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Epileptiform activity induces distance‐dependent alterations of the Ca 2+ extrusion mechanism in the apical dendrites of subicular pyramidal neurons
Author(s) -
Srinivas Kalyan V.,
Sikdar Sujit K.
Publication year - 2008
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2008.06519.x
Subject(s) - chemistry , biophysics , thapsigargin , neuroscience , endoplasmic reticulum , apical dendrite , electrophysiology , microbiology and biotechnology , biochemistry , cerebral cortex , biology
The cellular and molecular mechanisms that underlie acquired changes in Ca 2+ dynamics of different neuronal compartments are important in the induction and maintenance of epileptiform activity. Simultaneous electrophysiology and Ca 2+ imaging techniques were used to understand the basic properties of dendritic Ca 2+ signaling in rat subicular pyramidal neurons during epileptiform activity. Distance‐dependent changes in the Ca 2+ decay kinetics locked to spontaneous epileptiform discharges and back‐propagating action potentials were observed in the apical dendrites. A decrement in the mean τ value of Ca 2+ decay was observed in distal parts (95–110 μm) of the apical dendrites compared with proximal segments (30–45 μm) in in‐vitro epileptic conditions but not in control. Pharmacological agents that block Ca 2+ transporters, i.e. Na + / Ca 2+ exchangers (Benzamil), plasma membrane Ca 2+ ‐ATPase pumps (Calmidazolium) and smooth endoplasmic reticulum Ca 2+ ‐ATPase pumps (Thapsigargin), were applied locally to the proximal and distal part of the apical dendrites in both experimental conditions to understand the molecular aspects of the Ca 2+ extrusion mechanisms. The relative contribution of Na + /Ca 2+ exchangers in Ca 2+ extrusion was higher in the distal apical dendrites in the in‐vitro epileptic condition and this property modulated the excitability of the neuron in simulation. The Ca 2+ homeostatic mechanisms that restore normal Ca 2+ levels could play a major neuroprotective role in the distal dendrites that receive synaptic inputs.