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Excitatory action of hypocretin/orexin on neurons of the central medial amygdala
|Published in||Neuroscience. 2006, vol. 142, no. 4, p. 999-1004|
|Abstract||The neurons of the lateral hypothalamus that contain hypocretin/orexin (hcrt/orx) are thought to promote arousal through the excitatory action they exert on the multiple areas to which they project within the CNS. We show here that the hcrt/orx peptides can also exert a strong action on the amygdala, a structure known for its implication in emotional aspects of behavior. Indeed, the hcrt/orx peptides, applied in acute rat brain slices, excite a specific class of "low threshold burst" neurons in the central medial (CeM) nucleus which is considered as a major output of the amygdala. These excitatory effects are postsynaptic, mediated by Hcrt2/OX2 receptors and result from the closure of a potassium conductance. They occur on a class of neurons that are also excited by vasopressin acting through V1a receptors. These results suggest that the hcrt/orx system can act through the amygdala to augment arousal and evoke the autonomic and behavioral responses associated with fear, stress or emotion.|
|Keywords||Action Potentials/drug effects/physiology — Amygdala/drug effects/ metabolism — Animals — Arousal/drug effects/physiology — Excitatory Postsynaptic Potentials/drug effects/ physiology — Fear/drug effects/physiology — Intracellular Signaling Peptides and Proteins/ metabolism/pharmacology — Neural Pathways/drug effects/ metabolism — Neurons/drug effects/ metabolism — Neuropeptides/ metabolism/pharmacology — Organ Culture Techniques — Potassium Channels/drug effects/metabolism — Rats — Receptors, G-Protein-Coupled/drug effects/metabolism — Receptors, Neuropeptide/drug effects/metabolism — Receptors, Vasopressin/agonists/metabolism — Stress, Psychological/metabolism/physiopathology — Synaptic Transmission/drug effects/ physiology — Vasopressins/metabolism/pharmacology|
|BISETTI, A. et al. Excitatory action of hypocretin/orexin on neurons of the central medial amygdala. In: Neuroscience, 2006, vol. 142, n° 4, p. 999-1004. doi: 10.1016/j.neuroscience.2006.07.018 https://archive-ouverte.unige.ch/unige:10195|