Pharmacological upregulation of h-channels selectively reduces the excitability of pyramidal neuron dendrites (Articolo in rivista)

Type
Label
  • Pharmacological upregulation of h-channels selectively reduces the excitability of pyramidal neuron dendrites (Articolo in rivista) (literal)
Anno
  • 2002-01-01T00:00:00+01:00 (literal)
Alternative label
  • Poolos N.P. 1,2, Migliore M. 3,4, Johnston D. 1 (2002)
    Pharmacological upregulation of h-channels selectively reduces the excitability of pyramidal neuron dendrites
    in Nature neuroscience (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Poolos N.P. 1,2, Migliore M. 3,4, Johnston D. 1 (literal)
Pagina inizio
  • 767 (literal)
Pagina fine
  • 774 (literal)
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  • 5 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1: Baylor College of Medicine, Houston, TX, USA; 2: University of Washington, Seattle, WA, USA; 3. Yale University School of Medicine, New Haven, CT, USA; 4: CNR (literal)
Titolo
  • Pharmacological upregulation of h-channels selectively reduces the excitability of pyramidal neuron dendrites (literal)
Abstract
  • The dendrites of pyramidal neurons have markedly different electrical properties from those of the soma, owing to the non-uniform distribution of voltage-gated ion channels in dendrites. It is thus possible that drugs acting on ion channels might preferentially alter dendritic, but not somatic, excitability. Using dendritic and somatic whole-cell and cell- attached recordings in rat hippocampal slices, we found that the anticonvulsant lamotrigine selectively reduced action potential firing from dendritic depolarization, while minimally affecting firing at the soma. This regional and input-specific effect resulted from an increase in the hyperpolarization-activated cation current (I(h)), a voltage-gated current present predominantly in dendrites. These results demonstrate that neuronal excitability can be altered by drugs acting selectively on dendrites, and suggest an important role for I(h) in controlling dendritic excitability and epileptogenesis. (literal)
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