Trevor Atkinson
National Research Council
13 Papers
80 Citations
Trevor Atkinson is an academic researcher from National Research Council. The author has contributed to research in topics: Receptor & Low-affinity nerve growth factor receptor. The author has an hindex of 9, co-authored 13 publications.
Chat about Author
Papers
Transient NMDA receptor inactivation provides long-term protection to cultured cortical neurons from a variety of death signals.
Roger Tremblay,Balu Chakravarthy,Kimberley Hewitt,Joseph S. Tauskela,Paul Morley,Trevor Atkinson,Jon P. Durkin +6 more
TL;DR: A novel role for MK-801 and other NMDA receptor antagonists in preconditioning neurons to withstand a wide range of subsequent lethal insults is described, and it is likely that the stress associated with transient inactivation of NMDA receptors triggered a rapid compensatory survival response that provided long-term protection from a spectrum of insults.
92
Amyloid-beta peptides stimulate the expression of the p75(NTR) neurotrophin receptor in SHSY5Y human neuroblastoma cells and AD transgenic mice.
Balu Chakravarthy,Chantal Gaudet,Michel Ménard,Trevor Atkinson,Leslie Brown,Frank M. LaFerla,Ubaldo Armato,James F. Whitfield +7 more
TL;DR: It appears that it could be the accumulating Abeta(1-42) that increases or at least prevents the downregulation of p75 (NTR) receptors in key parts of AD brains.
85
Comparison of the changes in protein kinase c induced by glutamate in primary cortical neurons and by in vivo cerebral ischaemia
Balu Chakravarthy,Jian Wang,Roger Tremblay,Trevor Atkinson,Fuhu Wang,Hui Li,Alastair M. Buchan,Jon P. Durkin +7 more
TL;DR: The results indicate that the loss of PKC observed in in vivo ischaemia is likely to be due to excitotoxic damage and that this event can be closely mirrored in primary neuronal cultures damaged by glutamate.
26
The phosphatase inhibitor, okadaic acid, strongly protects primary rat cortical neurons from lethal oxygen-glucose deprivation.
TL;DR: OA increased the phosphorylation of both PI-3K/Akt and MAPK, and stimulated new protein synthesis, and acted independently of the CREB activation and FKHRL1 and GSK-3 inactivation which have been implicated in IGF-1 actions.
16
Relative expression of the p75 neurotrophin receptor, tyrosine receptor kinase A, and insulin receptor in SH-SY5Y neuroblastoma cells and hippocampi from Alzheimer's disease patients.
TL;DR: Findings suggest that increased expression of the p75NTR due to IR signaling inhibition by AβOs might be involved in the pathology of AD.
13