Home > Publications Database > Transplantation of dorsal root ganglia overexpressing the NaChBac sodium channel improves locomotion after complete SCI > print

001     269434
005     20240926164136.0
024 7 _ |a pmc:PMC11184342
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024 7 _ |a 10.1016/j.ymthe.2024.03.038
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037 _ _ |a DZNE-2024-00531
082 _ _ |a 610
100 1 _ |a Hingorani, Sonia
|b 0
245 _ _ |a Transplantation of dorsal root ganglia overexpressing the NaChBac sodium channel improves locomotion after complete SCI
260 _ _ |a New York, NY
|c 2024
|b Nature Publ. Group
336 7 _ |a article
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520 _ _ |a Spinal cord injury (SCI) is a debilitating condition currently lacking treatment. Severe SCI causes the loss of most supraspinal inputs and neuronal activity caudal to the injury, which, coupled with the limited endogenous capacity for spontaneous regeneration, can lead to complete functional loss even in anatomically incomplete lesions. We hypothesized that transplantation of mature dorsal root ganglia (DRGs) genetically modified to express the NaChBac sodium channel could serve as a therapeutic option for functionally complete SCI. We found that NaChBac expression increased the intrinsic excitability of DRG neurons and promoted cell survival and neurotrophic factor secretion in vitro. Transplantation of NaChBac-expressing dissociated DRGs improved voluntary locomotion 7 weeks after injury compared to control groups. Animals transplanted with NaChBac-expressing DRGs also possessed higher tubulin-positive neuronal fiber and myelin preservation, although serotonergic descending fibers remained unaffected. We observed early preservation of the corticospinal tract 14 days after injury and transplantation, which was lost 7 weeks after injury. Nevertheless, transplantation of NaChBac-expressing DRGs increased the neuronal excitatory input by an increased number of VGLUT2 contacts immediately caudal to the injury. Our work suggests that the transplantation of NaChBac-expressing dissociated DRGs can rescue significant motor function, retaining an excitatory neuronal relay activity immediately caudal to injury.
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650 _ 7 |a dorsal root ganglia
|2 Other
650 _ 7 |a functional recovery
|2 Other
650 _ 7 |a inhibitory and excitatory input
|2 Other
650 _ 7 |a neuronal survival
|2 Other
650 _ 7 |a neuronal transplantation
|2 Other
650 _ 7 |a sodium channel
|2 Other
650 _ 7 |a spinal cord injury
|2 Other
650 _ 7 |a Sodium Channels
|2 NLM Chemicals
650 _ 2 |a Ganglia, Spinal: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: metabolism
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: therapy
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: genetics
|2 MeSH
650 _ 2 |a Locomotion
|2 MeSH
650 _ 2 |a Sodium Channels: metabolism
|2 MeSH
650 _ 2 |a Sodium Channels: genetics
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Recovery of Function
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Gene Expression
|2 MeSH
650 _ 2 |a Myelin Sheath: metabolism
|2 MeSH
650 _ 2 |a Cell Survival
|2 MeSH
700 1 _ |a Paniagua Soriano, Guillem
|b 1
700 1 _ |a Sánchez Huertas, Carlos
|b 2
700 1 _ |a Villalba Riquelme, Eva María
|b 3
700 1 _ |a López Mocholi, Eric
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700 1 _ |a Martínez Rojas, Beatriz
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700 1 _ |a Alastrué Agudo, Ana
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700 1 _ |a Dupraz, Sebastián
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700 1 _ |a Ferrer Montiel, Antonio Vicente
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700 1 _ |a Moreno Manzano, Victoria
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773 _ _ |a 10.1016/j.ymthe.2024.03.038
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