Ca 2+ -Dependent Plasticity of Miniature Inhibitory Postsynaptic currents
following amputation of Dendrites in Central Neurons.
Soltesz, I., I. Mody.
Department of Anesthesiology and Pain Management, UT Southwestern Med.
Ctr., 5323 Harry Hines Blvd., Dallas, TX 75235-9068.
APStracts 2:0029N, 1995.
SUMMARY AND CONCLUSIONS
1) The effects of cutting off the bulk (more than 2/3) of the dendritic tree
(dendrotomy) on GABAergic miniture inhibitory postsynaptic currents (mIPCSs)
were studied in granule cells of the adult rat dentate gyrus in 400 m thick
slices in vitro . 2) Following dendrotomy carried out in warm (32C) control
artificial cerebro-spinal fluid (ACSF) only small antidromic population spikes
could be evoked in the granule cell layer and no viable whole-cell recordings
could be obtained. However, when dendrotomy was performed in cold (8-10C)
control ACSF, the amplitude of the antidromic population spikes increased and
stable whole-cell recordings became possible. 3) Whole-cell recordings, with
CsCl filled pipettes, from granule cells dendrotomized in cold control ACSF
revealed significant alterations, lasting over 10 hrs, in the decay kinetics
of mIPSCs. The change consisted of a calcium-dependent transformation of the
normal, single exponential decay into a prolonged double exponential which
effectively increased the charge transferred by the synaptic events (the total
area of the currents) by 67%. When 30 mM BAPTA was included in the pipette,
the changes in the mIPSCs decay kinetics could still be observed after
dendrotomy, indicating that the maintenance phase of this plasticity did not
depend on elevated intracellular calcium levels. 4) Viable whole-cell
recordings could also be obtained in dendrotomized granule cells when the
amputation of dendrites was carried out at 32C after incubation for 2 hrs with
the cell-permeant Ca 2+ chelator, BAPTA-AM (50 M), or the cutting process was
done in an ACSF containing either a combination of excitatory amino acid
receptor antagonists APV (25 M) + CNQX (10 M), a blocker of intracellular Ca
2+ release dantrolene-Na (20 M), or the voltage-gated Na + channel blocker
tetrodotoxin (TTX; 1 M). 5) Following dendrotomy in BAPTA-AM, APV+CNQX,
APV+CNQX+TTX and/or dantrolene, the changes in decay kinetics were prevented,
indicating that a rise in intracellular Ca 2+ concentration plays a pivotal
role in this plasticity. 6) Computer simulations of mIPSCs suggested that
changes in single channel kinetics alone can, in principle, account for the Ca
2+ -dependent changes in mIPSC decay kinetics. 7) These findings are
consistent with a lasting Ca 2+ -dependent increase in GABA A receptor
function in cells that survive physical injury to their dendrites.
Received 29 September 1994; accepted in final form 6 January 1995.
APS Manuscript Number J615-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 3 April 1995.