Winnie Wefelmeyer

Winnie Wefelmeyer

Research Associate


I am a postdoctoral researcher with Prof Juan Burrone, investigating structural, intrinsic and synaptic forms of homeostatic plasticity. Neurons have a large number of mechanisms available to avoid extreme forms of activity levels in the brain, such as epileptic states or a complete loss of brain activity. A number of these mechanisms take place directly at the site of action potential generation, the axon initial segment (AIS). Research in the lab has shown that the AIS can change its position along the axon, as well as its length. In addition to this structural plasticity, ion channel composition at the AIS can change in a homeostatic manner and will influence action potential generation. Finally, the AIS is also the target of a specific type of interneuron, the Chandelier cell, which has the potential to strongly oppose action potential initiation. My research currently focuses on how Chandelier cells change the way they influence network activity in vivo throughout postnatal development. Ultimately, understanding how neurons in the brain control their levels of excitability is crucial in understanding normal brain function as well as neurological disorders.


Research Gate:

Selected publications:

Pan-Vazquez A, Wefelmeyer W, Gonzalez Sabater V, Neves G, Burrone J (2020) Activity-Dependent Plasticity of Axo-axonic Synapses at the Axon Initial Segment. Neuron 106: 265-276.e6

Wright R, Newey SE, Ilie A, Wefelmeyer W, Raimondo JV, Ginham R, Mcllhinney RAJ, Akerman CJ (2017) Neuronal Chloride Regulation via KCC2 Is Modulated through a GABAB Receptor Protein Complex. J Neurosci 37: 5447-5462
Wefelmeyer W, Puhl CJ, Burrone J (2016) Homeostatic Plasticity of Subcellular Neuronal Structures: From Inputs to Outputs. Trends Neurosci 39: 656-667
Wefelmeyer W, Cattaert D, Burrone J (2015) Activity-dependent mismatch between axo-axonic synapses and the axon initial segment controls neuronal output. Proc Natl Acad Sci U S A 112: 9757-62