||This article may be too technical for most readers to understand. (November 2011)|
|Diagram of a gap junction|
An electrical synapse is a mechanical and electrically conductive link between two abutting neurons that is formed at a narrow gap between the pre- and postsynaptic neurons known as a gap junction. At gap junctions, such cells approach within about 3.5 nm of each other, a much shorter distance than the 20 to 40 nm distance that separates cells at chemical synapse. In many animals, electrical synapse-based systems co-exist with chemical synapses.
Compared to chemical synapses, electrical synapses conduct nerve impulses faster, but unlike chemical synapses they do not have gain (the signal in the postsynaptic neuron is the same or smaller than that of the originating neuron). Electrical synapses are often found in neural systems that require the fastest possible response, such as defensive reflexes. An important characteristic of electrical synapses is that most of the time, they are bidirectional, i.e. they allow impulse transmission in either direction. However, some gap junctions do allow for communication in only one direction.
Each gap junction (aka nexus junction) contains numerous gap junction channels which cross the membranes of both cells. With a lumen diameter of about 1.2 to 2.0 nm, the pore of a gap junction channel is wide enough to allow ions and even medium sized molecules like signaling molecules to flow from one cell to the next, thereby connecting the two cells' cytoplasm. Thus when the voltage of one cell changes, ions may move through from one cell to the next, carrying positive charge with them and depolarizing the postsynaptic cell.
Gap junction funnels are composed of two hemi-channels called connexons in vertebrates, one contributed by each cell at the synapse. Connexons are formed by six 7.5 nm long, four-pass membrane-spanning protein subunits called connexins, which may be identical or slightly different from one another.
- Without the need for receptors to recognize chemical messengers, signal transmission at electrical synapses is more rapid than that which occurs across chemical synapses, the predominant kind of junctions between neurons. The synaptic delay for a chemical synapse is typically about 2 ms, while the synaptic delay for an electrical synapse may be about 0.2 ms. However, the difference in speed between chemical and electrical synapses is not as marked in mammals as it is in cold-blooded animals.
- Because electrical synapses do not involve neurotransmitters, electrical neurotransmission is less modifiable than chemical neurotransmission
- The response is always the same sign as the source. For example, depolarization of the pre-synaptic membrane will always induce a depolarization in the post-synaptic membrane, and vice versa for hyperpolarization.
- The response in the postsynaptic neuron is generally smaller in amplitude than the source. The amount of attenuation of the signal is due to the membrane resistance of the presynaptic and postsynaptic neurons.
- Long-term changes can be seen in electrical synapses. For example, changes in electrical synapses in the retina are seen during light and dark adaptations of the retina.
The relative speed of electrical synapses also allows for many neurons to fire synchronously. Because of the speed of transmission, electrical synapses are found in escape mechanisms and other processes that require quick responses, such as the response to danger of the sea hare Aplysia, which quickly releases large quantities of ink to obscure enemies' vision.
Normally, current carried by ions could travel in either direction through this type of synapse. However, sometimes the junctions are rectifying synapses, containing voltage-gated ion channels that open in response to depolarization of an axon's plasma membrane, and prevent current from traveling in one of the two directions. Some channels may also close in response to increased calcium (Ca2+) or hydrogen (H+) ion concentration, so as not to spread damage from one cell to another.
The model of a reticular network of directly interconnected cells was one of the early hypotheses for the organization of the nervous system at the beginning of the 20th century. This reticular hypothesis was considered to conflict directly with the now predominant neuron doctrine, a model in which isolated, individual neurons signal to each other chemically across synaptic gaps. These two models came into sharp contrast at the award ceremony for the 1906 Nobel Prize in Physiology or Medicine, in which the award went jointly to Camillo Golgi, a reticularist and widely recognized cell biologist, and Santiago Ramón y Cajal, the champion of the neuron doctrine and the father of modern neuroscience. Golgi delivered his Nobel lecture first, in part detailing evidence for a reticular model of the nervous system. Ramón y Cajal then took the podium and refuted Golgi's conclusions in his lecture. Modern understanding of the coexistence of chemical and electrical synapses, however, suggests that both models are physiologically significant; it could be said that the Nobel committee acted with great foresight in awarding the Prize jointly.
There was substantial debate on whether the transmission of information between neurons was chemical or electrical in the first decades of the twentieth century, but chemical synaptic transmission was seen as the only answer after Otto Loewi's demonstration of chemical communication between neurons and heart muscle. Thus, the discovery of electrical communication was surprising.
See also 
- Central nervous system
- Gap junction
- Thalamic reticular nucleus
- Junctional complex
- Cardiac muscle
- Kandel, ER; Schwartz, JH; Jessell, TM (2000). Principles of Neural Science (4th ed.). New York: McGraw-Hill. ISBN 0-8385-7701-6.
- Hormuzdi SG, Filippov MA, Mitropoulou G, Monyer H, Bruzzone R (March 2004). "Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks". Biochim. Biophys. Acta 1662 (1-2): 113–37. doi:10.1016/j.bbamem.2003.10.023. PMID 15033583.
- Purves, Dale, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, and Leonard E. White (2008). Neuroscience. 4th ed. Sinauer Associates. pp. 85–8. ISBN 978-0-87893-697-7.
- Gibson JR, Beierlein M, Connors BW (January 2005). "Functional properties of electrical synapses between inhibitory interneurons of neocortical layer 4". J. Neurophysiol. 93 (1): 467–80. doi:10.1152/jn.00520.2004. PMID 15317837.
- Bennett MV, Zukin RS (February 2004). "Electrical coupling and neuronal synchronization in the Mammalian brain". Neuron 41 (4): 495–511. doi:10.1016/S0896-6273(04)00043-1. PMID 14980200.
- Kandel, Schwartz & Jessell 2000, pp. 178–180
- Kandel, Schwartz & Jessell 2000, p. 178
- Kandal, et al., Chapter 10
- Kandel, Schwartz & Jessell 2000, p. 180
- Activity-Dependent Long-Term Depression of Electrical Synapses, Julie S. Haas, et al., Science 334, 389 (2011); doi:10.1126/science.1207502
Further reading 
- Andrew L. Harris and Darren Locke (2009). Connexins, a guide. New York: Springer. p. 574. ISBN 978-1-934115-46-6.
- Haas, Julie S.; Baltazar Zavala, Carole E. Landisman (2011). "Activity-dependent long-term depression of electrical synapses". Science 334 (6054): 389–393. doi:10.1126/science.1207502. PMID 22021860. Retrieved 2011-10-22.
- Hestrin, Shaul (2011). "The strength of electrical synapses". Science 334 (6054): 315–316. doi:10.1126/science.1213894. PMID 22021844. Retrieved 2011-10-22.