Research reportEffect of rat spinal cord injury (hemisection) on the ex vivo uptake and release of [3H]noradrenaline from a slice preparation

- Spinal cord injury was simulated by hemisection in rats.
- Uptake and release of [3H]NA from spinal cord slices was measured.
- Hemisection increased resting and stimulated [3H]NA-release.
- Nisoxetine inhibited [3H]NA uptake.
- Data suggest reverse operation of noradrenaline transporter after spinal cord injury.

We measured the ex vivo uptake and release of [3H]noradrenaline ([3H]NA) from perfused rat spinal cord slice preparations at 1, 3 and 14 days after unilateral hemisection-induced spinal cord injury (SCI) compared with control slice preparations.After surgical hemisection under anaesthesia, the rats showed characteristic signs of hemiplegia, with no movement of the ipsilateral hindlimb. After 3 days, the electron microscopy images showed overall degeneration of neuronal organelles and the myelin sheath, but the synapses seemed to be intact. In ex vivo experiments, the spinal cord injury did not influence uptake but increased [3H]NA release at rest and in response to axonal stimulation. The effect of a selective noradrenaline reuptake inhibitor, nisoxetine, was studied to identify the mechanisms underlying the increase in NA release. Nisoxetine potentiated stimulation-evoked [3H]NA release from the non-injured tissue, but it gradually lost its effectiveness after injury, depending on the time (1 and 3 days) elapsed after hemisection, indicating that the noradrenaline transporter binding sites of the terminals become impaired after decentralisation.