Signal propagation along the axon (original) (raw)
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Action Potential Initiation and Propagation in CA3 Pyramidal Axons
Journal of Neurophysiology, 2007
Dentate gyrus granule cells transmit action potentials (APs) along their unmyelinated mossy fibre axons to the CA3 region. Although the initiation and propagation of APs are fundamental steps during neural computation, little is known about the site of AP initiation and the speed of propagation in mossy fibre axons. To address these questions, we performed simultaneous somatic and axonal whole-cell recordings from granule cells in acute hippocampal slices of adult mice at ∼23 • C. Injection of short current pulses or synaptic stimulation evoked axonal and somatic APs with similar amplitudes. By contrast, the time course was significantly different, as axonal APs had a higher maximal rate of rise (464 ± 30 V s −1 in the axon versus 297 ± 12 V s −1 in the soma, mean ± S.E.M.). Furthermore, analysis of latencies between the axonal and somatic signals showed that APs were initiated in the proximal axon at ∼20-30 μm distance from the soma, and propagated orthodromically with a velocity of 0.24 m s −1 . Qualitatively similar results were obtained at a recording temperature of ∼34 • C. Modelling of AP propagation in detailed cable models of granule cells suggested that a ∼4 times higher Na + channel density (∼1000 pS μm −2 ) in the axon might account for both the higher rate of rise of axonal APs and the robust AP initiation in the proximal mossy fibre axon. This may be of critical importance to separate dendritic integration of thousands of synaptic inputs from the generation and transmission of a common AP output.
Axonal Speeding: Shaping Synaptic Potentials in Small Neurons by the Axonal Membrane Compartment
Neuron, 2007
The role of the axonal membrane compartment in synaptic integration is usually neglected. We show here that in interneurons of the cerebellar molecular layer, where dendrites are so short that the somatodendritic domain can be considered isopotential, the axonal membrane contributes a significant part of the cell input capacitance. We examine the impact of axonal membrane on synaptic integration by cutting the axon with two-photon illumination. We find that the axonal compartment acts as a sink for signals generated at fast conductance synapses, thus increasing the initial decay rate of corresponding synaptic potentials over the value predicted from the resistance-capacitance (RC) product of the cell membrane; signals generated at slower synapses are much less affected. This mechanism sharpens the spike firing precision of fast glutamatergic inputs without resorting to multisynaptic pathways.
Tracking individual action potentials throughout mammalian axonal arbors
eLife, 2017
Axons are neuronal processes specialized for conduction of action potentials (APs). The timing and temporal precision of APs when they reach each of the synapses are fundamentally important for information processing in the brain. Due to small diameters of axons, direct recording of single AP transmission is challenging. Consequently, most knowledge about axonal conductance derives from modeling studies or indirect measurements. We demonstrate a method to noninvasively and directly record individual APs propagating along millimeter-length axonal arbors in cortical cultures with hundreds of microelectrodes at microsecond temporal resolution. We find that cortical axons conduct single APs with high temporal precision (~100 µs arrival time jitter per mm length) and reliability: in more than 8,000,000 recorded APs, we did not observe any conduction or branch-point failures. Upon high-frequency stimulation at 100 Hz, successive became slower, and their arrival time precision decreased by...
Sodium channel slow inactivation normalizes firing in axons with uneven conductance distributions
SummaryThe Na+channels that are important for action potentials show rapid inactivation, a state in which they do not conduct, although the membrane potential remains depolarized1,2. Rapid inactivation is a determinant of millisecond scale phenomena, such as spike shape and refractory period. Na+channels also inactivate orders of magnitude more slowly, and therefore have impacts on excitability over much longer time scales than those of a single spike or a single inter-spike interval3-9. Here, we focus on the contribution of slow inactivation to the resilience of axonal excitability10,11when ion channels are unevenly distributed across the axonal membrane. We study models in which the voltage-gated Na+and K+channels are unevenly distributed along axons with different variances, capturing the heterogeneity that biological axons display12. In the absence of slow inactivation many conductance distributions result in spontaneous tonic activity. Faithful axonal propagation is achieved wi...
Electrogenic Tuning of the Axon Initial Segment
The Neuroscientist, 2009
Action potentials (APs) provide the primary means of rapid information transfer in the nervous system. Where exactly these signals are initiated in neurons has been a basic question in neurobiology and the subject of extensive study. Converging lines of evidence indicate that APs are initiated in a discrete and highly specialized portion of the axon-the axon initial segment (AIS). The authors review key aspects of the organization and function of the AIS and focus on recent work that has provided important insights into its electrical signaling properties. In addition to its main role in AP initiation, the new findings suggest that the AIS is also a site of complex AP modulation by specific types of ion channels localized to this axonal domain.
Journal of Neuroscience, 2011
The shape of action potentials invading presynaptic terminals, which can vary significantly from spike waveforms recorded at the soma, may critically influence the probability of synaptic neurotransmitter release. Revealing the conductances that determine spike shape in presynaptic boutons is important for understanding how changes in the electrochemical context in which a spike is generated, such as subthreshold depolarization spreading from the soma, can modulate synaptic strength. Utilizing recent improvements in the signal-to-noise ratio of voltagesensitive dye imaging in mouse brain slices, we demonstrate that intracortical axon collaterals and en passant presynaptic terminals of layer 5 pyramidal cells exhibit a high density of Kv1 subunit-containing ion channels, which generate a slowly inactivating K ϩ current critically important for spike repolarization in these compartments. Blockade of the current by low doses of 4-aminopyridine or ␣-dendrotoxin dramatically slows the falling phase of action potentials in axon collaterals and presynaptic boutons. Furthermore, subthreshold depolarization of the soma broadened action potentials in collaterals bearing presynaptic boutons, an effect abolished by blocking Kv1 channels with ␣-dendrotoxin. These results indicate that action potential-induced synaptic transmission may operate through a mix of analog-digital transmission owing to the properties of Kv1 channels in axon collaterals and presynaptic boutons.
The Action Potential, Synaptic Transmission, and Maintenance of Nerve Function eBook
1. Nongated ion channels establish the resting membrane potential of neurons; voltage-gated ion channels are responsible for the action potential and the release of neurotransmitter. 2. Ligand-gated ion channels cause membrane depolarization or hyperpolarization in response to neurotransmitter. 3. Nongated ion channels are distributed throughout the neuronal membrane; voltage-gated channels are largely restricted to the axon and its terminals, while ligand-gated channels predominate on the cell body (soma) and dendritic membrane. 4. Membrane conductance and capacitance affect ion flow in neurons. 5. An action potential is a transient change in membrane potential characterized by a rapid depolarization followed by a repolarization; the depolarization phase is due to a rapid activation of voltage-gated sodium channels and the repolarization phase to an inactivation of the sodium channels and the delayed activation of voltage-gated potassium channels. 6. Initiation of an action potential occurs when an axon hillock is depolarized to a threshold for rapid activation of a large number of voltage-gated sodium channels.
Action potential generation requires a high sodium channel density in the axon initial segment
Nature Neuroscience, 2008
The axon initial segment (AIS) is a specialized region in neurons where action potentials are initiated. It is commonly assumed that this process requires a high density of voltage-gated sodium (Na 1) channels. Paradoxically, the results of patch-clamp studies suggest that the Na 1 channel density at the AIS is similar to that at the soma and proximal dendrites. Here we provide data obtained by antibody staining, whole-cell voltage-clamp and Na 1 imaging, together with modeling, which indicate that the Na 1 channel density at the AIS of cortical pyramidal neurons is~50 times that in the proximal dendrites. Anchoring of Na 1 channels to the cytoskeleton can explain this discrepancy, as disruption of the actin cytoskeleton increased the Na 1 current measured in patches from the AIS. Computational models required a high Na 1 channel density (~2,500 pS lm-2) at the AIS to account for observations on action potential generation and backpropagation. In conclusion, action potential generation requires a high Na 1 channel density at the AIS, which is maintained by tight anchoring to the actin cytoskeleton.
Journal of neurophysiology, 1990
1. The effect of presynaptic, axoaxonal inhibition, that exerts its action by producing a local conductance increase, on the behavior of action potentials at postsynaptic axon terminals is analyzed computationally. The significance of the location and strength of the presynaptic inhibition, as well as the morphology and membrane properties of the axonal terminals, are considered. 2. Keeping the specific properties of terminal membrane and axoplasm constant, the critical "silent" steady-state conductance change (gcrit) that blocks propagation is linearly scaled with the terminal diameter raised to the 3/2 power. At the midpoint of a 5 lambda long, 1 micron diameter axon that has the standard Hodgkin and Huxley (1952) kinetics at 18 degrees C (and an input conductance of 8.7 nS), gcrit is 72 nS. At 0 degrees C, gcrit = 200 nS, whereas at 30 degrees C gcrit = 30 nS. 3. The critical conductance change that blocks propagation depends steeply on the density of excitable channels...