title: Glutamatergic inputs contribute to phasic activity in vasopressin neurons.
abstract: Many neurons in the CNS display rhythmic patterns of activity to optimize excitation-secretion coupling. However, the mechanisms of rhythmogenesis are only partially understood. Magnocellular vasopressin (VP) neurons in the hypothalamus display a phasic activity that consists of alternative bursts of action potentials and silent periods. Previous observations from acute slices of adult hypothalamus suggested that VP cell rhythmicity depends on intrinsic membrane properties. However, such activity in vivo is nonregenerative. Here, we studied the mechanisms of VP neuron rhythmicity in organotypic slice cultures that, unlike acute slices, preserve functional synaptic connections. Comparative analysis of phasic firing of VP neurons in vivo, in acute slices, and in the cultures revealed that, in the latter, the activity was closely related to that observed in vivo. It was synaptically driven, essentially from glutamatergic inputs, and did not rely on intrinsic membrane properties. The glutamatergic synaptic activity was sensitive to osmotic challenges and kappa-opioid receptor activation, physiological stimuli known to affect phasic activity. Together, our data thus strongly suggest that phasic activity in magnocellular VP neurons is controlled by glutamatergic synaptic inputs rather than by intrinsic properties.
authors.affiliation: Inserm Unité 862, Neurocentre Magendie, Université de Bordeaux, 33077 Bordeaux, France. jean-marc.israel@inserm.fr
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Israel
authors.forename: Dominique A
authors.initials: DA
authors.lastname: Poulain
authors.forename: Stéphane H R
authors.initials: SH
authors.lastname: Oliet
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000344:Afferent Pathways / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D000701:Analgesics, Opioid / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D048430:Cell Shape / Q000502:physiology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006982:Hypertonic Solutions / Q000494:pharmacology; D007038:Hypotonic Solutions; D007150:Immunohistochemistry; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009924:Organ Culture Techniques; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D010507:Periodicity; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism; D017473:Receptors, Opioid, kappa / Q000819:agonists / Q000378:metabolism; D013495:Supraoptic Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
chemical_list: D000701:Analgesics, Opioid; D006982:Hypertonic Solutions; D007038:Hypotonic Solutions; D009292:Narcotic Antagonists; D011963:Receptors, GABA-A; D017473:Receptors, Opioid, kappa; D018698:Glutamic Acid