels into local compartments and maintains this localization perhaps either by direct cytoskeletal attachments or by a selective barrier to channel diffusion.

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Section: Discussionmentioning

confidence: 99%

“…Since the sodium channel system lends such unique excitability characteristics to the cell membrane (15), there is great interest in localizing and quantifying sodium channels at specific sites on the cell. This distribution of channels will determine some of the differential electrical properties of one part versus another part of a given excitable cell.…”

mentioning

confidence: 99%

Distribution and lateral mobility of voltage-dependent sodium channels in neurons [published erratum appears in J Cell Biol 1989 May;108(5):preceding 2001]

Angelides

Elmer

Loftus

et al. 1988

The Journal of Cell Biology

146

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“…Potassium citrate (2 M) rather than KCl-filled micro-electrodes were employed in order to eliminate C1 leakage from the micro-electrode (cf. Nishi et al 1974;Coombs, Eccles & Fatt, 1955).…”

Section: Methodsmentioning

confidence: 99%

Characterization and ionic basis of GABA‐induced depolarizations recorded in vitro from cat primary afferent neurones.

Gallagher¹,

Higashi²,

Nishi³

1978

The Journal of Physiology

311

133

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CIO-,. 7. Restoration of the GABA depolarization to its control level after augmentation by Cl-injection had a mean time constant of 27-8 + 2-6 min. Picrotoxin did not alter this value.8. When foreign anions were exchanged for Cl-in the perfusion solution, the ten anions smaller or equal to ClO3-, decreased the GABA depolarization by 50-90 % and increased its time course 1-5-20 x control. The only exception having a small radius was Br-which augmented the amplitude 10-30 %.9. The ten anions larger than C103-produced a biphasic effect, i.e. an initial Japan.J. P. GALLAGHER, H. HIGASHI AND S. NISHI augmentation followed by a marked (up to 100 %) depression of the response. Experiments with CH3COO-, CH3S04-, or HOCH2CH2SO3-, indicated that this depression was non-competitive.

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“…(Coombs, Eccles, and Fatt, 1955;Frank and Fuortes, 1956). This local spike will not spread over the rest of the cell, however, until the cell is depolarized by 30 or 40 Inv.…”

Section: Production 0]~ ~Otoneiyron Spikesmentioning

confidence: 99%

Steps in the Production of Motoneuron Spikes

Fuortes

Frank

Becker

1957

The Journal of General Physiology

303

147

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The first report on action potentials recorded with intracellular electrodes from motoneurons (Brock, Coombs, and Eccles, 1951) described orthodromic and antidromic spikes as identical except for presence of a synaptic potential at the foot of the spike evoked by orthodromic stimulation. It was later recognized (Brock et al., 1952 a and b) that a difference exists in the rising phase of spikes evoked by orthodromic or antidromic stimulation, and it was stated that antidromic spikes show an initial fast rise of about 35 mv., an inflection, and a further fast rise to peak, while the orthodromic spikes present an initial slow rise of about 10 mv. (the synaptic potential) an inflection there, and a further fast and smooth rise to peak. It was then suggested that " . . . the spike response of the neurone began at the inflection on the rising phase . . . . In the former [antidromic] the inflection indicates origin of the neuronal spike from the spike of the non-medullated axon, in the latter [orthodromic] its origin from the synaptic potential" (Brock el al., 1952 a, p. 440). This view was further developed in a later article (Brock et al., 1953) in which an attempt was also made to justify the difference of depolarization level required for initiation of soma firing following orthodromic or antidromic stimulation. Araki, Otani, and Furukawa (1953) working with toads noted that an inflection is often present also in the rising phase of orthodromically evoked spikes, and Araki and Otani (1955) recorded a similar inflection also in spikes evoked by direct stimulation of toad's motoneurons. They interpreted these findings by assuming that " . . . the non-myelinated segment is more excitable than the soma, so that the local current due to synaptic potential may excite it primarily, as suggested by Gesell" (Araki and Otani, 1955, p. 475). Frank and Fuortes (1955 b) confirmed the presence of an inflection in the rising phase of orthodromic spikes and showed in addition that orthodromically evoked spikes may be made to fall from the point of inflection just as occurs for antidromic

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The electrical properties of the motoneurone membrane

Cited by 417 publications

References 18 publications

Distribution and lateral mobility of voltage-dependent sodium channels in neurons [published erratum appears in J Cell Biol 1989 May;108(5):preceding 2001]

Distribution and lateral mobility of voltage-dependent sodium channels in neurons [published erratum appears in J Cell Biol 1989 May;108(5):preceding 2001]

Characterization and ionic basis of GABA‐induced depolarizations recorded in vitro from cat primary afferent neurones.

Steps in the Production of Motoneuron Spikes

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