Adenosine A2A receptor stimulation increases release of acetylcholine from rat hippocampus but not striatum, and does not affect catecholamine release
Adenosine A2A receptor stimulation increases release of acetylcholine from rat hippocampus but not striatum, and does not affect catecholamine release
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腺苷 A2A 受体刺激会增加大鼠海马而非纹状体乙酰胆碱的释放,并且不影响儿茶酚胺的释放
DOI:
10.1007/pl00004917
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发表时间:
1996
期刊:
影响因子:
--
通讯作者:
B. Fredholm
中科院分区:
文献类型:
--
作者:
Shaoyu Jin;B. Fredholm
Abstract Rat striatal and hippocampal slices, preincubated with [3H] dopamine (DA) {or [3H] noradrenaline (NA)} and [14C] choline, were superfused continuously and stimulated electrically. 2-chloroadenosine (2-CADO 0.001–100 μM), a non-selective adenosine receptor agonist, produced a concentration-dependent inhibition of the electrically evoked DA and acetylcholine (ACh) release from the striatal slices and of the electrically evoked NA and ACh release from the hippocampal slices. 8-cyclopentyl-1,3-dipropylxanthine (DPCPX 3, 30 and 200 nM), a selective adenosine A1 receptor antagonist, caused a concentration-dependent, parallel, rightward shift of the 2-CADO concentration-response curve, consistent with competitive antagonism. The pA2 values ranged between 8.4 and 8.8. In the case of ACh release from the hippocampus, but in no other case, was there an increase in release of radioactivity at low concentrations of 2-CADO in the presence of DPCPX. The stimulation in the hippocampus could be blocked by a selective adenosine A2A receptor antagonist KF 17837. By itself KF 17837 (0.1–100 μM) had no effect on electrically evoked NA release from hippocampal slices, but decreased electrically evoked ACh release. This inhibition was counteracted by DPCPX (1 μM).These results show that, under the conditions used, DA release in the striatum, and NA release in the hippocampus, as well as ACh release from the striatum are regulated by adenosine A1 but not by adenosine A2A receptors. By contrast, ACh release from the hippocampus is tonically regulated both by adenosine A1 receptors, which inhibit release, and by adenosine A2A receptors which stimulate release.
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DOI:
--
发表时间:
2005
期刊:
--
影响因子:
--
作者:
Bertil;-B.;Fredholm;Maria;-P.;Abbracchio;Geoffrey;Burnstock;John;-W.;Daly;-T.;Kendall
通讯作者:
Bertil;-B.;Fredholm;Maria;-P.;Abbracchio;Geoffrey;Burnstock;John;-W.;Daly;-T.;Kendall
DOI:
--
发表时间:
1993
期刊:
The Journal of pharmacology and experimental therapeutics
影响因子:
--
作者:
Jackson,EK;Herzer,WA;Suzuki,F
通讯作者:
Suzuki,F
影响因子:
3.6
作者:
M. Abbracchio;Roberta Brambilla;S. Ceruti;Hea Ok Kim;D. V. Lubitz;Kenneth A. Jacobson;Flaminio Cattabeni
通讯作者:
M. Abbracchio;Roberta Brambilla;S. Ceruti;Hea Ok Kim;D. V. Lubitz;Kenneth A. Jacobson;Flaminio Cattabeni
DOI:
--
发表时间:
1990
期刊:
The Journal of pharmacology and experimental therapeutics
影响因子:
--
作者:
Lupica,CR;Cass,WA;Zahniser,NR;Dunwiddie,TV
通讯作者:
Dunwiddie,TV
影响因子:
56.9
作者:
RAINNIE, DG;GRUNZE, HCR;GREENE, RW
通讯作者:
GREENE, RW