Enhanced Spontaneous Transmitter Release Is the Earliest Consequence of Neocortical Hypoxia That Can Explain the Disruption of Normal Circuit Function

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Fig. 1.
Fig. 1.

Hypoxia induces activation of ATP-sensitive K+ channels with a lag of ∼3 min.A, Under normoxic conditions, a cell-attached recording from a representative layer 5 neuron in a 400-μm-thick slice maintained at 37°C revealed brief, sporadic, “background” openings of potassium channel. The openings are inward because the pipette contained 140 mm K+, and the membrane was held at a Vr −20 mV (approximately −90 mV). Channel currents were filtered at 2 kHz (−3 dB) and digitized at 10 kHz. B, One minute of hypoxia causes no alteration in the potassium channel activity. C, After 3 min of hypoxia, the ATP-sensitive K+ channel began to activate, first as a single openings and minibursts; the frequency and duration of the bursts increased rapidly while hypoxia proceeded.D, In this patch, the ATP-sensitive K+ channel openings disappear completely only after 10 min of reoxygenation. E, Plot of K+ channel opening frequency before, during, and after a 4 min hypoxic episode. Each dot represents an averaged channel opening frequency during 500 msec. F, Changes in neuronal input resistance before, during, and after a 4 min hypoxic episode.

  1. The Journal of Neuroscience vol. 21 no. 13 4600-4608
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