Hypoxia and
ischemia occur in the spinal cord when blood vessels of the spinal cord are compressed under pathological conditions such as
spinal stenosis,
tumors, and traumatic
spinal injury. Here by using spinal cord slice preparations and patch-clamp recordings we investigated the influence of an
ischemia-simulating medium on dorsal horn neurons in deep lamina, a region that plays a significant role in sensory
hypersensitivity and pathological
pain. We found that the
ischemia-simulating medium induced large inward currents in dorsal horn neurons recorded. The onset of the
ischemia-induced inward currents was age-dependent, being onset earlier in older animals. Increases of sensory input by the stimulation of afferent fibers with electrical impulses or by
capsaicin significantly speeded up the onset of the
ischemia-induced inward currents. The
ischemia-induced inward currents were abolished by the
glutamate receptor antagonists CNQX (20 microM) and APV (50 microM). The
ischemia-induced inward currents were also substantially inhibited by the
glutamate transporter inhibitor
TBOA (100 microM). Our results suggest that
ischemia caused reversal operation of
glutamate transporters, leading to the release of
glutamate via
glutamate transporters and the subsequent activation of
glutamate receptors in the spinal dorsal horn neurons.