Anandamide centrally depresses the respiratory rhythm generator of neonatal mice

Abstract Endogenous cannabinoid receptors are widely distributed throughout the CNS, including the brainstem, and modulate a variety of functions, including breathing. In adult rats, activation of cannabinoid 1 receptors has been shown to depress breathing. Here in neonatal mice, we used in vitro el...

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Bibliographic Details
Published in:	Neuroscience Vol. 170; no. 4; pp. 1098 - 1109
Main Authors:	Tree, K, Caravagna, C, Hilaire, G, Peyronnet, J, Cayetanot, F
Format:	Journal Article
Language:	English
Published:	Amsterdam Elsevier Ltd 10-11-2010 Elsevier Elsevier - International Brain Research Organization
Subjects:	Adrenergic alpha-1 Receptor Antagonists Adrenergic alpha-1 Receptor Antagonists - pharmacology Adrenergic alpha-2 Receptor Antagonists Adrenergic alpha-2 Receptor Antagonists - pharmacology Adrenergic receptors Animals Animals, Newborn Arachidonic Acids Arachidonic Acids - pharmacology Arachidonic Acids - physiology Biochemistry Biochemistry, Molecular Biology Biological and medical sciences Cannabinoid Receptor Modulators - pharmacology Cannabinoid Receptor Modulators - physiology catecholamine endocannabinoid Endocannabinoids Fundamental and applied biological sciences. Psychology in vitro In Vitro Techniques Life Sciences Medulla Oblongata Medulla Oblongata - drug effects Medulla Oblongata - physiology Mice neonate Neurology Periodicity Polyunsaturated Alkamides Polyunsaturated Alkamides - pharmacology Prazosin Prazosin - pharmacology Receptor, Cannabinoid, CB1 Receptor, Cannabinoid, CB1 - metabolism Receptors, Adrenergic, alpha-1 Receptors, Adrenergic, alpha-1 - physiology Receptors, Adrenergic, alpha-2 Receptors, Adrenergic, alpha-2 - physiology Respiratory Center Respiratory Center - drug effects Respiratory Center - physiology respiratory rhythm generator Vertebrates: nervous system and sense organs Yohimbine Yohimbine - pharmacology phrenic bursts endocannabinoid delta-9-tetrahydrocannabinol artificial cerebro-spinal fluid RRG PBampl neonate cannabinoid receptor 1 CB 1R PB amplitude THC PB catecholamine NA PB frequency VLM in vitro aCSF noradrenaline ventrolateral medulla respiratory rhythm generator AEA anandamide PBfreq Breathing rate Rodentia Cannabinoid Catecholamine In vitro Anandamide Vertebrata Mammalia Endocannabinoid Mouse Animal
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Summary:	Abstract Endogenous cannabinoid receptors are widely distributed throughout the CNS, including the brainstem, and modulate a variety of functions, including breathing. In adult rats, activation of cannabinoid 1 receptors has been shown to depress breathing. Here in neonatal mice, we used in vitro electrophysiology, pharmacology, and immunohistochemistry to analyse the central effects of the endocannabinoid anandamide (AEA) on the activity of the medullary respiratory rhythm generator (RRG). First of all, in vitro electrophysiology on medullary preparations has revealed that bath application of AEA (30 μM, 15 min) significantly depressed respiratory activity. Secondly, applying pre-treatments with alpha-1 (Prazosin, 5 μM, 10 min) and alpha-2 (Yohimbine, 5 μM, 10 min) adrenoceptor antagonists prior to AEA application abolished the AEA-induced depression of the RRG. Finally, immunostaining revealed a dense network of fibres positive for the cannabinoid 1 receptor in the ventrolateral medulla (VLM), a region known to contain both the RRG and the modulatory A1/C1 catecholaminergic group. Moreover, cannabinoid 1 receptor positive fibres were found in close apposition with A1/C1 catecholaminergic cells, identified by the presence of tyrosine hydroxylase. In regard of our electrophysiological, pharmacological and immunostaining results, we conclude that AEA has a central depressive effect on the neonatal RRG, probably via the medullary A1/C1 catecholaminergic neurons which are already known to modulate the respiratory rhythm generator.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2010.08.045