Korean J Physiol Pharmacol.
1997 Apr;1(2):135-142.
The influence of N-6-cyclopentyladenosine and magnesium on
norepinephrine release in the rat hippocampus
- Affiliations
-
- 1Department of Pharmacology, Wonkwang University School of Medicine and
Medicine Resources Res. Cent., Iksan 5 South Korea.
Abstract
-
As it has been reported that the depolarization-induced norepinephrine
(NE) release is modulated by activation of presynaptic A-1-adenosine
heteroreceptor and various lines of evidence indicate that
A-2-adenosine receptor also presents in hippocampus, and that the
adenosine effect is magnesium dependent, the present study was
undertaken to delineate the role of adenosine receptors in the
modulation of hippocampal NE release. Slices from the rat hippocampus
were equilibrated with (3H)-NE and the release of the labelled product,
(3H)-NE, was evoked by electrical stimulation (3 Hz, 5 V cm-1, 2 ms,
rectangular pulses), and the influence of various agents on the evoked
tritium outflow was investigated. N-6-cyclopentyladenosine (CPA), in
concentrations ranging from 0.1 to 10 micrometer, decreased the (3H)-NE
release in a dose-dependent manner without changing the basal rate of
release, and these effects were significantly inhibited by
8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 2 micrometer) treatment. When the
magnesium concentration was reduced to 0.4 mM or completely removed,
the evoked NE release increased along with decreased basal rate of
release. In contrast, increasing the magnesium concentrations to 2.4
and 4 mM, decreased the evoked NE release. The CPA effects on evoked NE
release were reduced by magnesium removal, but potentiated by 2.4 mM
magnesium in the medium. 5-(N-cyclopropyl)-carboxamodiadenosine (CPCA,
1 & 10 micrometer), an A-2-agonist, decreased the evoked tritium outflow, and
this effect was also abolished by DPCPX pretreatment. CGS, a powerful
A-2-agonist, did not affect the evoked NE release. However, the effects
of CPCA and CGS on evoked NE release were significantly increased by
pretreatment of DPCPX in the magnesium-free medium. These results
indicate that inhibitory effect of A-1-adenosine receptor on NE release
is magnesium-dependent, and A-2-receptor may be present in the rat
hippocampus.