Figure 3. Functional and molecular recovery effects of KDS2010 (IMAGE)
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Electrophysiological analyses showed that spinal cord injury led to an excessive increase in tonic GABA currents (persistent inhibitory signaling), which were restored to normal levels after KDS2010 administration, thereby re-establishing excitatory–inhibitory balance between neurons (a). At the molecular level, KDS2010 reduced aberrant GABA production from astrocytes while simultaneously increasing the expression of proBDNF (a precursor of brain-derived neurotrophic factor), thereby shifting the injured spinal cord environment toward a state favorable for neural regeneration (b).
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