Publications by authors named "Tatiana M Shapiro"
After a severe, high-level spinal cord injury (SCI), plasticity to intraspinal circuits below injury results in heightened spinal sympathetic reflex activity and detrimentally impacts peripheral organ systems. Such sympathetic hyperreflexia is immediately apparent as an episode of autonomic dysreflexia (AD), a life-threatening condition characterized by sudden hypertension and reflexive bradycardia following below-level sensory inputs; for example, pressure sores or impacted fecal matter. Over time, plasticity within the spinal sympathetic reflex (SSR) circuit contributes to the progressive intensification of AD events, as the frequency and severity of AD events increase greatly beginning ∼2 weeks post-injury (wpi).
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- Dorsal root crush injuries prevent sensory axons from regenerating into the spinal cord, but activating dorsal root ganglion (DRG) neurons can enhance this growth in lab models.
- * In vivo experiments show that daily chemogenetic activation of DRG neurons for 12 weeks helps regenerate axons across damaged areas, leading to functional recovery in movement tasks.
- * The increase in axon growth is linked to changes in tubulin modifications, which suggest a mechanism for stimulating axon extension in response to neuronal activation.