title: Noradrenergic responses of neurones in the mediolateral part of the lateral septum: alpha1-adrenergic depolarization and rhythmic bursting activities, and alpha2-adrenergic hyperpolarization from guinea pig brain slices.
abstract: Bath application of noradrenaline on neurones of class A, B and C within the mediolateral part of the lateral septum from guinea pig brain slices elicited depolarization (through alpha1-adrenoceptors) or hyperpolarization (through alpha2-adrenoceptors) and rhythmic bursting activities (through alpha1-adrenoceptors). A co-existence of these two types of adrenoceptors (alpha1 and alpha2) mediating opposite effects on membrane excitability was sometimes observed on the same neurone. Three types (I, II and III) of neurones were identified on the basis of their bursting properties during noradrenaline application. With the bursting activities persisting under tetrodotoxin and their frequency being sensitive to changes in membrane potential, these neurones could be considered as conditional bursters. An afterdepolarizing potential could promote burst initiation in the three types of neurones. Neuronal input resistance decreased at the afterdepolarizing potential peak. Application of low-Na+ medium blocked the generation of bursts and afterdepolarizing potentials induced by noradrenaline in the three types of neurones. Furthermore, the bursts were dependent on the presence of Ca(2+) in the medium in a subpopulation of neurones. We conclude that afterdepolarizing potentials and bursts induced by noradrenaline are generated by a cationic conductance largely permeable to Na+ in neurones of the mediolateral part of the lateral septum.
authors.affiliation: INSERM U 422, Lille, France. carette@biserte.lille.inserm.fr
authors.forename: B
authors.initials: B
authors.lastname: Carette
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D004594:Electrophysiology; D005260:Female; D006168:Guinea Pigs; D009474:Neurons / Q000737:chemistry / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology*; D009924:Organ Culture Techniques; D010507:Periodicity; D010656:Phenylephrine / Q000494:pharmacology; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D012686:Septal Nuclei / Q000166:cytology / Q000502:physiology; D012964:Sodium / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D010656:Phenylephrine; D015016:Yohimbine; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D009532:Nickel; D012964:Sodium; D003000:Clonidine; D002118:Calcium; D009638:Norepinephrine