Calcium action potentials restricted to distal apical dendrites of rat neocortical pyramidal neurons

Authors


  • Authors’ present addresses
    J. Schiller: Department of Pharmacology, Guggenheim 7, Mayo Foundation, Rochester, MN 55905, USA.
    Y. Schiller: Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA.
    G. Stuart: Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra ACT 0200, Australia.

Abstract

  • 1Simultaneous whole-cell voltage and Ca2+ fluorescence measurements were made from the distal apical dendrites and the soma of thick tufted pyramidal neurons in layer 5 of 4-week-old (P28–32) rat neocortex slices to investigate whether activation of distal synaptic inputs can initiate regenerative responses in dendrites.
  • 2Dual whole-cell voltage recordings from the distal apical trunk and primary tuft branches (540–940 μm distal to the soma) showed that distal synaptic stimulation (upper layer 2) evoking a subthreshold depolarization at the soma could initiate regenerative potentials in distal branches of the apical tuft which were either graded or all-or-none. These regenerative potentials did not propagate actively to the soma and axon.
  • 3Calcium fluorescence measurements along the apical dendrites indicated that the regenerative potentials were associated with a transient increase in the concentration of intracellular free calcium ([Ca2+]i) restricted to distal dendrites.
  • 4Cadmium added to the bath solution blocked both the all-or-none dendritic regenerative potentials and local dendritic [Ca2+]i transients evoked by distal dendritic current injection. Thus, the regenerative potentials in distal dendrites represent local Ca2+ action potentials.
  • 5Initiation of distal Ca2+ action potentials by a synaptic stimulus required coactivation of AMPA- and NMDA-type glutamate receptor channels.
  • 6It is concluded that in neocortical layer 5 pyramidal neurons of P28–32 animals glutamatergic synaptic inputs to the distal apical dendrites can be amplified via local Ca2+ action potentials which do not reach threshold for axonal AP initiation. As amplification of distal excitatory synaptic input is associated with a localized increase in [Ca2+]i these Ca2+ action potentials could control the synaptic efficacy of the distal cortico-cortical inputs to layer 5 pyramidal neurons.

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