Synapse

From Wikipedia, the free encyclopedia
Jump to: navigation, search
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 is a structure that permits a neuron (or nerve cell) to pass an electrical or chemical signal to another cell (neural or otherwise).[1] 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.[2]

The word "synapse" (from Greek synapsis "conjunction," from synaptein "to clasp," from syn- "together" and haptein "to fasten") was introduced in 1897 by English physiologist Michael Foster at the suggestion of English classical scholar Arthur Woollgar Verrall.[3][4]

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 presynaptic 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.[5]

Chemical or electrical[edit]

There are two fundamentally different types of synapses:

  • In an electrical synapse, the presynaptic and postsynaptic cell membranes are connected by special channels called gap junctions that are capable of passing electric current, causing voltage changes in the presynaptic cell to induce voltage changes in the postsynaptic cell. The main advantage of an electrical synapse is the rapid transfer of signals from one cell to the next.[6]

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

Types of interfaces[edit]

Synapses can be classified by the type of cellular structure serving as the postsynaptic target, onto which the axon terminal projects. 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[edit]

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.[7]

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.[8]

Study models[edit]

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

Synaptic polarization[edit]

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.[9] 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.[10][11] 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.[10]

Additional images[edit]

See also[edit]

References[edit]

  1. ^ 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. 
  2. ^ 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. 
  3. ^ "synapse". Online Etymology Dictionary. Retrieved 2013-10-01. 
  4. ^ 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." 
  5. ^ 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. 
  6. ^ 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. 
  7. ^ 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. 
  8. ^ Krugers, Harm J.; Zhou, Ming; Joëls, Marian; Kindt, Merel (October 11, 2011). "Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones". Frontiers in Behavioural Neuroscience (Switzerland: Frontiers Media SA) 5: 62. doi:10.3389/fnbeh.2011.00062. PMC 3190121. Retrieved 2013-03-21. 
  9. ^ 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. 
  10. ^ a b 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. 
  11. ^ 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.