Intrinsic plasticity in human motor cortex

Introduction: Neuronal plasticity in animal experiments is usually divided into synaptic and intrinsic mechanisms. While synaptic plasticity results from enhanced or weakened synaptic transmission mediated by NMDA receptors (long-term potentiation (LTP) or -depression), intrinsic plasticity is caused by changes in voltage-gated ion channels. There exists a well characterized correlate of synaptic plasticity in human motor cortex, so called LTP-like plasticity, which can be measured as changes of motor evoked potential (MEP) amplitudes. In this work we investigated whether a correlate for intrinsic plasticity is detectable in human motor cortex.

Methods: Thirty healthy volunteers (mean age 23.5±3.2 years) completed either a motor practice task (MP) or paired associative stimulation (PAS). MP consisted of a net training time of 60 minutes in sessions of 5min each seperated by 5min breaks. For PAS, we applied 200 pairs of peripheral electric and central magnetic stimuli with 25ms interstimulus interval and a frequency of 0.25Hz. Following both protocols we recorded MEP amplitudes and motor threshold (MT) at three points in time over a total of 60 minutes.

Results: Both protocols led to significantly enhanced MEP amplitudes, which reached their maximum at 60 minutes post intervention (MP: 0.90 mV to 1.76 mV, p=0.004; PAS: 1.,02 mV to 2.07 mV, p<0.001). Furthermore, we observed significantly reduced values for MT after MP as well as after PAS (MP: 36.4% to 34.2%, p=0.007; PAS: 38.0% to 36.5%, p=0.02).

Conclusion: Both interventions, MP and PAS led to an increase of MEP amplitude and also to a significant reduction in MT, which occurred in parallel. Voltage-gated sodium and potassium channels are discussed as underlying mechanism of MT. Therefore, changes of MT after plasticity inducing protocols might represent a correlate of intrinsic plasticity in human motor cortex.