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| Research article summary (published 10 Sep 2009): |
Serotonin targets inhibitory synapses to induce modulation of network functions.
Full Abstract
The cellular effects of serotonin (5-HT), a neuromodulator with widespread influences in the central nervous system, have been investigated. Despite detailed knowledge about the molecular biology of cellular signalling, it is not possible to anticipate the responses of neuronal networks to a global action of 5-HT. Heterogeneous expression of various subtypes of serotonin receptors (5-HTR) in a variety of neurons differently equipped with cell-specific transmitter receptors and ion channel assemblies can provoke diverse cellular reactions resulting in various forms of network adjustment and, hence, motor behaviour. Using the respiratory network as a model for reciprocal synaptic inhibition, we demonstrate that 5-HT(1A)R modulation primarily affects inhibition through glycinergic synapses. Potentiation of glycinergic inhibition of both excitatory and inhibitory neurons induces a functional reorganization of the network leading to a characteristic change of motor output. The changes in network operation are robust and help to overcome opiate-induced respiratory depression. Hence, 5-HT(1A)R activation stabilizes the rhythmicity of breathing during opiate medication of pain.
Author information
Author/s: Manzke, Till (T); Dutschmann, Mathias (M); Schlaf, Gerald (G); Mörschel, Michael (M); Koch, Uwe R (UR); Ponimaskin, Evgeni (E); Bidon, Olivier (O); Lalley, Peter M (PM); Richter, Diethelm W (DW);
Affiliation: Department of Neuro- and Sensory Physiology, University of Göttingen, , 37073 Göttingen, Germany.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Philosophical transactions of the Royal Society of London. Series B, Biological sciences (Philos Trans R Soc Lond B Biol Sci), published in England. (Language: eng)
Reference: 2009-Sep; vol 364 (issue 1529) : pp 2589-602
Dates: Created 2009/08/04; Completed 2009/10/30;
PMID: 19651659, status: MEDLINE (last retrieval date: 10/30/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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