Synapse

This article is about synapses of the nervous system. For other uses, see Synapse (disambiguation).
Structure of a typical chemical synapse

In the nervous system, a synapse[1] is a structure that permits a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron. Some authors generalize this concept to include the communication from a neuron to any other cell type,[2] such as to a motor cell, although such non-neuronal contacts may be referred to as junctions (a historically older term). Santiago Ramón y Cajal proposed that neurons are not continuous throughout the body, yet still communicate with each other, an idea known as the neuron doctrine.[3] Synapses (at least chemical synapses) are stabilized in position by synaptic adhesion molecules (SAMs) projecting from both the pre- and post-synaptic neuron and sticking together where they overlap; SAMs may also assist in the generation and functioning of synapses.[4]

The word "synapse" – from the Greek synapsis (συνάψις), meaning "conjunction", in turn from συνάπτεὶν (συν ("together") and ἅπτειν ("to fasten")) – was introduced in 1897 by English physiologist Michael Foster at the suggestion of English classical scholar Arthur Woollgar Verrall.[5][6]

Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the plasma membrane of the signal-passing neuron (the presynaptic neuron) comes into close apposition with the membrane of the target (postsynaptic) cell. Both the presynaptic and postsynaptic sites contain extensive arrays of molecular machinery that link the two membranes together and carry out the signaling process. In many synapses, the presynaptic part is located on an axon, but some postsynaptic sites are located on a dendrite or soma. Astrocytes also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating neurotransmission.[7]

Chemical or electrical

An example of chemical synapse- by the release of neurotransmitter like Acetyl Choline or glutamic acid.

There are two fundamentally different types of synapses:

Synaptic communication is distinct from ephaptic coupling, in which communication between neurons occurs via indirect electric fields.

Types of interfaces

Synapses can be classified by the type of cellular structures serving as the pre- and post-synaptic components. The vast majority of synapses in the mammalian nervous system are classical axo-dendritic synapses (axon synapsing upon a dendrite), however a variety of other arrangements exist. These include but are not limited to axo-axonic, dendro-dendritic, axo-secretory, somato-dendritic, dendro-somatic, and somato-somatic synapses.

The axon can synapse onto a dendrite, onto a cell body, or onto another axon or axon terminal, as well as into the bloodstream or diffusely into the adjacent nervous tissue.

Different types of synapses

Role in memory

Main article: Hebbian theory

It is widely accepted that the synapse plays a role in the formation of memory. As neurotransmitters activate receptors across the synaptic cleft, the connection between the two neurons is strengthened when both neurons are active at the same time, as a result of the receptor's signalling mechanisms. The strength of two connected neural pathways is thought to result in the storage of information, resulting in memory. This process of synaptic strengthening is known as long-term potentiation.[9]

By altering the release of neurotransmitters, plasticity of synapses can be controlled in the presynaptic cell. The postsynaptic cell can be regulated by altering the function and number of its receptors. Changes in postsynaptic signaling are most commonly associated with N-methyl-d-aspartic acid receptor (NMDAR)-dependent long-term potentiation (LTP) and long-term depression (LTD), which are the most analyzed forms of plasticity at excitatory synapses.[10]

Study models

For technical reasons, synaptic structure and function has historically been studied at unusually large model synapses, for example:

Synaptic polarization

The function of neurons depends upon cellular polarization. The distinctive structure of nerve cells allows action potentials to travel directionally (from dendrites to axons), and for these signals to then be received and carried on by post-synaptic neurons or received by effector cells. Nerve cells have long been used as models for cellular polarization, and of particular interest are the mechanisms underlying the polarized localization of synaptic molecules. PIP2 signalling regulated by IMPase plays an integral role in synaptic polarity.

Phosphoinositides (PIP, PIP2, and PIP3) are molecules that have been shown to affect neuronal polarity.[12] A gene (ttx-7) was identified in Caenorhabditis elegans that encodes myo-inositol monophosphatase (IMPase), an enzyme that produces inositol by dephosphorylating inositol phosphate. Organisms with mutant ttx-7 genes demonstrated behavioral and localization defects, which were rescued by expression of IMPase. This led to the conclusion that IMPase is required for the correct localization of synaptic protein components.[13][14] The egl-8 gene encodes a homolog of phospholipase Cβ (PLCβ), an enzyme that cleaves PIP2. When ttx-7 mutants also had a mutant egl-8 gene, the defects caused by the faulty ttx-7 gene were largely reversed. These results suggest that PIP2 signaling establishes polarized localization of synaptic components in living neurons.[13]

Additional images

See also

References

  1. ↑ Foster, M.; Sherrington, C.S. (1897). Textbook of Physiology, volume 3 (7th ed.). London: Macmillan. p. 929.
  2. ↑ Schacter, Daniel L.; Gilbert, Daniel T.; Wegner, Daniel M. (2011). Psychology (2nd ed.). New York: Worth Publishers. p. 80. ISBN 978-1-4292-3719-2. LCCN 2010940234. OCLC 696604625.
  3. ↑ Elias, Lorin J.; Saucier, Deborah M. (2006). Neuropsychology: Clinical and Experimental Foundations. Boston: Pearson/Allyn & Bacon. ISBN 978-0-20534361-4. LCCN 2005051341. OCLC 61131869.
  4. ↑ Cold Spring Harb Perspect Biol. 2012 Apr; 4(4) ; http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312681/
  5. ↑ "synapse". Online Etymology Dictionary. Retrieved 2013-10-01.
  6. ↑ Tansey, E.M. (1997). "Not committing barbarisms: Sherrington and the synapse, 1897". Brain Research Bulletin (Amsterdam: Elsevier) 44 (3): 211–212. doi:10.1016/S0361-9230(97)00312-2. PMID 9323432. The word synapse first appeared in 1897, in the seventh edition of Michael Foster's Textbook of Physiology.
  7. ↑ Perea, G.; Navarrete, M.; Araque, A. (August 2009). "Tripartite synapses: astrocytes process and control synaptic information". Trends in Neurosciences (Cambridge, MA: Cell Press) 32 (8): 421–431. doi:10.1016/j.tins.2009.05.001. PMID 19615761.
  8. ↑ Silverthorn, Dee Unglaub (2007). Human Physiology: An Integrated Approach. Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson (4th ed.). San Francisco: Pearson/Benjamin Cummings. p. 271. ISBN 978-0-8053-6851-2. LCCN 2005056517. OCLC 62742632.
  9. ↑ Lynch, M. A. (January 1, 2004). "Long-Term Potentiation and Memory". Physiological Reviews 84 (1): 87–136. doi:10.1152/physrev.00014.2003. PMID 14715912.
  10. ↑ Krugers, Harm J.; Zhou, Ming; Joëls, Marian; Kindt, Merel (October 11, 2011). "Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones". Frontiers in Behavioral Neuroscience (Switzerland: Frontiers Media SA) 5: 62. doi:10.3389/fnbeh.2011.00062. PMC 3190121. PMID 22013419. Retrieved 2013-03-21.
  11. ↑ Stanley, EF (1992). "The calyx-type synapse of the chick ciliary ganglion as a model of fast cholinergic transmission.". Canadian Journal of Physiology and Pharmacology. 70 Suppl: S73–7. doi:10.1139/y92-246. PMID 1338300.
  12. ↑ Arimura, Nariko; Kaibuchi, Kozo (December 22, 2005). "Key regulators in neuronal polarity". Neuron (Cambridge, MA: Cell Press) 48 (6): 881–884. doi:10.1016/j.neuron.2005.11.007. PMID 16364893.
  13. 1 2 Kimata, Tsubasa; Tanizawa, Yoshinori; Can, Yoko; et al. (June 1, 2012). "Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans". Genetics (Bethesda, MD: Genetics Society of America) 191 (2): 509–521. doi:10.1534/genetics.111.137844. PMID 22446320.
  14. ↑ Tanizawa, Yoshinori; Kuhara, Atsushi; Inada, Hitoshi; et al. (December 1, 2006). "Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans". Genes & Development (Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press) 20 (23): 3296–3310. doi:10.1101/gad.1497806. PMC 1686606. PMID 17158747. Retrieved 2013-10-01.
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