Long‐term potentiation of transmitter release induced by adrenaline in bull‐frog sympathetic ganglia.

Kuba, Kenji; Kumamoto, Eiichi

doi:10.1113/jphysiol.1986.sp016095

Cited by 55 publications

(23 citation statements)

References 33 publications

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“…There are clearly similarities between the acute effects of phorbol esters reported here and elsewhere and the increase in transmitter release associated with long-term potentiation in the hippocampus (Malenka et al, 1986a) and in sympathetic ganglia (Briggs et al, 1985;Kuba and Kamamoto, 1986). Indeed, it has been hypothesized that PKC is important in the genesis ofthis type of synaptic plasticity.…”

Section: Discussionsupporting

confidence: 81%

Down regulation of protein kinase C in neuronal cells: effects on neurotransmitter release

et al. 1987

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We investigated the effects of phorbol esters on protein kinase C (PKC) activity and on neurotransmitter release from cultured neuronal cells. Both differentiated and undifferentiated PC12 pheochromocytoma cells contained high levels of protein PKC. Under normal conditions all the enzyme activity was found in the cytoplasm. Addition of the phorbol esters phorbol 12-myristate-13-acetate (TPA) or phorbol 12,13- dibutyrate (PDBu) caused a rapid translocation of PKC from the cytoplasm to the particulate fraction. Continued culture of cells with these phorbol esters resulted in the decline of total PKC activity. After 10–20 hr of culture, both membrane and cytoplasmic PKC activity had declined to background levels. cAMP-dependent and Ca2+/calmodulin- dependent protein kinase activities were only slightly affected by chronic phorbol ester treatment. Addition of active phorbol esters to PC12 cells produced an enhancement of the depolarization-induced release of 3H-norepinephrine. Following chronic phorbol ester treatment, the ability of these substances to enhance evoked catecholamine release was lost. Furthermore, depolarizing stimuli released considerably less 3H-norepinephrine than in control untreated cells. Phorbol esters also enhanced depolarization-induced 3H- norepinephrine release from primary cultures of rat sympathetic neurons. Chronic treatment of these neurons with phorbol esters also resulted in the loss of their ability to enhance transmitter release and in a large reduction in the extent of depolarization-evoked transmitter release. Chronic phorbol ester treatment also resulted in the disappearance of PKC from sympathetic neurons, but had little effect on cAMP-dependent or Ca2+/calmodulin-dependent kinase activities. These results demonstrate that PKC-deficient neurons can be prepared. The data also demonstrate that depolarization-induced neurotransmitter release is mediated by both protein kinase C-dependent and independent pathways.

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Section: Discussionsupporting

confidence: 81%

Down regulation of protein kinase C in neuronal cells: effects on neurotransmitter release

et al. 1987

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“…In vertebrates, cyclic AMP appears to increase neurotransmitter and hormone release generally (see Reese & Cooper, 1984;Mulder & Schoffelmeer, 1985). Indeed, pharmacological elevation of cyclic AMP in the sympathetic ganglia of frog and rat was associated with an increase in the quantal content of nicotinic excitatory postsynaptic potentials (e.p.s.ps) (Akagi & Kudo, 1985;Kuba & Kumamoto, 1986).…”

Section: Receptor-mediated Regulationmentioning

confidence: 99%

“…The idea that cyclic AMP may mediate the 3-adrenoceptor-induced potentiation of nicotinic transmission is prompted by several findings: (1) P-adrenoceptor agonists stimulate cyclic AMP synthesis potently and efficaciously in the whole sympathetic ganglion (Briggs et al, 1982;Volle et al, 1982); (2) preganglionic denervation reduces the amount of cyclic AMP formed following exposure to ,-adrenoceptor agonists (Quenzer et al, 1980); (3) P-adrenoceptor agonists and cyclic AMP both increase the quantal content of nicotinic transmission in the frog sympathetic ganglion (Kuba & Kumamoto, 1986), and both increase nicotinic transmission and evoked ACh release in the rat sympathetic ganglion (this study). However, other evidence indicates that Padrenoceptor agonists may also act postsynaptically in the sympathetic ganglion (Brown & Dunn, 1983a), and that the potentiation is not mediated by cyclic AMP (Brown & Dunn, 1983b (Lynch & Baudry, 1984;Stanton & Sarvey, 1985a,b;Akers et al, 1986;Malenka et al, 1986), there is persuasive evidence in Aplysia that cyclic AMP mediates a longlasting presynaptic potentiation through inhibition of K+ channels (Kandel & Schwartz, 1982;Abrams et al, 1984;Schuster et al, 1985;Walters & Byrne, 1985; cf.…”

Section: Receptor-mediated Regulationmentioning

confidence: 99%

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Briggs

McAfee

McCaman

1988

British J Pharmacology

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1 Using the rat superior cervical ganglion in vitro, the relative efficacy of nicotinic synaptic transmission was estimated by recording the postganglionic compound action potential and the amount of endogenous acetylcholine (ACh) released. These two parameters were correlated in individual ganglia by sampling the bathing medium for the assay of ACh while simultaneously recording the postganglionic response.2 The P-adrenoceptor agonist isoprenaline potentiated both the evoked release of ACh and the postganglionic response by about 20% during preganglionic stimulation at 0.2 Hz. 3 The adenosine receptor agonist 2-chloroadenosine inhibited ACh release and the postganglionic response by about 35%. 4 Tetanic preganglionic stimulation for a few seconds induced a long-term potentiation of nicotinic responses and of ACh release. Both of these potentiations were dependent upon extracellular Ca2l during the tetani. 5 Forskolin and analogues of cyclic AMP also caused a long-lasting potentiation of both the evoked release ofACh and the postganglionic response, indicating that cyclic AMP may regulate transmission by a presynaptic mechanism. The specificity of the cyclic AMP analogues was tested using various butyryl-and bromo-purine nucleotides. 6 The effects of forskolin and 8-bromo-cyclic AMP did not appear to be dependent upon extracellular Ca2+. 7 The potentiation caused by forskolin was consistently augmented by three phosphodiesterase inhibitors -AH 21-132, papaverine and SQ 20-006. However, the effect of forskolin was not consistently enhanced by theophylline, nor was it reduced by the adenylate cyclase inhibitor SQ 22-536. 8 The neurogenic long-term potentiation was augmented by two of the phosphodiesterase inhibitors that also augmented the forskolin-induced potentiation -papaverine and SQ 20-006. 9 It was concluded that cyclic AMP can enhance nicotinic transmission, and can do so by increasing the evoked release of ACh. However, it was not possible to prove that cyclic AMP mediates the longterm potentiation induced by tetanic preganglionic stimulation.

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“…Exogenously applied adrenaline reduced the evoked ACh release from preganglionic nerve terminals in mammalian and bullfrog sympathetic ganglia (CHRIST and NIsHI, 1971;KUBA et al, 1981;KUBA and KUMAMOTO, 1986). If adrenaline was released from nerve elements during peptidergic depolarization, the released adrenaline could inhibit the ACh output.…”

Section: Discussionmentioning

confidence: 98%

Peptidergic inhibition of cholinergic transmission in bullfrog sympathetic ganglia.

Hasuo

Akasu

1988

Jpn.J.Physiol

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Intracellular and voltage-clamp recordings were made from sympathetic B neurons to investigate an interaction between peptidergic and cholinergic responses in bullfrog sympathetic ganglia. Stimulations of both 3rd-5th (0.2 Hz) and 8th (30 Hz) spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of fast EPSPs was decreased during the course of the late slow EPSP in a majority of sympathetic neurons. The mean depression of the fast EPSP amplitude was 51 + 4 % (n = 24). The quantal content of the fast EPSP was also depressed by 54±3% (n =10) during the late slow EPSP. Acetylcholineinduced depolarization (ACh potential) and current (ACh current) produced by an ionophoretic application of ACh were not reduced during the late slow EPSP. Bath-application of LH-RH (40 nM-4 µM) depressed the fast EPSP in a concentration-dependent manner; at a concentration of 1 µM, it produced a 63±8° (n =8) depression of the quantal content of the fast EPSP. LH-RH (1-4, tM) depressed the frequency of the miniature (M) EPSPs by 25±4% (n =5) of control. Antagonists for luteinizing hormonereleasing hormone (LH-RH) receptor, ]-LH-RH, prevented the presynaptic inhibition of the fast EPSP induced by LH-RH. These results suggest that the fast EPSP is depressed during the late slow EPSP by decreasing the evoked release of ACh from presynaptic nerve terminals in bullfrog sympathetic ganglia.

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Long‐term potentiation of transmitter release induced by adrenaline in bull‐frog sympathetic ganglia.

Cited by 55 publications

References 33 publications

Down regulation of protein kinase C in neuronal cells: effects on neurotransmitter release

Down regulation of protein kinase C in neuronal cells: effects on neurotransmitter release

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Peptidergic inhibition of cholinergic transmission in bullfrog sympathetic ganglia.

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