Synapse

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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]

There are two fundamentally different types of synapses:

  • In a chemical synapse, electrical activity in the presynaptic neuron is converted (via the activation of voltage-gated calcium channels) into the release of a chemical called a neurotransmitter that binds to receptors located in the plasma membrane of the postsynaptic cell. The neurotransmitter may initiate an electrical response or a secondary messenger pathway that may either excite or inhibit the postsynaptic neuron. Chemical synapses can be classified according to the neurotransmitter released: glutamatergic (excitatory), GABAergic (inhibitory), cholinergic (e.g. vertebrate neuromuscular junction) and adrenergic (releasing norepinephrine). Because of the complexity of receptor signal transduction, chemical synapses can have complex effects on the postsynaptic cell.
  • 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.

Specialized synapses[edit]

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

Role in memory[edit]

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]

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.