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Modulation of sensory input to the spinal cord by presynaptic ionotropic glutamate receptors.
Arch Ital Biol. 2005 May; 143(2):103-12.AI

Abstract

Sensory input from peripheral nerves to the dorsal horn of the spinal cord is mediated by a variety of agents released by the central terminals of dorsal root ganglion (DRG) neurons. These include, but are not limited to, amino acids, especially glutamate, peptides and purines. The unraveling of the mechanisms of synaptic transmission by central terminals of DRG neurons has to take into account various ways in which the message from the periphery can be modulated at the level of the first central synapse. These include postsynaptic and presynaptic mechanisms. Homomeric and heteromeric complexes of receptor subunits for the different transmitters released by DRG neurons and interneurons, clustered at the postsynaptic site of central synapses, can be expressed in different combinations and their rate of insertion into the postsynaptic membrane is activity-regulated. Inhibitory mechanisms are an important part of central modulation, especially via presynaptic inhibition, currently believed to involve GABA released by inhibitory intrinsic neurons. Recent work has established the occurrence of another way by which sensory input can be modulated, i.e. the expression of presynaptic ionotropic and metabotropic receptors in central terminals of DRG neurons. Microscopic evidence for the expression, in these terminals, of various subunits of ionotropic glutamate receptors documents the selective expression of glutamate receptors in functionally different DRG afferents. Electrophysiological and pharmacological data suggest that activation of presynaptic ionotropic glutamate receptors in central terminals of DRG neurons may result in inhibition of release of glutamate by the same terminals. Glutamate activating presynaptic receptors may spill over from the same or adjacent synapses, or may be released by processes of astroglial cells surrounding synaptic terminals. The wide expression of presynaptic ionotropic glutamate receptors, especially in superficial laminae of the dorsal horn, where Adelta- and C fibers terminate, provides an additional or alternative mechanism, besides GABA-mediated presynaptic inhibition, for the modulation of glutamate release by these fibers. Since, however, presynaptic ionotropic glutamate receptors are also expressed in terminals of GABAergic intrinsic interneurons, a decrease of GABA release resulting from activation of these receptors in the same laminae, may also play a role in central sensitization and hyperalgesia.

Authors+Show Affiliations

Department of Cell and Developmental Biology, Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. rustioni@med.unc.edu

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16106991

Citation

Rustioni, A. "Modulation of Sensory Input to the Spinal Cord By Presynaptic Ionotropic Glutamate Receptors." Archives Italiennes De Biologie, vol. 143, no. 2, 2005, pp. 103-12.
Rustioni A. Modulation of sensory input to the spinal cord by presynaptic ionotropic glutamate receptors. Arch Ital Biol. 2005;143(2):103-12.
Rustioni, A. (2005). Modulation of sensory input to the spinal cord by presynaptic ionotropic glutamate receptors. Archives Italiennes De Biologie, 143(2), 103-12.
Rustioni A. Modulation of Sensory Input to the Spinal Cord By Presynaptic Ionotropic Glutamate Receptors. Arch Ital Biol. 2005;143(2):103-12. PubMed PMID: 16106991.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of sensory input to the spinal cord by presynaptic ionotropic glutamate receptors. A1 - Rustioni,A, PY - 2005/8/19/pubmed PY - 2005/9/29/medline PY - 2005/8/19/entrez SP - 103 EP - 12 JF - Archives italiennes de biologie JO - Arch Ital Biol VL - 143 IS - 2 N2 - Sensory input from peripheral nerves to the dorsal horn of the spinal cord is mediated by a variety of agents released by the central terminals of dorsal root ganglion (DRG) neurons. These include, but are not limited to, amino acids, especially glutamate, peptides and purines. The unraveling of the mechanisms of synaptic transmission by central terminals of DRG neurons has to take into account various ways in which the message from the periphery can be modulated at the level of the first central synapse. These include postsynaptic and presynaptic mechanisms. Homomeric and heteromeric complexes of receptor subunits for the different transmitters released by DRG neurons and interneurons, clustered at the postsynaptic site of central synapses, can be expressed in different combinations and their rate of insertion into the postsynaptic membrane is activity-regulated. Inhibitory mechanisms are an important part of central modulation, especially via presynaptic inhibition, currently believed to involve GABA released by inhibitory intrinsic neurons. Recent work has established the occurrence of another way by which sensory input can be modulated, i.e. the expression of presynaptic ionotropic and metabotropic receptors in central terminals of DRG neurons. Microscopic evidence for the expression, in these terminals, of various subunits of ionotropic glutamate receptors documents the selective expression of glutamate receptors in functionally different DRG afferents. Electrophysiological and pharmacological data suggest that activation of presynaptic ionotropic glutamate receptors in central terminals of DRG neurons may result in inhibition of release of glutamate by the same terminals. Glutamate activating presynaptic receptors may spill over from the same or adjacent synapses, or may be released by processes of astroglial cells surrounding synaptic terminals. The wide expression of presynaptic ionotropic glutamate receptors, especially in superficial laminae of the dorsal horn, where Adelta- and C fibers terminate, provides an additional or alternative mechanism, besides GABA-mediated presynaptic inhibition, for the modulation of glutamate release by these fibers. Since, however, presynaptic ionotropic glutamate receptors are also expressed in terminals of GABAergic intrinsic interneurons, a decrease of GABA release resulting from activation of these receptors in the same laminae, may also play a role in central sensitization and hyperalgesia. SN - 0003-9829 UR - https://www.unboundmedicine.com/medline/citation/16106991/Modulation_of_sensory_input_to_the_spinal_cord_by_presynaptic_ionotropic_glutamate_receptors_ L2 - http://www.architalbiol.org/aib/article/view/143103/16106991 DB - PRIME DP - Unbound Medicine ER -