# Changes in Spinal Neural Circuit Plasticity in a Rat Sciatic Nerve Transection Model

## TL;DR

This study examines how spinal neural circuits change in rats after sciatic nerve injury, finding distinct plasticity patterns in motor neurons and cholinergic interneurons.

## Contribution

The study reveals localization-dependent plasticity in cholinergic interneurons following sciatic nerve transection.

## Key findings

- Motor neuron cell-body volume decreased by 29% at 6 weeks post-SNT.
- Lateral CINs showed increased vGlut1 inputs without cell loss, while medial CINs showed delayed vGlut1 increases and cell number reduction.
- CST axonal number and volume remained unchanged after SNT.

## Abstract

Changes in neural plasticity crucially modulate functional recovery after central nerve injury. To describe morphological peripheral nerve injury‐related changes, we comprehensively elucidated post‐sciatic nerve transection (post‐SNT) plasticity changes in the lumbar spinal corticospinal tract (CST), motor neurons, and cholinergic interneurons (CINs).

In a rat SNT model, we compared post‐SNT changes in lumbar spinal cord plasticity at 2, 4, and 6 weeks with those in the Sham group. Using neural tracers and immunohistochemistry, we labeled and analyzed the CST axonal number and volume, motor neuron cell‐body volume and synaptic inputs, and cholinergic interneuron (CIN) (medial and lateral, based on the distance from the central canal) number and synaptic inputs.

Compared to the Sham group, the SNT groups showed no significant post‐SNT changes in CST axonal number and volume. Motor neuron cell‐body volume decreased by 29% at 6 weeks post‐SNT, and vesicular glutamate transporter 1 (vGlut1) and vesicular acetylcholine transporter (vAchT) synaptic inputs decreased by 82–93% and 27–42%, respectively, from 2 weeks post‐SNT onward. From 2 weeks post‐SNT onward, cell numbers were maintained, although vGlut1 synaptic inputs increased by 98%–68% in lateral CINs. At 6 weeks post‐SNT, a 44% reduction in cell numbers and a simultaneous 107% increase in vGlut1 synaptic inputs were noted in medial CINs.

Following SNT, although CST axonal numbers remained unchanged, plasticity changes were observed in motor neurons and in CINs. CINs exhibited distinct plasticity changes depending on their localization.

Following sciatic nerve transection (SNT), corticospinal tract (CST) labeling in the lumbar gray matter remained unchanged, whereas motor neurons showed soma atrophy with reduced perisomatic vesicular glutamate transporter 1 (vGlut1) and vesicular acetylcholine transporter (vAchT) inputs. In contrast, cholinergic interneurons (CINs) exhibited localization‐dependent plasticity: lateral CINs showed an early increase in vGlut1 inputs without cell loss, while medial CINs showed a delayed increase in vGlut1 inputs accompanied by reduced cell number.