KCC2 on Axotomized Motoneurons Is Regulated Differently Than in Systems Previously Described

Material below summarizes the article Removal of the Potassium Chloride Co-Transporter From the Somatodendritic Membrane of Axotomized Motoneurons Is Independent of BDNF/TrkB Signaling but Is Controlled by Neuromuscular Innervation, published on September 20, 2019, in eNeuro and authored by Erica Tracey Akhter, Ronald W. Griffith, Arthur W. English, and Francisco J. Alvarez.

Highlights

• Potassium chloride-cotransporter 2 (KCC2) mRNA and protein are downregulated within days of peripheral axotomy of spinal motoneurons.

• KCC2 downregulation on axotomized motoneurons is not dependent on microgliosis or BDNF/TrkB signaling by difference to pathways reported previously in other disease and pathology associated with KCC2 dysregulation.

• Extensive KCC2 depletion is tied to the regenerative state and recovers after motor axons reinnervate muscle, suggesting that GABA/glycinergic synapse action in the absence of KCC2 might contribute to axon regeneration.

About the Contributors

Erica Tracey Akhter, PhD

Erica Tracey Akhter is an instructor at Georgia State University. She obtained her PhD from Emory University, where she worked on the topic of this article and looked for novel mechanisms driving motor axon regeneration.

Arthur William English, PhD

Arthur William English is a professor in the department of cell biology with a joint appointment in rehabilitation medicine at the University of Illinois, where he also obtained his PhD.

Francisco Javier Alvarez, PhD

Francisco Javier Alvarez is a professor in the department of physiology at Emory University. Alvarez obtained his PhD from the Complutense University of Madrid, for work performed at the Cajal institute, in Madrid, and St. Thomas’s Hospital, in London.