Matthew Pamenter

Dr. Matthew PamenterDr. Matthew Pamenter's primary research focus is the study of natural adaptations to low oxygen stress that enable central nervous system function and viability in hypoxic/anoxic environments. Specifically, he uses hypoxia-tolerant comparative model organisms (goldfish, turtle, naked mole rat) and oxygen-sensitive mammalian cells and tissues (mouse, rat, human) to investigate mechanisms involved in hypoxia tolerance and neuroprotection.

The long-term aim of Dr. Pamenter's research is to discover pathways or molecular candidates that enable endogenous systemic tolerance to low oxygen stress in hypoxia-adapted species. Such lessons may also be translated to hypoxia-intolerant mammals in order to reduce or reverse damage caused by pathological conditions that compromise oxygen supply to the brain (e.g., stroke, traumatic brain injury, sleep apnea), thereby greatly increasing potential funding sources for my research into basic physiology questions.


Affiliation

University: University of British Columbia
Faculty: Science
Department: Zoology
Position: Post-Doctoral Fellow


Recent Publications

Pamenter ME and Powell FL (2013). Invited review: Signaling mechanisms of long-term facilitation of breathing with intermittent hypoxia. F1000 Reports. 5:23.

Pamenter ME, Perkins GA, Gu XQ, Ellisman MH and Haddad GG (2013). DIDS (4,4’-diisothiocyano-2,2’-stilbenedisulfonic acid) induces apoptotic cell death in cultured hippocampal neurons and is not protective against ischemic stress. PLoS One. 8(4):e60804.

Pamenter ME, Perkins GA, McGinness AK, Gu XQ, Ellisman MH and Haddad GG (2012). Autophagy and apoptosis are induced in neurons and astrocytes treated with an in vitro mimic of the ischemic penumbra. PLoS One. 7(12):e51469.

Pamenter ME, Hogg DW, Gu XQ, Buck LT and Haddad GG (2012). Painted turtle cortex is resistant to an in vitro mimic of the ischemic mammalian penumbra. Journal of Cerebral Blood Flow and Metabolism. 32(11)2033-2043.

Pamenter ME, Hogg DW, Ormond J, Shin DS, Woodin MA and Buck LT (2011). Endogenous GABA(A) and GABA(B) receptor-mediated electrical suppression is critical to neuronal anoxia tolerance. Proceedings of the National Academy of Sciences (USA). 108(27):11274-11279.