抄録
We intended to elucidate the mechanism how hypoxia and ischemia affect the neural function of the spinal cord. Transverse slices of the juvenile rat cervical spinal cord were stained with a voltage-sensitive dye. Preparations were superfused with a control mock cerebrospinal fluid (mock CSF) (O2=95%, CO2=5%, glucose 11mM). We recorded processes of electrical stimulation induced neural excitation propagation on the transverse plain of the spinal cord using a high-speed optical recording system. We, then, analyzed the effect of hypoxia by superfusing the preparations with a hypoxic mock CSF (N2=95%, CO2=5%, glucose 11mM) as well as the effect of ischemia with an ischemic mock CSF (N2=95%, CO2=5%, glucose free). Under the control condition, two components were identified in the depolarizing optical responses to dorsal root stimulation: a fast component of short duration and a slow component of long duration. Hypoxic condition as well as short term ischemic exposure reversibly reduced the slow component without affecting the fast component. However, long term ischemic exposure irreversibly reduced not only the slow component but the fast component. Because the fast component represents pre-synaptic, and the slow component represents post-synaptic neural activity, it was suggested that hypoxia and ischemia disturb synaptic transmission in the neuronal network of the spinal cord. [Jpn J Physiol 54 Suppl:S109 (2004)]
