IUPS/APS Newsroom March 29-April 6
San Diego Convention Center
Hall E Registration Area/Flex Unit
Telephone: 619.525.6228
Contact: Donna Krupa
(703) 967-2751 (cell)
(301) 634-7209 (office, outside IUPS dates)
Why Can’t Humans Be More
Like (Western Painted) Turtles?
The
right answer could yield better anesthetics, stroke/heart attack recovery
San Diego (April 3, 2005) – For a human, mere minutes
without oxygen (called anoxia) resulting from cardiac arrest, cerebral
stroke or being trapped under water can lead to profound tissue damage and
even death. However a Western painted turtle can survive anoxia for months
without apparent tissue damage. Why, and how?
“Key to surviving anoxia is the shutting off of
energy-utilizing cellular activities, such as the synthesis of proteins and
perhaps most importantly reducing the activity of energy intensive ion
pumps,” according to Leslie T. Buck, a physiologist at University of
Toronto’s Zoology Department. Whereas turtles and many other animals have
shutoff mechanisms, humans and many mammals don’t.
“However, basic biochemical pathways are common to
almost all species, certainly among reptiles (turtles), fish, birds and
mammals,” Buck said, adding: “Therefore, the basic signals and pathways that
permit anoxia-tolerance in the turtle must also be present in mammals.”
In studying the natural mechanisms of anoxia tolerance,
Buck’s lab focused on a particular ion channel, the N-methyl-D-aspartate (NMDA)
receptor. This receptor/channel is strongly associated with anoxic damage
in the mammalian brain by permitting a very large flow of calcium ions into
the cell during anoxia. Unlike anoxia-sensitive mammals, this doesn’t occur
in the western painted turtle’s brain.
*Paper presentation: “NMDA receptor
regulation by mitochondrial KATP channels and adenosine receptors in
cortical neurons of the anoxia-tolerant western painted turtle,” 12:30
p.m.-3 p.m. Sunday April 3, Physiology 381.3/board #A558. On view 7:30 a.m.
- 4 p.m. Others in the research team are Damian Shin and Matthew Pamenter.
Featured topic: Buck is also participating in
“Mechanisms of metabolic depression: comparative aspects,” Sunday April 3,
room 30 B/C beginning at 10:30 a.m. His presentation is scheduled for noon.
Buck is presenting the research at the 35th Congress of the International
Union of Physiological Sciences in San Diego, March 31 - April 5, 2005.
New potassium channel blockage short-circuits
turtle’s shutoff mechanism
A known protective factor is adenosine, a compound that
accumulates in both mammalian and reptile (turtle) brains in response to low
oxygen levels. It reduces the inflow of calcium through NMDA receptors
during anoxia and is associated with brain protection. “However, our work
suggests that adenosine isn’t the only protective factor. Even with the
adenosine pathways inhibited, calcium influx in anoxic turtle brain still
decreases,” Buck noted.
Mathew Pamenter, a graduate student in the lab, had the
idea to investigate a relatively newly discovered potassium channel
(mitochondrial KATP channel) as a possible regulator of NMDA
receptor activity during anoxia. “When this new channel was inhibited, the
protective decrease in calcium influx previously observed in anoxic turtle
brain didn’t occur,” Buck said. “This result indicates that this channel
plays a key role in the natural anoxia-tolerance of the turtle and opens a
new research direction in this area.”
Next steps. Buck said one avenue of
investigation is to see whether the potassium channels may be part of an
oxygen sensing mechanism, which some believe. “Our ultimate goal is to
determine the natural cellular pathways responsible for oxygen sensing and
the shutting off of energy consuming processes in the turtle,” Buck said.
“Then I want to apply this knowledge to human clinical situations, such as
improving outcomes of cerebral stroke and cardiac infarct, and the
development of better anesthetics.”
Funding. Research was supported by a Natural Sciences and
Engineering Research Council of Canada (NSERC) grant.
***
The 35th Congress of the International Union of
Physiological Sciences is in San Diego, March 31 - April 5, 2005. The
Congress (http://www.iups2005.org/)
is organized by the six member societies of the U.S. National Committee of
the IUPS,
the American Physiological Society,
the Society for Neuroscience,
the Microcirculatory Society,
the Society of General Physiologists,
the Biomedical Engineering Society, and
the Society for Integrative and Comparative Biology, under the auspices
of the U.S. National Academy of Sciences.
The IUPS conference, held every four years, runs
concurrently this year with Experimental Biology 2005 at the San Diego
Convention Center.
The American Physiological Society (APS), which is
hosting IUPS, was founded in 1887 to foster basic and applied science, much
of it relating to human health. The Bethesda, MD-based Society has more than
10,000 members and publishes nearly 4,000 articles every year in its 14
peer-reviewed journals. In May, APS received the Presidential Award
for Excellence in Science, Mathematics and Engineering Mentoring (PAESMEM).
***
Editor’s Note: For further information or to
schedule an interview with a member of the research team, please contact
Donna Krupa at the IUPS/APS newsroom @ 619.525.6228 (March 31-April
6), or (703) 967-2751 (cell) or (301) 634-7209 (office), or Stacy Brooks at
240.432.9697 (cell) or 301.634.7253 (office).
A searchable online program for IUPS and EB is at
http://www.faseb.org/meetings/eb2005/call/default.htm
