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Journal of Neuroscience, Vol 15, 2777-2787, Copyright © 1995 by Society for Neuroscience
IPSPs strongly inhibit climbing fiber-activated [Ca2+]i increases in the dendrites of cerebellar Purkinje neurons
JC Callaway, N Lasser-Ross and WN Ross
Department of Physiology, New York Medical College, Valhalla 10595, USA.
The interaction between the excitatory climbing fiber (CF) response and
stellate cell inhibition was studied in guinea pig Purkinje cells in
sagittal slices from the cerebellar vermis. Sharp microelectrode recordings
from the soma or dendrites were combined with high-speed fluorescence
imaging of intracellularly injected fura-2. In this way both the electrical
responses and the associated [Ca2+]i changes could be monitored at the same
time. Usually simultaneously activated inhibition caused almost no change
to the somatically recorded CF response. However, the inhibition caused a
strong reduction in the CF- associated [Ca2+]i increase which normally was
widespread in the dendrites. This effect was graded; stronger inhibition
caused a larger and more widespread reduction in the [Ca2+]i change that
was greatest in the more distal dendrites. Sometimes the reduction was over
90% in the distal dendrites and occasionally it was localized to only a
single dendritic branch. Both the inhibitory postsynaptic potential (IPSP)
and the associated reduction in the CF-induced [Ca2+]i change were blocked
by bicuculline, a GABAA receptor antagonist. Dendritic recordings showed
that each CF response evoked a 2-3 msec wide action potential. The
amplitude of this action potential was reduced in a graded manner by the
IPSP in parallel with the reduction in the [Ca2+]i change. Varying the time
between the activation of the IPSP and the CF response showed that both the
reduction in the [Ca2+]i change and the action potential amplitude occurred
in a narrow time window of about 8-10 msec, about the rise time of the
IPSP. Together these results indicate that the CF response activates a fast
dendritic Ca2+ spike that causes most of the [Ca2+]i increase, both of
which can be blocked by an inhibitory shunting conductance. This
interaction provides a means whereby Ca(2+)-dependent dendritic mechanisms
can be modulated without affecting the immediate output of the Purkinje
cell.
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