Increased responses in the somatosensory thalamus immediately after spinal cord injury

Abstract

Spinal cord injury (SCI) involves large-scale deafferentation of supraspinal structures in the somatosensory system, producing well-known long-term effects at the thalamo-cortical level. We recently showed that SCI provokes immediate changes in cortical spontaneous and evoked responses and here, we have performed a similar study to define the immediate changes produced in the thalamic ventro-postero-lateral nucleus (VPL) that are associated with the forepaw and hindpaw circuits. Extracellular electrophysiological recordings from the VPL reflected the spontaneous activity and the responses to peripheral electrical stimulation applied to the paws. Accordingly, the activity of the neuronal populations recorded at specific thalamic locations that correspond to the forepaw and hindpaw circuits was recorded under control conditions and immediately after thoracic SCI. The results demonstrate that peripheral inputs from both extremities overlap on neuronal populations in the somatosensory thalamus. In addition, they show that the responses of thalamic neurons to forepaw and hindpaw stimuli are increased immediately after SCI, in association with a specific decrease in spontaneous activity in the hindpaw locations. Finally, the increased thalamic responses after SCI have a state-dependent component in relation with cortical activity. Together, our results indicate that the thalamic changes occurring immediately after SCI could contribute to the cortical changes also detected immediately after such spinal lesions.

Feasibility of imaging evoked activity throughout the rat brain using electrical impedance tomography

“…LFP recordings of forepaw activity stimulated at 0.5 Hz in the VPL by Alonso-Calvino et al (2016) had an amplitude around 250 μV, a similar amplitude to the 266 AE 71 μV observed here. At 20 Hz stimulation frequency the amplitude of the evoked potential recorded decreased to 168 AE 51 μV.…”

Cortex-dependent recovery of unassisted hindlimb locomotion after complete spinal cord injury in adult rats

“…Future work should expand on the molecular mechanisms of this cortical plasticity, establishing the role of pre-synaptic and post-synaptic processes as well as the possible contribution of astrocytes and neuron-glia interaction in the cortical reorganization observed here. Overall, even though subcortical plasticity is likely to have contributed to the observed functional recovery (Kambi et al, 2014; Alonso-Calviño et al, 2016), our results suggest that at least part of the plasticity induced by our therapies after spinal cord injury is genuinely cortical.…”

Optical Imaging of the Motor Cortex Following Antidromic Activation of the Corticospinal Tract after Spinal Cord Injury

“…SCI induces cellular and molecular events via both primary and secondary injury cascades (Davis et al, 1996; Alonso-Calvino et al, 2016). This cascade process leads to inflammatory reactions, neuronal apoptosis, and reactive astrogliosis, which may cause impaired regeneration, tissue loss, and functional disabilities (Chen et al, 2016).…”

“…These areas were diminished in the 1-W SCI group, wherein expression times were also significantly delayed. The delayed activating optical signals might be resulted from reduced populations of surviving neurons and increased demyelination after SCI (Alonso-Calvino et al, 2016; Chen et al, 2016). However, improved activating optical signals 4 weeks after SCI may have reflected spontaneous recovery, such as newly formed neuronal reorganization and neuroplasticity of the remaining neuronal synapses in the adjacent injury site (Murray et al, 2011; He et al, 2017).…”