Figure 3.

ISF flow is disturbed due to demyelination damage. In the Cuprizon-mediated demyelination rat model, the integrity of the myelin sheath in the internal capsule area was interrupted, as observed using EM and Black Gold staining (B), resulting in myelin sheath splitting, myelin balloon formation and separation from axon. The destruction of the barrier structure accompanied by abnormal ISF flow was observed using LSCM (C). The internal capsule area between Cn and Tha showed demyelination compared to that in the non-demyelination group (A). The traced ISF in one ISS division could be transported to the other (Cn and Tha), i.e., the fluorescent probe in Tha was observed in the adjacent Cn area, and vice versa (C). In the control group, tracer-based MRI showed that the high intensity after Gd-DTPA administration into Cn was limited within the corresponding drainage division and its margin adjacent to the internal capsule was sharp in the control group (upper row, D). No D value could be detected in the D mapping (E). However, in the demyelination group, the high intensity spanned the internal capsule and emerged in Tha (lower row, D). D values could be detected in D mapping. In demyelinated rats (A), communication between the two divisions emerged after the integrity of the myelin sheath in the inner capsule was interrupted, and the ISF in one ISS division could travel to the other. In the Cn division, ISF flow to the cortex was reduced. Thus, local homeostasis was interrupted. Comparison of λ, α, D and k values between control group and demyelination group (columns a-d), clearance rates (k) of the demyelination group were significantly higher (d) (P <0.01), while the others showed no significant difference (a-c) (P>0.05).