Recent papers have described spiking behaviour on the dendrites of neurons. This page provides some background (for an introduction see [1]), and then speculates on some possible implications.
The purpose of this is page is to encourage discussion.
I will update the page and credit the contributors from time to time: please use the email address at the end to send comments.
The traditional view of spikes being generated at the axon hillock, and actively transmitted along the axon, but only passively transmitted (if transmitted at all) along the dendrite appears to be only partially correct. Although the idea of antidromic spikes invading the dendrite from the soma is not new (reviewed in [2]), Stuart and Sakmann [3] describe what appear to be fast Na
Antidromic spikes provide a mechanism for Hebbian synaptic modification [5]: the conjunction of the antidromic spike and an EPSP (excitatory post-synaptic potential) leads to the increase in the efficacy of an excitatory synapse. Markram et al [6] go further, suggesting firstly that NMDA receptors are crucial to this synaptic modification, and further that the occurrence of the presynaptic EPSP 10ms before the action potential leads to increased efficacy of the excitatory synapse, whereas the occurrence of the presynaptic EPSP 10ms after the AP (action potential) leads to a decrease in efficacy.
Smith [7] suggests that this provides a basis for differential Hebbian learning [8].
Antidromic spikes provide a neurophysiological basis for a form of Hebbian learning in which EPSPs partially responsible for the cell firing are rewarded by having their efficacy increased. One interpretation for this is in terms of an arrow of time. An event which (slightly) precedes another event results in first one neuron then another neuron firing due to their connections from the environment. If this occurs a number of times, and if the two neurons are linked by an excitatory synapse, then this connection will be strengthened.
Could this time-asymmetry be at the root of our perceptual sense of time? The time intervals involved (about 10ms) are of the right order of magnitude for human time-perception.
Alternatively, could the relative timings underlie the timing effects found in classical conditioning? Could they be at the root of the differences in effect found when the unconditioned stumulus (US) precedes or does not precede the conditioned stimulus (CS)?
What would the effect of disabling the invasion of the axon-hillock spike into the dendrite be? If, as Markram et al [6] suggest, the dendritic spike is important in EPSP alteration, would its absence lead to stasis in the state of excitatory synapses? Can one separately inhibit the AP on the axon from the AP on the dendrite? If so, what would the perceptual effect be?
If the antidromic spike is required for laying down memory traces, might its inhibition be a mechanism for the absence of memory traces during forms of anaesthesia? Could it underlie a possible pharmacological way of inhibiting the laying down of memory traces?
[1] Koch C., Computation and the single neuron, Nature, 385, 16 January 1997, 20-23, 1997.
[2] Llinas R.R., The intrinsic electrophysiological properties of mammalian neurons:insights into central nervous system function, Science, 242, 1654-1664, 1988.
[3] Stuart G.J., Sakmann B., Active propagation of somatic action potentials into neocortical pyramidal cell dendrites, Nature, 367, January 1994, 69-72, 1994.
[4] Mainen Z.F., Joerges J., Huguenard J.R., Sejnowski T.J., A model of spike initiation in neorcortical pyramidal neurons , Neuron, 15, 6, 1427-1439, 1995.
[5] Magee J.C., Johnston D., A synaptically controlled, associative signal for Hebbian plasticity in hippocampal neurons , Science, 275, 5297, 209-213, 1997.
[6] Markram H., Luebke J., Frotscher M., Sakmann B., Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs, Science, 275, 5297, 213-215, 1997.
[7] Smith L.S. Short-term synaptic depression and antidromic action potentials, unpublished letter, 1997 (.ps.Z available).
[8] Klopf A.H., A neuronal model of classical conditioning, Psychobiology, 16, 2, 85-125, 1988.
The purpose of this page is to get some discussion started! Please use email!
Home Page for Dr. Leslie Smith(lss@cs.stir.ac.uk).This page last updated 21 May 1997. You are visitor number 3811 to this page since 3 March 1997.