Adenosine acts in at least three different ways at A1 receptors in order to reduce excitability and signal transfer. In the hippocampus, it causes in a steady state outward (potassium) current which is blocked by barium ions and not sensitive to voltage; (ii) an increase in the calcium and cyclic AMP‐dependent current 1AHP which is responsible for a long lasting afterhyperpolarization and the accommodation of action potential firing; (iii) a presynaptic reduction of excitatory but not inhibitory transmitter release. The mechanism of this effect is unclear. It is, in contrast to the former, not sensitive to pertussis toxin. When the adenosine elicited potassium currents at the postsynaptic site are blocked, slow inward currents, normally carried by calcium, are unaffected by adenosine. A2 receptor mediated actions have not been found in the hippocampus. While the precise analysis of these effects has been done largely on rats they were all found in human hippocampal slices as well. © 1993 Wiley‐Liss, Inc.
|Original language||English (US)|
|Number of pages||4|
|Journal||Drug Development Research|
|State||Published - Mar 1993|
- cyclic AMP
ASJC Scopus subject areas
- Drug Discovery