Carter, Brett, Ph.D.

Group Leader at ENI


  • 2002 Undergraduate studies in chemical engineering, Georgia Institue of Technology, Atlanta, USA
  • 2004-2006 Research Assistant with David Clapham, Children’s Hospital Boston, USA
  • 2006-2011 PhD in Neurobiology with Bruce Bean, Harvard, Boston, USA
  • 2011-2017 Postdoctoral training with Craig Jahr, Vollum Institute, Portland, USA
  • since 2017 Research group leader, European Neuroscience Institute, Göttingen, Germany




Major Research Interests

Our research focuses on synaptic function and the changes that can occur after synaptic plasticity. We study intact glutamatergic synapses in brain slices using a combination of electrophysiology, 2-photon imaging, and pharmacology. In particular, we are interested in understanding the role of NMDA receptors in signaling synaptic depression.

Homepage Department/Research Group

http://www.eni.gwdg.de/groups/synaptic-physiology-and-plasticity



Selected Recent Publications


  • Sun W, Wong JM, Gray JA, Carter BC (2018). Incomplete block of NMDA receptors by intracellular MK-801. Neuropharmacology 143: 122-129
  • Carter BC and Jahr CE (2016). Postsynaptic, not presynaptic NMDA receptors are required for spike timing dependent LTD induction. Nat Neurosci. 19: 1218-1224
  • Carter BC, Giessel AJ, Sabatini BL, Bean BP (2012). Transient sodium current at subthreshold voltages: activation by EPSP waveforms. Neuron 75(6): 1081-1093
  • Desai BN, Krapivinsky G, Navarro B, Krapivinsky L, Carter BC, Febvay, S, Delling M, Penumaka A, Ramsey IS, Manasian Y, Clapham DE (2012). Cleavage of TRPM7 releases the kinase domain from the ion channel and regulates its participation in Fas-induced apoptosis. Dev Cell 22(6): 1149-1162
  • Carter BC and Bean BP (2011). Incomplete inactivation and rapid recovery of voltage-dependent sodium channels during high-frequency firing in cerebellar Purkinje neurons. J Neurophysiol. 105(2): 860-871
  • Carter BC and Bean BP (2009). Sodium entry during action potentials of mammalian neurons: incomplete inactivation and reduced metabolic efficiency in fast-spiking neurons. Neuron 64(6): 898-909