Peripheral nerve injury induces immediate increases in layer v neuronal activity.

BACKGROUND: Peripheral nerve injury leads to changes in neuronal activity in the contralateral and ipsilateral primary somatosensory cortices (S1), which may lead to enduring sensory dysfunction and pain. Plasticity in the barrel and visual cortices has been shown to occur in a layer-specific manner. However, little is known about the layer specific changes associated with limb injury.
OBJECTIVE: To determine the layer-specific changes in neuronal activity associated with short-term plasticity induced by peripheral nerve injury in the rat.
METHODS: In vivo electrophysiology recordings (multiunit activity and local field potential) and high-resolution functional magnetic resonance imaging techniques were applied to characterize neuronal and hemodynamic responses across the depth of S1 contralateral and ipsilateral to the injury.
RESULTS: Within 60 minutes following injury, atypical increases in neuronal and hemodynamic responses in the deprived S1, ipsilateral to the noninjured limb, were observed in response to stimulation of the noninjured limb. The most prominent increases in neuronal activity in the deprived S1 occurred in layer V.
CONCLUSION: Layer V neurons provide the major output of S1 and they send and receive transcallosal input. Thus, the immediate changes in neuronal firing patterns in layer V induced by the injury, can adversely affect the activity of subcortical regions and also interfere with normal cortical processing and interhemispheric communication. Therefore, a rehabilitation strategy that targets layer V neurons activity and starts immediately after the injury may benefit the functional outcome.