The interpretation of spike potentials of motoneurones.
About: This article is published in The Journal of Physiology.The article was published on 1957-12-03 and is currently open access. It has received 369 citations till now. The article focuses on the topics: Spike (software development).
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TL;DR: The action potential of the squid giant axon is formed by just two voltage-dependent conductances in the cell membrane, yet mammalian central neurons typically express more than a dozen different types of voltage- dependent ion channels.
Abstract: The action potential of the squid giant axon is formed by just two voltage- dependent conductances in the cell membrane, yet mammalian central neurons typically express more than a dozen different types of voltage-dependent ion channels. This rich repertoire of channels allows neurons to encode information by generating action potentials with a wide range of shapes, frequencies and patterns. Recent work offers an increasingly detailed understanding of how the expression of particular channel types underlies the remarkably diverse firing behaviour of various types of neurons.
1,426 citations
TL;DR: Experiments using simultaneous patch-pipette recordings show that the site of action potential initiation is in the axon, even when synaptic activation is powerful enough to elicit dendritic electrogenesis, and that following initiation, action potentials actively backpropagate into the dendrites of many neuronal types, providing a retrograde signal of neuronal output to thedendritic tree.
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TL;DR: Modeling studies and simultaneous somatic and axonal recordings showed that distal Nav1.6 promotes action potential initiation, whereas proximal Nav 1.2 promotes its backpropagation to the soma.
Abstract: The distal end of the axon initial segment (AIS) is the preferred site for action potential initiation in cortical pyramidal neurons because of its high Na(+) channel density. However, it is not clear why action potentials are not initiated at the proximal AIS, which has a similarly high Na(+) channel density. We found that low-threshold Na(v)1.6 and high-threshold Na(v)1.2 channels preferentially accumulate at the distal and proximal AIS, respectively, and have distinct functions in action potential initiation and backpropagation. Patch-clamp recording from the axon cut end of pyramidal neurons in the rat prefrontal cortex revealed a high density of Na(+) current and a progressive reduction in the half-activation voltage (up to 14 mV) with increasing distance from the soma at the AIS. Further modeling studies and simultaneous somatic and axonal recordings showed that distal Na(v)1.6 promotes action potential initiation, whereas proximal Na(v)1.2 promotes its backpropagation to the soma.
584 citations
TL;DR: In this paper, simultaneous dual and triple patch pipette recordings from different locations on neocortical layer 5 pyramidal neurons in brain slices from 4-week-old rats (P26-30) at physiological temperatures were used to study the initiation and propagation of action potentials evoked by extracellular synaptic stimulation.
Abstract: 1. Initiation and propagation of action potentials evoked by extracellular synaptic stimulation was studied using simultaneous dual and triple patch pipette recordings from different locations on neocortical layer 5 pyramidal neurons in brain slices from 4-week-old rats (P26-30) at physiological temperatures. 2. Simultaneous cell-attached and whole-cell voltage recordings from the apical trunk (up to 700 microns distal to the soma) and the soma indicated that proximal synaptic stimulation (layer 4) initiated action potentials first at the soma, whereas distal stimulation (upper layer 2/3) could initiate dendritic regenerative potentials prior to somatic action potentials following stimulation at higher intensity. 3. Somatic action potentials, once initiated, propagated back into the apical dendrites in a decremented manner which was frequency dependent. The half-width of back propagating action potentials increased and their maximum rate of rise decreased with distance from the soma, with the peak of these action potentials propagating with a conduction velocity of approximately 0.5 m s-1. 4. Back-propagation of action potentials into the dendritic tree was associated with dendritic calcium electrogenesis, which was particularly prominent during bursts of somatic action potentials. 5. When dendritic regenerative potentials were evoked prior to somatic action potentials, the more distal the dendritic recording was made from the soma the longer the time between the onset of the dendritic regenerative potential relative to somatic action potential. This suggested that dendritic regenerative potentials were initiated in the distal apical dendrites, possibly in the apical tuft. 6. At any one stimulus intensity, the initiation of dendritic regenerative potentials prior to somatic action potentials could fluctuate, and was modulated by depolarizing somatic or hyperpolarizing dendritic current injection. 7. Dendritic regenerative potentials could be initiated prior to somatic action potentials by dendritic current injections used to simulate the membrane voltage change that occurs during an EPSP. Initiation of these dendritic potentials was not affected by cadmium (200 microM), but was blocked by TTX (1 microM). 8. Dendritic regenerative potentials in some experiments were initiated in isolated from somatic action potentials. The voltage change at the soma in response to these dendritic regenerative events was small and subthreshold, showing that dendritic regenerative events are strongly attenuated as they spread to the soma. 9. Simultaneous whole-cell recordings from the axon initial segment and the soma indicated that synaptic stimulation always initiated action potentials first in the axon. The further the axonal recording was made from the soma the greater the time delay between axonal and somatic action potentials, indicating a site of action potential initiation in the axon at least 30 microns distal to the soma. 10. Simultaneous whole-cell recordings from the apical dendrite, soma and axon initial segment showed that action potentials were always initiated in the axon prior to the soma, and with the same latency difference, independent of whether dendritic regenerative potentials were initiated or not. 11. It is concluded that both the apical dendrites and the axon of neocortical layer 5 pyramidal neurons in P26-30 animals are capable of initiating regenerative potentials. Regenerative potentials initiated in dendrites, however, are significantly attenuated as they spread to the soma and axon. As a consequence, action potentials are always initiated in the axon before the soma, even when synaptic activation is intense enough to initiate dendritic regenerative potentials. Once initiated, the axonal action potentials are conducted orthogradely into the axonal arbor and retrogradely into the dendritic tree.
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TL;DR: This article concludes a series of papers concerned with the flow of electric current through the surface membrane of a giant nerve fibre by putting them into mathematical form and showing that they will account for conduction and excitation in quantitative terms.
Abstract: This article concludes a series of papers concerned with the flow of electric current through the surface membrane of a giant nerve fibre (Hodgkinet al, 1952,J Physiol116, 424–448; Hodgkin and Huxley, 1952,J Physiol116, 449–566) Its general object is to discuss the results of the preceding papers (Section 1), to put them into mathematical form (Section 2) and to show that they will account for conduction and excitation in quantitative terms (Sections 3–6)
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TL;DR: The present experiments show that the antidromic activation of certain groups of motoneurons does condition the reflex discharges of other moto-neurons, and it is not necessary to infer from the early onset of inhibition that a specific inhibitory action is produced by the arrival of impulses at the synapses made by the recurrent collaterals with other neurons.
Abstract: SOME spinal motoneurons are equipped with recurrent collaterals which arise from the axon near its origin and terminate in association with other neurons of the ventral horn (cf. Cajal, 1909). An impulse that sweeps over the motor axon must also invade its collaterals. Does it then affect the excita-bility of the neurons in association with which the collaterals terminate? Miiller (1835) could produce no muscular contractions by stimulating the central end of a cut motor root. Others have likewise failed to find evidence that an antidromic volley produces either a centrifugal discharge in motor axons or activity in other nerve tracts In the absence of known excitatory effects it has been suggested that impulses in recurrent collaterals might lead to inhibition of the activity in the neurons to which they pass (Graham Brown, 1914; Gesell, 1940). The collaterals would then be an important part of the mechanism for reciprocal innervation. Forbes and his collaborators (1933) put the suggestion of Graham Brown to a careful experimental test. They found that a contralaterally evoked reflex discharge into the tibia1 nerve is not conditioned by antidromic volleys arriving at the cord in the motor axons of the peroneal nerve. The present experiments show that the antidromic activation of certain groups of motoneurons does condition the reflex discharges of other moto-neurons. The conditioning effect is often inhibitory. It is then neither preceded by facilitation nor delayed; inhibition is present when the antidromic volley reaches the cord approximately simultaneously with an afferent volley which fires the testing motoneurons directly after a single synaptic delay. The inhibition must then be caused by events occurring during the synaptic delay at the motoneurons-a period of only 0.9 msec. or less (Lorente de No, 1938; Renshaw, 1940). The conditioning volley cannot have fired either the tested motoneurons or premotor interneurons in time for the refractori-ness (subnormality) which follows activity to mediate the response deficit (cf. Gasser, 1937a, b; Lorente de No, 1936). In a discussion of this phenomenon it would be misleading to focus attention only upon the possible role of recurrent collaterals. It is not necessary to infer from the early onset of inhibition that a specific inhibitory action is produced by the arrival of impulses at the synapses made by the recurrent collaterals with other neurons. As Grundfest (1940) has pointed out, an alternative explanation for findings of this sort is suggested by the fact that
487 citations