Description:
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<jats:list-item><jats:p>The stimulation‐evoked overflow of [<jats:sup>3</jats:sup>H]‐noradrenaline from slices of the rabbit hippocampus is inhibited by α<jats:sub>2</jats:sub>‐autoreceptors as well as by adenosine (A<jats:sub>1</jats:sub>)‐receptors. Slices of rabbit hippocampus were labelled with [<jats:sup>3</jats:sup>H]‐noradrenaline, superfused continuously and stimulated twice electrically (rectangular pulses; 2 ms, 3 Hz, 24 mA, 5 V cm<jats:sup>−1</jats:sup>).</jats:p></jats:list-item>
<jats:list-item><jats:p>Treatment of hippocampal slices with N‐ethylmaleimide (NEM, 30 μ<jats:sc>m</jats:sc>; 30 min), which functionally disturbs certain N‐proteins, decreased the inhibitory action of adenosine receptor agonists like (‐)‐N<jats:sup>6</jats:sup>‐(R‐phenylisopropyl)‐adenosine ((‐)‐PIA) and adenosine on noradrenaline release. Release inhibition caused by (‐)‐PIA (0.03‐1 μ<jats:sc>m</jats:sc>) was antagonized by NEM in a non‐competitive manner in the absence and in the presence of the α<jats:sub>2</jats:sub>‐adrenoceptor antagonist yohimbine.</jats:p></jats:list-item>
<jats:list-item><jats:p>The adenosine receptor antagonist 8‐phenyltheophylline significantly increased the evoked noradrenaline release by about 15% in control slices by diminishing the inhibitory action of endogenous adenosine. In NEM‐treated slices this effect of 8‐phenytheophylline was not seen. In the presence of (‐)‐PIA (0.1 μ<jats:sc>m</jats:sc>), i.e. under conditions of an increased inhibitory tone, release facilitation by 8‐phenyltheophylline was decreased by NEM compared to that in the respective controls.</jats:p></jats:list-item>
<jats:list-item><jats:p>Occupation of the A<jats:sub>1</jats:sub>‐receptor with (‐)‐PIA prior to and during the NEM treatment did not protect the A<jats:sub>1</jats:sub>‐receptor‐coupled signal transduction system from being affected by NEM.</jats:p></jats:list-item>
<jats:list-item><jats:p>In the presence of the α<jats:sub>2</jats:sub>‐adrenoceptor antagonist yohimbine, the inhibitory action of (‐)‐PIA was strongly increased.</jats:p></jats:list-item>
<jats:list-item><jats:p>The above results suggest the involvement of a regulatory N‐protein in the A<jats:sub>1</jats:sub>‐receptor‐mediated inhibition of noradrenaline release and an interaction between the α<jats:sub>2</jats:sub>‐autoreceptor and the A<jats:sub>1</jats:sub>‐receptor‐coupled signal transduction system, possibly at the level of a N‐protein.</jats:p></jats:list-item>
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