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MFA98
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Literature
38 records
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of the firing properties of rat neocortical pyramidal neurones.
intracellular recordings in layer V pyramidal neurones and whole-cell
voltage-clamp recordings in dissociated pyramidal neurones. The
intracellularly recorded neurones were classified on the basis of their firing
characteristics as intrinsically bursting (IB) and regular spiking (RS). The
RS neurones were further subdivided into adapting (RSAD) or non-adapting
(RSNA), depending on the presence or absence of spike frequency adaptation.
Since burst firing in neocortical pyramidal neurones has previously been
suggested to depend on the persistent fraction of Na+ current (INa, p),
pharmacological manipulations with drugs affecting INa inactivation have been
employed. 2. ATX II, a toxin derived from Anemonia sulcata, selectively
inhibited INa fast inactivation in dissociated neurones. In current-clamp
experiments on neocortical slices, ATX II enhanced the naturally occurring
burst firing in IB neurones and revealed the ability of RSNA neurones to
discharge in bursts, whereas in RSAD neurones it increased firing frequency,
without inducing burst discharges. During the ATX II effect, in all the three
neuronal subclasses, episodes of a metastable condition occurred,
characterized by long-lasting depolarizing shifts, triggered by action
potentials, which were attributed to a peak in the toxin-induced inhibition of
INa inactivation. The ATX II effect on IB and RSNA neurones was compared with
that induced by veratridine and iodoacetamide. Veratridine induced a small
increase in the INa and a large shift to the left in the voltage dependence of
INa activation. Accordingly, its major effect on firing characteristics was
the induction of prolonged tonic discharges, associated with burst
facilitation less pronounced than that induced by ATX II. The alkylating agent
iodoacetamide was able to induce a selective small increase in the INa,p, with
a similar but less pronounced effect than ATX II on firing behaviour. 3. The
present results show that pharmacological manipulations capable of slowing
down INa inactivation significantly enhance burst behaviour in IB neurones and
promote burst firing in otherwise non-bursting RSNA neurones. We suggest that
IB and, to a lesser extent, RSNA neurones are endowed with a relatively large
fraction of INa,p which, in physiological conditions, is sufficient to sustain
bursting in IB but not in RSNA neurones.
