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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
Coincidence detection in neurobiology is a mechanism to encode neural information based on separate yet concurrent input signals on a target neuron. This concept is a breakthrough in the understanding of neural processes and the formation of computational maps in the brain. The study of coincidence detection has contributed to fields such as neurobiology, neurophysiology, and neuroethology.
Philosophy
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Coincidence detection relies on two separate inputs converging on a common target. In some cases, the timing of these two inputs is important because the inputs may push the membrane potential of a target neuron over the threshold required to create an action potential. If the two inputs fire at two different times, the depolarization of the first input may have time to drop significantly. This could prevent the membrane potential of the target neuron from reaching the action potential threshold even with the help of the second depolarizing input. In other situations, specific timing of the signals is not as important. The target neuron simply needs to receive neural signaling from two separate neurons. This may lead to long-term potentiation or long-term depression through associativity and affect learning and neuroplasticity.
Computational Maps
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When a sound is heard, sound waves may reach the ears at different times. This is referred to as the interaural time difference(ITD). Coincidence detection has been shown to be a major factor in sound localization along the azimuth plane due to a neural interpretation of an ITD. In 1948, Lloyd Jeffress proposed a model that converted timing differences into a spatial map that could be found within the brain. Jeffress claimed that delay lines from both the right and left ear converge on coincidence detectors that fire maximally when receiving simultaneous inputs from both ears. Due to a finite conduction speed within axons, different coincidence detector neurons would fire when sound came Synaptic Plasticity and Associativity
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An important property of long-term potentiation is associativity. A weak neuronal stimulation onto a 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. This process suggests that two neuronal pathways converging on the same cell may both strengthen if stimulated coincidentally. This is a simple model that provides an explanation for learning and memory.
Molecular Mechanism of Long-term Potentiation
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LTP in the hippocampus requires a prolonged depolarization that can expel the Mg2+ block of postsynaptic NMDA receptors. The removal of the Mg2+ block allows the flow of Ca2+ into the cell. A large elevation of calcium levels activate protein kinases that ultimately increase the number of postsynaptic AMPA receptors. This increases the sensitivity of the postsynaptic cell to glutamate. As a result, both synapses strengthen. The prolonged depolarization needed for the expulsion of Mg2+ from NMDA receptors requires a high frequency stimulation (Purves 2004). Associativity becomes a factor because this can be achieved through two simultaneous inputs that may not be strong enough to activate LTP by themselves.
Molecular Mechanism of Long-term Depression
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Long-term depression also works through associative properties although it is not always the reverse process of LTP. LTD in the cerebellum requires simultaneous stimulation of parallel fibers and climbing fibers. Glutamate released from the parallel fibers activates AMPA receptors which depolarize the postsynaptic cell. The parallel fibers also activate metabotropic glutamate receptors that release the second messengers IP3 and DAG. The climbing fibers stimulate a large increase in postsynaptic Ca2+ levels when activated. The Ca2+, IP3, and DAG work together in a signal transduction pathway to internalize AMPA receptors and decrease the sensitivity of the postsynaptic cell to glutamate (Purves 2004).
Further Reading
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- http://www.neurophys.wisc.edu/yin/jorissmithyin98.pdf
- http://jp.physoc.org/cgi/content/abstract/518/1/109
- http://bbsonline.cup.cam.ac.uk/Preprints/OldArchive/bbs.neur4.crepel.html
- http://www.jneurosci.org/cgi/content/full/26/16/4166
Neuroethology | ||
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Concepts in Neuroethology |
Feedforward · Coincidence detector · Umwelt · Instinct · Feature detector · Central pattern generator (CPG) ·NMDA receptor · Lateral inhibition · Fixed action pattern · Krogh's Principle·Hebbian theory· Sound localization | |
History of Neuroethology |
Theodore Holmes Bullock · Walter Heiligenberg ·Niko Tinbergen· Konrad Lorenz· Eric Knudsen·
Donald Griffin · Donald Kennedy · Karl von Frisch · Erich von Holst · Jörg-Peter Ewert | |
Methods in Neuroethology | ||
Model Systems in Neuroethology |
Animal Echolocation · Waggle Dance· Electric Fish · Vision in toads · Neuroethology of Frog Audition · Infrared sensing in snakes |
References
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- Joris et al. 1998. Coincidence Detection in the Auditory System: 50 Years after Jeffress. 21:1235-1238.
- Purves et al. 2004. Neuroscience. Sinauer Associates Inc: Sunderland, MA. pp. 575-608.
- Zupanc, G.K.H. 2004. Behavioral Neurobiology: An Integrative Approach. Oxford University Press: Oxford, UK. pp. 133-150
See Also
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- Neurobiology
- Sound localization
- Long-term potentiation
- Long-term depression
- Hebbian theory
- Coincidence circuit
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