### A. Overview

Extracellular purines (adenosine, ADP, and ATP) and pyrimidines (UDP and UTP) are important signaling molecules that mediate diverse biological effects via cell-surface receptors termed purine receptors. In this review particular emphasis is placed on the discrepancy between the

/pdf/receptors-for-purines-and-pyrimidines-56f78tnpew.pdf

Receptors for Purines and Pyrimidines

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Slices of the caudate nucleus of rabbits were preincubated with 3H-choline and then superfused. Stimulation by electrical pulses at 3 Hz or by 25 mmol/l potassium elicited an increase in tritium outflow which was calcium-dependent and, in the case of electrical stimulation, tetrodotoxin-sensitive. The dopamine receptor agonist apomorphine (0.01-1 mumol/l) decreased, whereas the antagonist haloperidol increased the electrically evoked overflow of tritium. Nomifensine and cocaine, used at concentrations known to inhibit the re-uptake of dopamine, also reduced the evoked overflow of tritium, and this reduction was antagonized by haloperidol. Combined pretreatment with reserpine and alpha-methyltyrosine methylester (alpha-MT), which lowered dopamine levels by 99.5%, increased the electrically evoked overflow, as did bretylium which is shown here to block action potential-induced release of dopamine. The facilitation by haloperidol and bretylium as well as the inhibition by nomifensine and cocaine were diminished or abolished after pretreatment with reserpine plus alpha-MT. Apomorphine decreased, and haloperidol increased, the potassium-evoked overflow of tritium; the effects were not changed by tetrodotoxin. The results indicate that the striatal dopamine receptors which, when activated, depress the release of acetylcholine, are akin to the D-2 type. Endogenous dopamine also acts on the receptors as shown by several manipulations with known effects on dopaminergic transmission. A large fraction of these dopamine receptors may be located on the cholinergic axon terminals.

Modulation by endogenous dopamine of the release of acetylcholine in the caudate nucleus of the rabbit

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Modulation of acetylcholine release via adenosine receptors was studied in rabbit hippocampal slices, which were preincubated with 3H-choline and then continuously superfused. Electrical field stimulation of the slices elicited a release of acetylcholine, which was inhibited in a concentration-dependent manner by various adenosine receptor agonists. The effects of the agonists were antagonized by the methylxanthines. From the order of potency: cyclohexyladenosine > (−)phenylisopropyl-adenosine ((−)PIA) > 5′-N-ethylcarboxamideadenosine (NECA) > 2-chloradenosine > (+)phenylisopropyladenosine > adenosine, the inhibitory adenosine receptor may be classified as A1-(R1-)receptor. In experiments on rabbit caudate nucleus slices, adenosine receptor agonists only slightly decreased the evoked acetylcholine release. The presence of an inhibitory tone of endogenous adenosine on hippocampal acetylcholine release is supported by the following findings: 1) the methylxanthines theophylline, 8-phenyltheophylline and 3-isobutylmethyl-xanthine (IBMX) increased the evoked acetylcholine release in concentrations below those required for phosphodiesterase inhibition. 2) Adenosine uptake inhibitors, in contrast, decreased the evoked transmitter release. 3) Deamination of endogenous adenosine by addition of adenosine deaminase to the medium enhanced the acetylcholine release. In conclusion, acetylcholine release in the hippocampus is depressed at the level of the cholinergic nerve terminals by endogenous adenosine via A1-(Ri-)receptors.

Endogenous adenosine as a modulator of hippocampal acetylcholine release.

The effect of islet-activating protein (IAP) on α2-adrenoceptor mediated modulation of noradrenaline release in the rabbit hippocampus was studied. Slices of the hippocampus were incubated for 6 h with IAP, subsequently loaded with3H-noradrenaline and superfused continuously. IAP-pretreatment significantly enhanced the electrically evoked transmitter release and diminished the facilitatory effect of the α2-adrenoceptor antagonist yohimbine. In addition, the inhibitory effect of the α2-adrenoceptor agonist clonidine was reduced. These results provide circumstantial evidence that an inhibitory guanine-nucleotide-binding protein, most probably N1 of a presynaptically located adenylate cyclase, is involved in the α2-autoreceptor mediated modulation of noradrenaline release.

Islet-activating protein (pertussis toxin) diminishes alpha 2-adrenoceptor mediated effects on noradrenaline release.



Noradrenaline (NA) release and its modulation via presynaptic opioid receptors were studied in rabbit hippocampal slices, which were preincubated with [3H]NA, continuously superfused in the presence of 30 μM cocaine and stimulated electrically. The evoked release of [3H]NA was strongly reduced by the preferential K-agonists ethylketocyclazocine, dynorphin A1-13, dynorphin A, trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide (U-50,488), and (–)-5,9-dimethyl-2′-OH-2-tetrahydrofurfuryl-6,7-benzomorphan [(–)-MR 2034], whereas (+)-MR 2035 [the (+)-enantiomer of (–)-MR 2034] was ineffective. In contrast, the preferential δ-agonists Leu-enkephalin, Met-enkephalin, and D-Ala2,-D-Leu5-enkephalin (DADLE) as well as the μ-agonists morphine, normorphine, D-Ala2Gly-ol5-enkephalin (DAGO), and β-casomorphin1-4 amide (morphiceptin) were much less potent. However, in similar experiments on rat hippocampal slices DAGO (1 μM) was much more potent than ethylketocyclazocine (1 μM) or DADLE (1 μM). (–)-N-(3-furylmethyl)-α-noretazocine [(–)-MR 2266], 1 μM, a preferential K-antagonist, antagonized the effect of ethylketocyclazocine more potently than (–)-naloxone or (+)-MR 2267 [the (+)-enantiomer of (–)-MR 2266]. Given alone, (–)-MR 2266 slightly and (+)-MR 2267 (1 μM each) greatly enhanced NA release, apparently due to α2-adrenoceptor blockade since their effects were completely abolished in the presence of yohimbine (0.1 μM). The effects of DADLE (1 μM) and DAGO (1 μM) were also antagonized by (–)MR 2266 (0.1 μM) but not by the δ-antagonist N,N-diallyl-Tyr-Aib-Phe-Leu-OH (ICI 174864), 0.3 μM. It is concluded that NA release in the rabbit hippocampus is inhibited via K-receptors; our results do not support the presence of modulatory μ- and δ-receptors in this tissue. However, in the rat hippocampus μ-receptors may modulate NA release.

Characterization of Opioid Receptors Modulating Noradrenaline Release in the Hippocampus of the Rabbit

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