Coincidence detection in neurobiology

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For the electronic device, see Coincidence circuit.

Coincidence detection is a

computational maps
in the brain.

Principles of coincidence detection

Fig. 1: Spatial and temporal summation. Two EPSPs innervated in rapid succession sum to produce a larger EPSP, or an action potential in the postsynaptic cell.

Coincidence detection relies on separate inputs converging on a common target. For example (Fig. 1), in a basic neural circuit with two input neurons—A and B—that have excitatory synaptic terminals converging on a single output neuron (C), if each input neuron's EPSP is sub-threshold for an action potential at C, then C cannot fire unless the two inputs from A and B are temporally close. The synchronous arrival of these two inputs may push the membrane potential of a target neuron over the threshold required to create an action potential. Conversely, if the two inputs temporally arrive too far apart, the depolarization of the first input may have time to drop significantly, preventing the membrane potential of the target neuron from reaching the action potential threshold. Hence, the function of coincidence detection is to reduce the jitter caused by spontaneous neuronal activity, and while random sub-threshold stimulations from cells may not often fire coincidentally, coincident synaptic inputs derived from a unitary external stimulus ensure that a target neuron will fire as a result of the stimulus.

Distal coincidence detection

The above description applies well to feedforward inputs to neurons, which provide inputs from either sensory nerves or lower-level regions in the brain. About 90% of interneural connections are, however, not feedforward but predictive (or modulatory, or attentional) in nature. These connections receive inputs mainly from nearby cells in the same layer as the receiving cell, and also from distant connections which are fed through Layer 1. The dendrites which receive these inputs are quite distant from the cell body, and therefore they exhibit different electrical and signal-processing behaviour compared with the proximal (or feedforward) dendrites described above.

In a short section (perhaps 40 

μm
long) of distal dendrite, the reaction to activations coming in on synapses to the dendritic spines acts to raise the overall local potential with each incoming signal. This rising potential acts against a background of decay in the potential back to the resting level. If sufficient signals are received within a short period of time (i.e. before the overall voltage decays to background), the voltage of the segment will rise above a threshold, giving rise to a non-linear dendritic spike, which travels, effectively undiminished, all the way to the cell body, and which causes it to become partially depolarised.

This is perhaps the most important form of dendritic coincidence detection in the brain. The more easily understood proximal activation acts over much longer time periods, and is thus much less sensitive to the time factor in coincidence detection.

Sound localization

Fig. 2: If a sound arrives at the left ear before the right ear, the impulse in the left auditory tract will reach X sooner than the impulse in the right auditory tract reaches Y. Neurons 4 or 5 may therefore receive coincident inputs.

Coincidence detection has been shown to be a major factor in

medial superior olive in mammals.[4]

Synaptic plasticity and associativity

In 1949,

pyramidal neuron may not induce long-term potentiation. However, this same stimulation paired with a simultaneous strong stimulation from another neuron will strengthen both synapses.[5]
This process suggests that two neuronal pathways converging on the same cell may both strengthen if stimulated coincidentally.

Molecular mechanism of long-term potentiation

glutamate. As a result, both synapses strengthen. The prolonged depolarization needed for the expulsion of Mg2+ from NMDA receptors requires a high frequency stimulation.[6]
Associativity becomes a factor because this can be achieved through two simultaneous inputs that may not be strong enough to activate LTP by themselves.

Besides the NMDA-receptor based processes, further cellular mechanisms allow of the association between two different input signals converging on the same neuron, in a defined timeframe. Upon a simultaneous increase in the intracellular concentrations of cAMP and Ca2+, a transcriptional coactivator called TORC1 (

adenylate cyclase activation, might also account for the detection of the repetitive stimulation of a given synapse
.

Adenylyl cyclase (also commonly known as adenyl cyclase and adenylate cyclase) has been implicated in memory formation as a coincidence detector.[8][9][10][11]

Molecular mechanism of long-term depression

Long-term depression also works through associative properties although it is not always the reverse process of LTP. LTD in the

signal transduction pathway to internalize AMPA receptors and decrease the sensitivity of the postsynaptic cell to glutamate.[6]

See also

References

  1. PMID 9012854
    .
  2. PMID 18904764
    .
  3. PMID 3186725
    .
  4. ^ Zupanc, G.K.H. 2004. Behavioral Neurobiology: An Integrative Approach. Oxford University Press: Oxford, UK. pp. 133-150
  5. S2CID 4339789
    .
  6. ^
    ISBN 9780878937257
    .
  7. PMID 17360587
    .
  8. PMID 17615394
    .
  9. S2CID 10849274
    .
  10. PMID 11264454
    .
  11. S2CID 12407397
    .

Further reading
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