α₂‐Adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia

Abstract

1 The adrenaline-induced hyperpolarization (AdH), slow inhibitory postsynaptic potential (slow i.p.s.p.) and hyperpolarizing phase of the response to methacholine (MChH) in Rana pipiens sympathetic ganglia were studied by means of the sucrose-gap technique. Yohimbine (0

Pharmacological differences between two muscarinic responses of the rat superior cervical ganglion in vitro

“…The pharmacology of the depolarizing response has been studied in detail (Brown et al, 1980a,b), but that ofthe smaller hyperpolarization has received less attention. The purpose of our experiments was to compare the pharmacology of the two potentials and to examine the possible involvement of catecholamines in the mediation ofthe hyperpolarizing response (see Weight & Padjen, 1973;Cole & Shinnick-Gallagher, 1980;Ivanov & Skok, 1980;Ashe & Libet, 1982;Rafuse & Smith, 1986). A preliminary account of some of this work has been published (Newberry et al, 1985).…”

Elevation of intracellular cyclic AMP concentration fails to inhibit adrenaline‐induced hyperpolarization in amphibian sympathetic neurones

“…All drugs, except forskolin, were dissolved in Ringer solution of the following composition (mm): NaCl 100, KCI 2, CaCl2 1.8, tris(hydroxymethyl)-aminomethane-HCI (Tris) (pH 7.2) 16, and (+)-glucose 10. Desmethylimipramine (DMI; 500nM) was added to the Ringer solution to potentiate the response to adrenaline (Smith, 1984;Rafuse & Smith, 1986). Forskolin was initially dissolved in dimethylsulphoxide (DMSO) and further diluted in Ringer solution such that the final concentration of DMSO was 1% by volume.…”

“…As shown in Figure 1, forskolin 50M produced a 10 fold increase in basal cyclic AMP levels and a subsequent 30s exposure to adrenaline (1 M) reduced cyclic AMP accumulation in forskolin-stimulated ganglia by approximately 35%. Propranolol (1 M) and DMI (500 nM) were added to the Ringer solution to prevent activation of,-adrenoceptors (Brown et al, 1979) and inactivation of adrenaline by uptake (Rafuse & Smith, 1986).…”

“…If the amphibian x2-adrenoceptor (Rafuse & Smith, 1986) is coupled to adenylate cyclase via G,, then pretreatment with pertussis toxifn, which ADPribosylates certain G-proteins (Katada & Ui, 1982;Gilman, 1987), might be expected to prevent the adrenaline-induced reduction in cyclic AMP concentration in propranolol/forskolin/DMI treated ganglia. Figure 1 shows that the effect of adrenaline was greatly reduced in ganglia which had been Control F F, Ad F, PTX F, PTX, Ad Figure 1 Effects of forskolin (F), adrenaline (Ad) and pertussis toxin (PTX) on cyclic AMP concentration in bullfrog sympathetic ganglia.…”

“…We have tested the involvement of adenylate cyclase inhibition in the production of an CX2-adrenoceptor-mediated response in a simple and convenient preparation, the amphibian sympathetic ganglion. In this tissue, the hyperpolarization induced by adrenaline (Adh, Koketsu & Nakamura, 1976;Smith, 1984;Rafuse & Smith, 1986;Selyanko et al, 1988) has characteristics similar to a2-adrenoceptor-mediated responses in mammalian neurones (Aghajanian & VanderMaelen, 1982;North et al, 1987). If the transduction mechanism associated with the Adh involves adenylate cyclase inhibition, the transduction process would involve a decrease in the concentration of intracellular cyclic AMP.…”