Dr James Higham University positionPhD student DepartmentsHome pagehttps://www.neuroscience.cam.ac.uk/directo... Research ThemeInterestsI am a Research Associate in Pharmacology interested in the interaction between novel inflammatory mediators and sensory neurons, with the aim of better understanding nociceptive signalling during inflammatory disease. My PhD with Dr David Bulmer was primarily focussed on investigating the interaction between Angiotensin II and sensory neurons in vitro, using genetically engineered neurons (in collaboration with Prof John Wood and Prof James Cox, UCL) and pharmacological tools in tandem with calcium imaging, patch-clamp electrophysiology and immunofluorescence. Research Focus
EquipmentCalcium imaging Cell culture Electrophysiological recording techniques Immunohistochemistry Whole cell patch clamp Collaborators
Associated News ItemsPublications2019Edgar Buhl*, James P Higham*, James J L Hodge (2019), “Alzheimer's Disease-Associated Tau Alters Drosophila Circadian Activity, Sleep and Clock Neuron Electrophysiology” Neurobiol of Dis Vol 130 James Higham, Giriraj Sahu, Rima-Marie Wazen, Pina Colarusso, Alice Gregorie, Bartholomew S. J. Harvey, Lucy Goudswaard, Gemma Varley, David N Sheppard, Ray W Turner and Neil V Marrion (2019), “Preferred formation of heteromeric channels between co-expressed SK1 and IKCa channel subunits provides a unique pharmacological profile of Ca2+-activated K+ channels” Mol Pharm 97(5): 115-126 James P. Higham*, Bilal R. Malik*, Edgar Buhl, Jennifer M. Dawson, Anna S. Ogier, Katie Lunnon and James J. L. Hodge (2019), “Alzheimer’s Disease Associated Genes Ankyrin and Tau Cause Shortened Lifespan and Memory Loss in Drosophila” Front Cell Neuro Vol 13; pp260 James P. Higham†, Sergio Hidalgo†, Edgar Buhl and James J. L. Hodge* (2019), “Restoration of Olfactory Memory in Drosophila Overexpressing Human Alzheimer’s Disease Associated Tau by Manipulation of L-Type Ca2+ Channels” Front Cell Neuro Vol 13; pp409 2017James P Higham (2017), “Letter: Tangled tau: Active pathology or footprint of disease?” Alzheimer's and Demantia 3(4): 658-659 |