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Spike-timing-dependent plasticity

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Spike-timing-dependent plasticity (STDP) is a biological process that adjusts the strength of connections between neurons in the brain. STDP adjusts connection strengths based on the relative timing of a particular neuron's input and output. Neurons in the communicate with brief electrical pulses referred to as spikes and the STDP process utilises this. Under the STDP process, if an input spike to a neuron tends, on average, to occur immediately before that neuron's output spike, then that particular input is made somewhat stronger. If an input spike tends, on average, to occur immediately after an output spike, then that particular input is made somewhat weaker. Thus, inputs that might be causing the spiking of a neuron are made even more likely to contribute in the future, while inputs that are not causing the neuron to spike are made less likely to contribute in the future. The process continues until a subset of the initial set of connections remain, while the influence of all others is reduced to 0.

The overall effect is to reduce a neuron's inputs to those that are most correlated. Although the process occurs throughout the brain, its implementation is achieved at the level of individual neurons, as the process is intrinsic and there is no need for any central oversight. The STDP process is analogous to evolution in that initial random variation undergoes a process of negative selection using a simple mechanism that creates complex and useful final organisation without the need for any central oversight, design, or control.

History

Early experiments on associative plasticity were carried out by W. B. Levy and O. Steward in 1983[1] and examined the effect of relative timing of pre and postsynaptic action potentials at millisecond level on plasticity. Bruce McNaughton contributed much to this area, too. Y.Dan and M. Poo in 1992 on neuromuscular, D. Debanne, B. Gähwiler and S. Thompson in 1994 on the hippocampus, showed that asynchronous pairing of postsynaptic and synaptic activity induced long-term synaptic depression. However, STDP was more definitively demonstrated by Henry Markram in his postdoc period till 1993 in Bert Sakman's lab (SFN and Phys Soc abstracts in 1994–1995) which was only published in 1997.[2] C. Bell and co-workers also found a form of STDP in the cerebellum. Henry Markram used dual patch clamping techniques to repetitively activate pre-synaptic neurons 10 milliseconds before and after the post-synaptic target neurons, and found the strength of the synapse increased. When the activation order was reversed so that the pre-synaptic neuron was activated 10 milliseconds after its post-synaptic target neuron, the strength of the pre-to-post synaptic connection decreased. Further work, by Guoqiang Bi, Li Zhang, and Huizhong Tao in Mu-Ming Poo's lab in 1998,[3] continued the mapping of the entire time course relating pre- and post-synaptic activity and synaptic change, to show that in their preparation synapses that are activated within 5-40 ms before a postsynaptic spike are strengthened, and those that are activated within a similar time window after the spike are weakened. This phenomenon has been observed in various other preparations, with some variation in the time-window relevant for plasticity. Several reasons for timing-dependent plasticity have been suggested. For example, STDP might operate as a learning rule that maximizes the mutual information between inputs and outputs of simple networks, and provide a function for Hebbian learning and development[4]. Works from Y. Dan's lab advanced to study STDP in in vivo systems.[5]

Mechanisms

Postsynaptic NMDA receptors are highly sensitive to the membrane potential (see coincidence detection in neurobiology). Due to their high permeability for calcium, they generate a local chemical signal that is largest when the back-propagating action potential in the dendrite arrives shortly after the synapse was active (pre-post spiking). Large postsynaptic calcium transients are known to trigger synaptic potentiation (LTP). The mechanism for spike-timing-dependent depression is less well understood, but often involves either postsynaptic voltage-dependent calcium entry/mGluR activation, or retrograde endocannabinoids and presynaptic NMDARs.

From Hebbian Rule to STDP

According to the Hebbian Rule synapses increase their efficiency if the synapse persistently causes the postsynaptic target neuron to generate action potentials. An often used but not entirely accurate simplification is those who fire together, wire together. With recent advancements in technology we can more precisely measure the spike timing of neurons. As it turns out, the synaptic connection between two neurons is more likely to strengthen if the presynaptic neuron fires off shortly before the postsynaptic neuron. Revisiting, the Hebbian rule, we can tweak it to accommodate the new model. Synapses increase their efficacy if the presynaptic neuron is activated momentarily before the postsynaptic neuron is activated. OR Synapses in which the pre-synaptic input fired before the postsynaptic cell get stronger; in the inverse situation, the synapse gets weaker.

See also

References

  1. ^ Levy WB, Steward O (1983). "Temporal contiguity requirements for long-term associative potentiation/depression in the hippocampus". Neuroscience. 8 (4): 791–7. doi:10.1016/0306-4522(83)90010-6. PMID 6306504. {{cite journal}}: Unknown parameter |month= ignored (help) [1]
  2. ^ Markram H, Lübke J, Frotscher M, Sakmann B (1997). "Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs". Science. 275 (5297): 213–5. doi:10.1126/science.275.5297.213. PMID 8985014. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ Bi GQ, Poo MM (15 December 1998). "Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type". J. Neurosci. 18 (24): 10464–72. PMID 9852584.
  4. ^ Song S, Miller KD, Abbott LF (2000). "Competitive Hebbian learning through spike-timing-dependent synaptic plasticity". Nat. Neurosci. 3 (9): 919–26. doi:10.1038/78829. PMID 10966623. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ Meliza CD, Dan Y (2006), "Receptive-field modification in rat visual cortex induced by paired visual stimulation and single-cell spiking", Neuron, 49 (2): 183–189, doi:10.1016/j.neuron.2005.12.009

Further reading

  • Senn W, Markram H, Tsodyks M (2001). "An algorithm for modifying neurotransmitter release probability based on pre- and postsynaptic spike timing". Neural Comput. 13 (1): 35–67. doi:10.1162/089976601300014628. PMID 11177427. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • Lisman J, Spruston N (2005). "Postsynaptic depolarization requirements for LTP and LTD: a critique of spike timing-dependent plasticity". Nat. Neurosci. 8 (7): 839–41. PMID 16136666. {{cite journal}}: Unknown parameter |month= ignored (help)
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