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Volume 17, Number 15,
Issue of August 1, 1997
pp. 5782-5791
Copyright ©1997 Society for Neuroscience
Muscarinic Modulation of Spike Backpropagation in the Apical
Dendrites of Hippocampal CA1 Pyramidal Neurons
Received Feb. 24, 1997; revised May 5, 1997; accepted May 20, 1997.
Hiroshi Tsubokawa and
William N. Ross
Department of Physiology, New York Medical College, Valhalla, New
York 10595
In pyramidal neurons from the CA1 region of the rat hippocampus,
Na+-dependent action potentials backpropagate over the
dendrites in an activity-dependent manner. Consequently, later spikes
in a train have smaller amplitudes when recorded in the apical arbors. We studied the effect of the cholinergic agonist carbachol (CCh) on
this pattern of activity when spikes were evoked synaptically or
antidromically in the transverse slice preparation. Concentrations as
low as 1 µM were effective in reversing the modulation,
making the amplitude of all spikes in a train equal and independent of the frequency of spike firing. CCh did not change the propagation of
the first spike in a train. These effects of CCh were blocked by 1 µM atropine, showing that only muscarinic receptors were involved. The effects of CCh on the pattern of spike propagation were
observed in the proximal and middle dendrites, but recordings in the
distal dendrites (>300 µm from the soma) showed that CCh did not
boost the amplitude in this region. Intracellular BAPTA (10 mM) or EGTA (10 mM) had no effect on
activity-dependent backpropagation but blocked the effect of CCh.
Backpropagating spikes caused increases in
[Ca2+]i at all dendritic locations. In
the middle and distal dendrites these increases normally peaked at the
time of the first few large action potentials. In association with the
enhancement of spike backpropagation, CCh increased the amplitude and
duration of the train-evoked [Ca2+]i
changes. These effects of CCh on dendritic spike potentials and
associated [Ca2+]i changes may be
important in modulating synaptic integration and plasticity in these
neurons.
Key words:
pyramidal neuron;
dendrite;
carbachol;
muscarine;
hippocampus;
backpropagation;
calcium concentration;
action
potential
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