It has been a long time coming, but a good chunk of the work I did for my Ph.D. has finally hit the press in this week's issue of the Journal of Neuroscience.  It is satisfying to finally see my work published in a peer-reviewed journal.


Abstract

The work for this paper began about 5 years ago when I was still at the University of Calgary.  The first time we submitted the paper back in 2002, the reviewers wanted to see biochemical evidence in addition to the electrophysiology that I had already undertaken.  Luckily, when I arrived at UBC after the lab had moved from Calgary, a talented post-doc with expertise in biochemistry by the name of Francisco Cayabyab joined the lab.  He agreed to teach me biochemistry and contribute his own expertise to the project.  The two of us became a synergistic data-producing team, and today's paper is the first (of hopefully many) tangible results of our effort.  I think it proves that success in science requires regular golf and steak-and-egg lunches.

What the paper is about (in plain english):
When the brain is deprived of oxygen, bad things happen.  Toxic chemicals are released that kill neurons (brain cells) by stimulating them to death.  However, the brain is not defenseless.  It can protect itself by releasing agents that prevent the toxic chemicals from over-stimulating neurons.  These agents are called neuroprotective agents. 

One of the most important such neuroprotective agents in the nervous system is adenosine.  Adenosine is a potent inhibitor of excitation, which is why it is so good at protecting neurons from over-stimulation.  Adenosine prevents the release of chemicals from neurons.  Normally these chemicals (neurotransmitters) are required for neurons to communicate.  However these chemicals become toxic if present in excess amounts, which is what happens during a stroke.

Previously, it was not known how adenosine prevents the release of neurotransmitters.  This paper shows that adenosine works by turning on a molecular switch (p38 mitogen-activated protein kinase), which then prevents neurotransmitters from being released.  If the action of this protein could somehow be increased during oxygen deprivation (which occurs during a stroke, seizure, or head injury), it could prevent cells from dying.  It is important to understand the steps by which adenosine (the brain's natural defense against oxygen deprivation) decreases the release of neurotransmitters because it could eventually lead to a therapy that prevents brain damage caused by strokes.

On a more fundamental level, this paper increases our understanding of how the amount of neurotransmitter that is released from neuronal terminals can be regulated.  This is important because changes in the amount of neurotransmitter released is responsible for many brain processes, including learning and memory.