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TBGW03
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Literature
38 records
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enhancing persistent Na+ conductance or by blocking BK channels
selected neocortical neurons in cats in vivo and in slices of adult ferret and
cat brain. Fast rhythmic bursting (FRB) has been recorded in certain
superficial and deep principal neurons and in aspiny presumed local circuit
neurons; it can be evoked by depolarizing currents or by sensory stimulation
and has been proposed to depend on a persistent g(Na) that causes spike
depolarizing afterpotentials. We constructed a multicompartment 11-conductance
model of a layer 2/3 pyramidal neuron, containing apical dendritic
calcium-mediated electrogenesis; the model can switch between rhythmic spiking
(RS) and FRB modes of firing, with various parameter changes. FRB in this
model is favored by enhancing persistent g(Na) and also by measures that
reduce [Ca(2+)](i) or that reduce the conductance of g(K(C)) (a fast voltage-
and Ca(2+)-dependent conductance). Axonal excitability plays a critical role
in generating fast bursts in the model. In vitro experiments in rat layer 2/3
neurons confirmed (as shown previously by others) that RS firing could be
switched to fast rhythmic bursting, either by buffering [Ca(2+)](i) or by
enhancing persistent g(Na). In addition, our experiments confirmed the model
prediction that reducing g(KC) (with iberiotoxin) would favor FRB. During the
bursts, fast prepotentials (spikelets) could occur that did not originate in
apical dendrites and that appear to derive from the axon. We suggest that
modulator-induced regulation of [Ca(2+)] dynamics or of BK channel
conductance, for example via protein kinase A, could play a role in
determining the firing pattern of neocortical neurons; specifically, such
modulation could play a role in regulating whether neurons respond to strong
stimulation with fast rhythmic bursts.
