Coincidence detection in neurobiology

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


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
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 from different positions along the azimuth (Joris 1998). Masakazu Konishi's study on barn owls shows that this is true. Sensory information from the hair cells of the ears travels to the ipsilateral nucleus magnocellularis. From here, the signals project ipsilaterally and contralaterally to two nucleus laminari. Each nucleus laminaris contains coincidence detectors that receive auditory input from the left and the right ear. Since the ispilateral axons enter the nucleus laminaris dorsally while the contralateral axons enter ventrally, sounds from various positions along the azimuth correspond directly to stimulation of different depths of the nucleus laminaris. From this information, a neural map of auditory space was formed. The function of the nucleus laminaris parallels that of the medial superior olive in mammals (Zupanc 2004).

Synaptic Plasticity and Associativity
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
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
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).