The triple monoamine re-uptake inhibitor DOV 216,303 promotes functional recovery after spinal cord contusion injury in mice

  title={The triple monoamine re-uptake inhibitor DOV 216,303 promotes functional recovery after spinal cord contusion injury in mice},
  author={Tak-Ho Chu and Karen Cummins and Peter K. Stys},
  journal={Neuroscience Letters},
4 Citations
Role of Descending Serotonergic Fibers in the Development of Pathophysiology after Spinal Cord Injury (SCI): Contribution to Chronic Pain, Spasticity, and Autonomic Dysreflexia
How damage to serotonergic fibers can enable a state of over-excitation that interferes with adaptive learning and contributes to the development of pain, spasticity, and the dysregulation of autonomic function is discussed.
Acute spinal cord injury: Pathophysiology and pharmacological intervention
Several pharmacological and non-pharmacological therapies, which have either been previously investigated or have a potential in the management of this debilitating injury in the near future, are focused on.


The Recovery of 5-HT Immunoreactivity in Lumbosacral Spinal Cord and Locomotor Function after Thoracic Hemisection
Results indicate that return of 5-HT fibers and terminals predict the time course and extent of locomotory recovery after thoracic spinal cord hemisection.
Fluoxetine inhibits matrix metalloprotease activation and prevents disruption of blood-spinal cord barrier after spinal cord injury.
Fluoxetine improved functional recovery in part by inhibiting matrix metalloprotease activation and preventing blood-spinal cord barrier disruption after spinal cord injury, and may represent a potential therapeutic agent for preserving blood-brain barrier integrity following ischaemic brain injury and spinal Cord injury in humans.
Fluoxetine prevents oligodendrocyte cell death by inhibiting microglia activation after spinal cord injury.
It is demonstrated that fluoxetine alleviates oligodendrocyte cell death by inhibiting microglia activation and p38-MAPK activation, followed by pro-NGF production after SCI, and provide a potential usage of fluxetine for a therapeutic agent after acute SCI in humans.
Matrix Metalloproteinases Limit Functional Recovery after Spinal Cord Injury by Modulation of Early Vascular Events
Evidence is provided that MMP-9 plays a key role in abnormal vascular permeability and inflammation within the first 3 d after spinal cord injury, and that blockade of MMPs during this critical period attenuates these vascular events and leads to improved locomotor recovery.
Spontaneous Axonal Regeneration in Rodent Spinal Cord After Ischemic Injury
There is a considerable amount of spontaneous regeneration after spinal cord lesions in rodents and that the fibers remain several months after injury, suggesting that descending central fibers contribute to this endogenous repair of ischemic spinal cord injury.
Basso Mouse Scale for locomotion detects differences in recovery after spinal cord injury in five common mouse strains.
The differing behavioral response to SCI suggests inherent genetic factors significantly impact locomotor recovery and must be considered in studies with inbred or genetically engineered mouse strains.
Plasticity of motor systems after incomplete spinal cord injury
Functional and anatomical evidence exists that spontaneous plasticity can be potentiated by activity, as well as by specific experimental manipulations, which prepare the way to a better understanding of rehabilitation treatments and to the development of new approaches to treat spinal cord injury.