1 Using a grease-gap technique, we have investigated the effects of purine and pyrimidine nucleotides on the d.c. potential of the rat isolated superior cervical ganglion (SCG). 2 Of the purines tested, adenosine, adenosine 5'-triphosphate (ATP), P,y-methylene-adenosine 5'-triphosphate (P,y-MeATP) at up to 300 gM produced concentration-dependent hyperpolarizations, whereas 2-methyl-thio-ATP (2-Me.S.ATP) and a,p-methylene-ATP (a,,B-MeATP) depolarized ganglia. Of the pyrimidines tested, uridine 5'-triphosphate (UTP) produced concentration-dependent depolarizations and cytosine 5'-triphosphate (CTP) at 1000 tLM produced considerably smaller but significant depolarizations. In contrast uridine 5'-monophosphate (UMP) at 1000 AM hyperpolarized ganglia. The relative order of potency of purines and pyrimidines to depolarize ganglia was:-UTP> az,-MeATP>> CTP> 2-Me.S.ATP and to hyperpolarize ganglia was:-adenosine = P,By-MeATP> ATP> UMP.3 The ability of purines and pyrimidines to alter the depolarizing response caused by muscarine and of purines to alter depolarization induced by y-aminobutyric acid (GABA) was determined. The relative order of potency of nucleotides in depressing submaximal depolarization caused by muscarine (100 nM) was: adenosine = ATP>P,y-MeATP whereas 2-Me.S.ATP, a,4-MeATP and UTP did not significantly alter depolarization caused by muscarine. At 100ZM 3,Ty-MeATP and adenosine but not ATP potentiated GABA-induced depolarizations. 4 Hyperpolarizations caused by adenosine, ATP, P,y-MeATP and UMP and depolarizations caused by aj-MeATP were enhanced in medium containing reduced concentrations of calcium (0.1 mM) and potassium (2 mM). In this medium 8-phenyltheophylline abolished hyperpolarizations caused by adenosine and reversed hyperpolarizations caused by ATP into depolarizations. Suramin (300 tLM), a P2-purinoceptor antagonist, significantly reduced the depolarizing response caused by a,t-MeATP and significantly increased hyperpolarizations caused by ATP and ,B,-MeATP. Suramin (300 AM) did not significantly alter depolarizations caused by l,l-dimethyl-4-phenylpiperazinium (10 ILM), potassium (3 mM) or muscarine (100 nM) and significantly potentiated depolarizations caused by UTP (100IM).5 It is concluded that the rat SCG contains PI-purinoceptors that hyperpolarize the ganglion and diminish sensitivity to muscarine, and P2X-purinoceptors that depolarize the SCG. There is also some evidence to suggest the presence of receptors for UTP, i.e., pyrimidinoceptors, which depolarize SCG neurones.
