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Fig. 7. Involvement of KATP channels, but not adenosine receptors, in
anoxic hyperpolarisation of neonatal respiratory neurons and frequency
depression of respiratory rhythm. (A) Chemical anoxia due to 1 mmol
l–1 CN– notably depresses respiratory
frequency in the brainstem–spinal cord preparation from newborn rats. In
the presence of CN–, this effect is reversed by the
KATP channel blocker gliclazide (200 µmol l–1).
(B) In a neuron in the region of the pre-Bötzinger complex (PBC) of a
non-rhythmic medullary slice, tolbutamide blocks the outward current and
conductance increase underlying the anoxic hyperpolarisation. Membrane
conductance is measured by injection of hyperpolarising dc current pulses. (C)
In a pre-inspiratory neuron (also classified as `biphasic-expiratory';
Ballanyi et al., 1999), the
anoxia-induced hyperpolarisation and conductance increase abolishes rhythmic
fluctuations of membrane potential. After recovery from anoxia (wash),
administration of adenosine (500 µmol l–1) fails to mimic
the anoxic hyperpolarisation, conductance increase or block of
respiratory-related membrane potential fluctuations. A, data from L. Secchia
and K. Ballanyi; B,C, data from K. Ballanyi.
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