Depolarization-induced release of endocannabinoids by murine dorsal motor nucleus of the vagus nerve neurons differentially regulates inhibitory and excitatory neurotransmission

Autor: André Jean, Bruno Lebrun, Jérôme Trouslard, Julien Roux, Nicolas Wanaverbecq
Přispěvatelé: Centre de recherche en neurobiologie - neurophysiologie de Marseille (CRN2M), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Neurobiologie, Communication Chimique, (LNB), Centre National de la Recherche Scientifique (CNRS), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2009
Předmět:
Male
MESH: Capsaicin
MESH: 6-Cyano-7-nitroquinoxaline-2
3-dione

MESH: Neurons
MESH: Endocannabinoids
MESH: Receptor
Cannabinoid
CB1

Kynurenic Acid
Receptors
Presynaptic

Mice
0302 clinical medicine
Piperidines
Receptor
Cannabinoid
CB1

MESH: Vagus Nerve
MESH: Animals
MESH: Inhibitory Postsynaptic Potentials
2. Zero hunger
6-Cyano-7-nitroquinoxaline-2
3-dione

Neurons
0303 health sciences
MESH: Kynurenic Acid
Vagus Nerve
MESH: Naphthalenes
MESH: Excitatory Amino Acid Antagonists
MESH: Glutamic Acid
Endocannabinoid system
[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry
Molecular Biology/Biomolecules [q-bio.BM]

Pyridazines
MESH: Piperidines
MESH: Benzoxazines
Excitatory postsynaptic potential
GABAergic
Rimonabant
MESH: Efferent Pathways
Morpholines
Glutamic Acid
MESH: Morpholines
Arachidonic Acids
Tetrodotoxin
Biology
Neurotransmission
Naphthalenes
Inhibitory postsynaptic potential
MESH: Calcium Signaling
Efferent Pathways
03 medical and health sciences
Cellular and Molecular Neuroscience
Glutamatergic
MESH: Mice
Inbred C57BL

MESH: Pyridazines
MESH: Receptors
Presynaptic

Cannabinoid Receptor Modulators
Animals
MESH: Arachidonic Acids
Calcium Signaling
MESH: Excitatory Postsynaptic Potentials
[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry
Molecular Biology/Biochemistry [q-bio.BM]

MESH: Mice
030304 developmental biology
Pharmacology
Excitatory Postsynaptic Potentials
MESH: Male
MESH: Tetrodotoxin
Vagus nerve
Benzoxazines
Mice
Inbred C57BL

Dorsal motor nucleus
2-Amino-5-phosphonovalerate
Inhibitory Postsynaptic Potentials
MESH: Brain Stem
Pyrazoles
MESH: 2-Amino-5-phosphonovalerate
Capsaicin
Neuroscience
Excitatory Amino Acid Antagonists
030217 neurology & neurosurgery
MESH: Pyrazoles
Brain Stem
Endocannabinoids
Zdroj: Neuropharmacology
Neuropharmacology, 2009, 56 (8), pp.1106-15. ⟨10.1016/j.neuropharm.2009.03.009⟩
Neuropharmacology, Elsevier, 2009, 56 (8), pp.1106-15. ⟨10.1016/j.neuropharm.2009.03.009⟩
ISSN: 0028-3908
Popis: International audience; Numerous studies, focused on the hypothalamus, have recently implicated endocannabinoids (EC) as orexigenic factors in the central control of food intake. However, the EC system is also highly expressed in the hindbrain autonomic integrator of food intake regulation, i.e. the dorsal vagal complex (DVC). Previous studies have shown that exogenous cannabinoids, by acting on cannabinoid 1 receptor (CB1R), suppress GABAergic and glutamatergic neuronal transmission in adult rat dorsal motor nucleus of the vagus nerve (DMNV), the principal efferent compartment of the DVC. However, no endogenous release of EC has been demonstrated in DVC to date. Using patch-clamp techniques on mouse coronal brainstem slices, we confirmed that both inhibitory and excitatory neurotransmission were depressed by WIN 55,212-2, a CB1R agonist. We demonstrated that DMNV neurons exhibited a rapid and reversible depolarization-induced suppression of electrically evoked GABAergic IPSCs (eIPSCs), classically known as DSI (depolarization-induced suppression of inhibition), while spontaneous or miniature IPSCs activity remained unaltered. Further, no depolarization-induced suppression of glutamatergic eEPSCs (DSE) occurred. Our results indicate that DSI was blocked by SR141716A (Rimonabant), a selective CB1R antagonist, and was dependent on calcium elevation in DMNV neurons, suggesting a release of EC in the DVC. Moreover, the analysis of the paired-pulse ratio, of the coefficient of variation and of the failure rate of eIPSCs support the fact that EC-mediated suppression of GABAergic inhibition takes place at the presynaptic level. These results show for the first time that DMNV neurons release EC in an activity-dependent manner, which in turn differentially regulates their inhibitory and excitatory synaptic inputs.
Databáze: OpenAIRE