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Departments of 1 Pediatrics (Section of Respiratory Medicine) and 2 Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510
To study the physiological effects of chronic
intermittent hypoxia on neuronal excitability and function in mice, we
exposed animals to cyclic hypoxia for 8 h daily (12 cycles/h) for
~4 wk, starting at 2-3 days of age, and examined the properties
of freshly dissociated hippocampal neurons in vitro. Compared with
control (Con) hippocampal CA1 neurons, exposed (Cyc) neurons showed
action potentials (AP) with a smaller amplitude and a longer duration and a more depolarized resting membrane potential. They also have a
lower rate of spontaneous firing of AP and a higher rheobase. Furthermore, there was downregulation of the Na+ current
density in Cyc compared with Con neurons (356.09 ± 54.03 pA/pF in
Cyc neurons vs. 508.48 ± 67.30 pA/pF in Con, P < 0.04). Na+ channel characteristics, including activation,
steady-state inactivation, and recovery from inactivation, were similar
in both groups. The deactivation rate, however, was much larger in Cyc
than in Con (at 
100 mV, time constant for deactivation = 0.37 ± 0.04 ms in Cyc neurons and 0.18 ± 0.01 ms in Con
neurons). We conclude that the decreased neuronal excitability in mice
neurons treated with cyclic hypoxia is due, at least in part, to
differences in passive properties (e.g., resting membrane potential)
and in Na+ channel expression and/or regulation. We
hypothesize that this decreased excitability is an adaptive response
that attempts to decrease the energy expenditure that is used for
adjusting disturbances in ionic homeostasis in low-O2 conditions.
sodium channels; excitability; oxygen deprivation
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