Submitted on September 21, 2004
Accepted on February 14, 2005
Adenosine and ATP sensitive potassium channels modulate dopamine release in the anoxic turtle (Trachemys scripta) striatum
Sarah L Milton1* and Peter L Lutz1
1 Department of Biological Sciences, Florida Atlantic University, Boca Raton, FL, USA
* To whom correspondence should be addressed. E-mail: smilton{at}fau.edu.
Excessive dopamine is known to cause hypoxic/ischemic damage to mammalian brain. The freshwater turtle Trachemys scripta, however, maintains basal striatal DA levels in anoxia. We investigated DA balance during early anoxia when energy status in the turtle brain is compromised. The roles of ATP-sensitive potassium channels and adenosine receptors were investigated as these factors affect DA balance in mammalian neurons. Striatal extracellular DA was determined by microdialysis with HPLC in the presence or absence of the specific DA transport blocker GBR 12909, the KATP blocker BDM, or the non-specific AD receptor blocker theophylline. We found that in contrast to long-term anoxia, blocking DA reuptake did not significantly increase extracellular levels in 1 hr anoxic turtles. Low DA levels in early anoxia were maintained instead by activation of KATP channels and AD receptors. Blocking KATP resulted in a 227% increase in extracellular DA in 1 hr anoxic turtles, but had no effect after 4 hr of anoxia. Similarly, blocking AD receptors increased DA during the first hr of anoxia but did not change DA levels at 4 hr anoxia. Support for the role of KATP channels in DA balance comes from normoxic animals treated with KATP opener; infusing diazoxide but not adenosine into the normoxic turtle striatum resulted in an immediate DA decrease to 14% of basal values within 1.5 hrs. Alternative strategies to maintain low extracellular levels may prevent catastrophic DA increases when intracellular energy is compromised while permitting the turtle to maintain a functional neuronal network during long-term anoxia.
