Noradrenergic modulation of neuronal responses to n-methyl-d-aspartate in the vestibular nuclei: An electrophysiological and immunohistochemical study
Neuroscience. 2014-04-01; 265: 172-183
DOI: 10.1016/j.neuroscience.2014.01.054
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1. Neuroscience. 2014 Apr 18;265:172-83. doi: 10.1016/j.neuroscience.2014.01.054.
Epub 2014 Feb 7.
Noradrenergic modulation of neuronal responses to n-methyl-d-aspartate in the
vestibular nuclei: an electrophysiological and immunohistochemical study.
Barresi M(1), Grasso C(2), Licata F(3), Li Volsi G(4).
Author information:
(1)Department of Biomedical Sciences, Section of Physiology, University of
Catania, Italy. Electronic address: .
(2)Department of Biomedical Sciences, Section of Physiology, University of
Catania, Italy. Electronic address: .
(3)Department of Biomedical Sciences, Section of Physiology, University of
Catania, Italy. Electronic address: .
(4)Department of Biomedical Sciences, Section of Physiology, University of
Catania, Italy. Electronic address: .
Excitatory responses evoked by N-methyl-d-aspartate (NMDA) in the vestibular
nuclei (VN) of the rat were studied in vivo during microiontophoretic application
of noradrenaline (NA) and/or its agonists and antagonists. Ejection of
NA-modified excitatory responses mediated by NMDA receptors (NMDAR) in all
neurons tested; the effect was enhancement in 59% of cases and depression in the
remaining 41%. Enhancements prevailed in all VN with the exception of the lateral
vestibular nucleus, where both effects were recorded in an equal number of cases.
The enhancing action of NA on NMDAR-mediated responses was mimicked by the
noradrenergic beta-receptor agonist isoproterenol, the beta1 specific agonist
denopamine and the alpha2 agonist clonidine. These effects were blocked
respectively by the generic beta-receptor antagonist timolol, the beta1
antagonist atenolol and the alpha2 antagonist yohimbine. In contrast, application
of the alpha1 receptor agonist cirazoline and the specific alpha1 antagonist
prazosin respectively mimicked and partially antagonized the depression of
NMDAR-mediated excitations induced by NA. Double-labeling immunohistochemical
techniques demonstrated broad colocalization of NMDAR (specifically NR1 and NR2
subunits) with noradrenergic receptors (alpha1, alpha2 and beta1) in many VN
neurons; only minor differences were found between nuclei. These results indicate
that NA can produce generalized modulation of NMDAR-mediated excitatory
neurotransmission in VN, which may in turn modify synaptic plasticity within the
nuclei.
Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
DOI: 10.1016/j.neuroscience.2014.01.054
PMID: 24508745 [Indexed for MEDLINE]