Synaptic Potentials in Sympathetic Ganglia: Are They Mediated by Cyclic Nucleotides?

Abstract

The hypothesis that cyclic nucleotides are intracellular second messengers mediating the generation of synaptic potentials was studied in the sympathetic ganglia of the bullfrog. Synaptic potentials and the effect of administering cyclic nucleotides and agents which affect cyclic nucleotide metabolism were recorded by the sucrose gap technique. The administration of adenosine 3',5'-monophosphate (cyclic AMP), guanosine 3',5'-monophosphate (cyclic GMP), or several of their derivatives produced little or no change in membrane potential. Prostaglandin E1 did not block the generation of postsynaptic potentials. Theophylline produced membrane effects that were different from those associated with postsynaptic potential generation; it also reduced the slow excitatory postsynaptic potential (EPSP) and potentiated the slow inhibitory postsynaptic potential (IPSP). The administration of papaverine, however, reduced both the slow EPSP and the slow IPSP. Although synaptic stimulation increases both cyclic GMP and cyclic AMP in these neurons, these results raise the possibility that these cyclic nucleotides may have functionla roles other than mediation of synaptic potentials.

Muscarinic Receptors in Rat Sympathetic Ganglia

“…Unfortunately, the relatively small fall in 86Rb-efflux (-30%), superimposed on a rather fluctuating background flux-rate, has so far limited our attempts to analyze the receptive-mechanism in detail. (b) Cyclic GMP In contrast to previous reports (Weight et al, 1974;Kebabian et al, 1975) Hashiguchi, Ushiyama, Kobayashi & Libet, 1978; but see Busis, Weight & Smith, 1978), the response differs in nature from that to muscarinic agonists (Dun, Kaibara & Karczmar, 1978). A further doubt regarding an intermediary role for cyclic GMP is that the response to muscarinic agonists was enhanced on removing Ca2", and was not reduced even when tested in a Ca2 +-free/EDTA solution, conditions under which cyclic GMP formation is greatly reduced (see for example, Kebabian et al, 1975).…”

“…A further doubt regarding an intermediary role for cyclic GMP is that the response to muscarinic agonists was enhanced on removing Ca2", and was not reduced even when tested in a Ca2 +-free/EDTA solution, conditions under which cyclic GMP formation is greatly reduced (see for example, Kebabian et al, 1975). It seems likely, as suggested by Busis et al (1978), that changes in cyclic GMP levels (where they occur) are coincidental with muscarinic depolarization rather than causative. (c) Hyperpolarization The initial response to addition of muscarinic agonists usually consisted of a ganglion hyperpolarization.…”

Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

“…Brown etal., 1979, andMcAfee et al, 1980, for further discussion of this point). External application of cyclic AMP or its derivatives has usually been observed to produce either a ganglion hyperpolarization (McAfee & Greengard, 1972;Machova & Kristofova, 1973;, or no clear effect (Dun, Kaibara & Karczmar, 1977;Gallagher & Shinnick-Gallagher, 1977;Busis, Weight & Smith, 1978), though a depolarization has been reported by Akasu & Koketsu (1977) in frog ganglia and by Hsu & Mclsaac (1978) in rat ganglia. Such a depolarization was occasionally observed in the present experiments, but this was antagonized by theophylline suggesting that, like the previouslyobserved hyperpolarization it resulted from activation of external adenosine receptors.…”

The nitric oxide‐cyclic GMP pathway and synaptic plasticity in the rat superior cervical ganglion

“…In both cases, synaptic transmission was potentiated, the values (17 + 1% before and 19 + 2% afterwards; n = 6) (Figure 6a, b) not being significantly different. The NO cyclic GMP pathway and synaptic transmission in the rat SCG ""'li At one time, the SCG was a popular model tissue for trying to understand the role of cyclic nucleotides in synaptic transmission, although no clear picture emerged (Busis et al, 1978). The identification of NO as a neural messenger molecule capable of eliciting cyclic GMP accumulation by activating soluble guanylyl cyclase has added a previously missing element.…”