Evidence for adenosine A2 receptor involvement in the hypomobility effects of adenosine analogues in mice.

@article{Durcan1989EvidenceFA,
  title={Evidence for adenosine A2 receptor involvement in the hypomobility effects of adenosine analogues in mice.},
  author={Michael J. Durcan and Philip F. Morgan},
  journal={European journal of pharmacology},
  year={1989},
  volume={168 3},
  pages={
          285-90
        }
}
Pharmacological characterization of a simple behavioral response mediated selectively by central adenosine A1 receptors, using in vivo and in vitro techniques.
TLDR
It was found that two peripheral adenosine receptor antagonists, 8-(p-sulphophenyl)-1, 3-dipropylxanthine (DPSPX) and 8-PST, did not alter CPA-induced hypolocomotion, and this confirmed that pharmacological reversal of the adenosines A1 receptor-mediated response involved a central site of drug action.
Cocaine-induced hyperactivity is more influenced by adenosine receptor agonists than amphetamine-induced hyperactivity.
TLDR
It is shown that all adenosine receptor agonists (A1 and A2) reduce cocaine- and amphetamine-induced locomotor activity and indicate that cocaine-induced hyperactivity is more influenced by adenosines receptor agonist (particularly A1 receptors) than Amphetamine- induced hyperactivity.
Adenosine agonists reduce conditioned avoidance responding in the rat
Pharmacology of adenosine receptors of the rat isolated superior cervical ganglion
TLDR
This study has examined the effect of purines and pyrimidines on the rat superior cervical ganglion in vitro and found adenosine and its analogues produced concentration dependent hyperpolarisations, suggesting that protein kinase C is involved in the interaction ofadenosine with muscarine.
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The regional distribution of [3H]NECA binding and the affinities of adenosine agonists and antagonists for inhibition of binding indicate that the site labeled by [3NECA belongs to the high affinity, or A2a, subclass of A2 receptor.
Interactions in the behavioral effects of methylxanthines and adenosine derivatives.
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The behavioral effects of L-PIA appeared to be mediated in the brain and were not secondary to the cardiovascular effects, indicating a difference in the behavioral profile of these two agents.
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TLDR
D dose-response curves were constructed for the antagonism by caffeine or 8-SPT of the hypotension and bradycardia caused by infusing adenosine i.v. or by giving bolus i.p.v, indicating that the site at which the drug antagonizes the cardiovascular effects ofadenosine is peripheral.
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    The Journal of pharmacology and experimental therapeutics
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TLDR
Some of the anticonvulsant actions of L-phenylisopropyladenosine are not reversed by the adenosine antagonist theophylline, and are not shared by the other analogs, these may reflect actions mediated by other, perhaps nonpurinergic receptors.
NECA-induced hypomotility in mice: Evidence for a predominantly central site of action
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