Spinal cord injury significantly alters the properties of reticulospinal neurons: delayed repolarization mediated by potassium channels

After spinal cord injury (SCI), lamprey reticulospinal (RS) neurons responded to subthreshold depolarizing current pulses with a transient depolarization, which included an initial depolarization that was due to passive channels followed by a delayed repolarization that was mediated by voltage-gated potassium channels. The conductance of these channels ( g K ) was significantly increased for RS neurons after SCI and contributed to a reduction in excitability, which is expected to provide supportive conditions for subsequent axonal regeneration.