Site of adrenaline blockade in the superior cervical ganglion of the rabbit

Christ, Daryl; Nishi, S.

doi:10.1113/jphysiol.1971.sp009371

Cited by 105 publications

(37 citation statements)

References 20 publications

(21 reference statements)

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“…These concentrations of NA produced tic hyperpolarization and without any reduction in tions amounting to respectively, 12 ± 2% postsynaptic excitabiiity or in the response to ion-:3% (n = 5) and 21 ± 5% (n = 4). Data for tophoretic acetylcholine (Christ &Nishi, 1971 of the compound action potential, in spite of an almost negligible ganglionic hyperpolarization (Brown & Caulfield, 1981).…”

Section: Discussion Inhibitory Effect As It Did In the Absencementioning

confidence: 99%

Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Medgett

1983

British J Pharmacology

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1 Conditions under which transmission in rat isolated superior cervical ganglia may be affected by activation of presynaptic a-and 3-adrenoceptors have been investigated by means of an extracellular recording method. 2 Clonidine caused a small hyperpolarization of the ganglia (mean EC50-2 nM) in unstimulated preparations; with continuous preganglionic stimulation at 0.2 Hz, clonidine markedly decreased the height of the compound action potential (mean EC50-18 nM).3 Phentolamine (0.1 -3 pM) per se increased the height of the compound action potential by up to 15 %, and antagonized the inhibitory effects of adrenaline and clonidine.4 Using a higher frequency of stimulation (0.5 Hz), the effect of phentolamine (1juM) was unchanged, whereas the inhibitory effectiveness of adrenaline on the height of the compound action potential was reduced. 5(±)-Propranolol (0.1 pIM) did not affect the height of the compound action potential, whereas the inhibitory effects of high concentrations of adrenaline were enhanced. 6 During an infusion of clonidine (1MM), adrenaline (1-100Mm) and, less effectively, noradrenaline (10-100 pM) increased the height of the compound action potential by up to 14%; these effects were antagonized by propranolol (0.1 Mm).7 In the presence of noradrenaline (10 and 30 MM) adrenaline (1001M) caused a small (up to 5%) enhancement of the height of the compound action potential.8 The results obtained are consistent with the existence of presynaptic a-and P-adrenoceptors on preganglionic terminals. The x-adrenoceptor may be part of a trans-synaptic inhibitory feedback mechanism; however the functional role of the facilitatory P-adrenoceptor is not clear.

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Section: Discussion Inhibitory Effect As It Did In the Absencementioning

confidence: 99%

Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Medgett

1983

British J Pharmacology

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“…low Ca2+ solution, Co2+ and catecholamines. Adrenaline and noradrenaline have been shown to inhibit release of transmitter from a number of synapses, including the liberation of acetylcholine (ACh) from sympathetic ganglia (Christ & Nishi, 1971;Dun & Nishi, 1974;Dun & Karezmar, 1977).…”

Section: Discussionmentioning

confidence: 99%

Post‐tetanic depolarization in sympathetic neurones of the guinea‐pig

Dun

Minota

1982

The Journal of Physiology

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SUMMARY1. Repetitive intracellular stimulation at a frequency of 5-30 Hz for 1-10 s evoked in neurones of the isolated inferior mesenteric and superior cervical ganglia of the guinea-pig three types of post-spike membrane potential changes: (i) hyperpolarization, (ii) hyperpolarization followed by a slow depolarization, and (iii) a second hyperpolarization following the initial two responses.2. The initial post-spike hyperpolarization had a mean duration of 2-0 s and was often associated with a fall in membrane resistance; it could be elicited in every sympathetic neurone studied. This response was termed the post-tetanic hyperpolarization (PTH).3. The slow depolarization which could be induced only in a portion of neurones had a mean amplitude and duration of 2-2 mV and 27-5 s, respectively; it was termed the post-tetanic depolarization (PTD).4. PTD was associated with a fall in membrane resistance, augmented by membrane hyperpolarization, and reduced by depolarization; its mean extrapolated equilibrium potential was -38 mV.5. PTD was not blocked by nicotinic and muscarinic antagonists, or a-and /1-adrenergic receptor antagonists, whereas it was suppressed by adrenaline, noradrenaline, Co2+ and a low Ca2+ solution. 6. The amplitude of the single spike after-hyperpolarization in normal Krebs solution as well as in high K+ solution was increased during PTD; furthermore, conditioning hyperpolarization to the level of EK increased the amplitude of PTD in normal Krebs as well as in high K+ solution.7. PTD with similar amplitude, time course and membrane characteristics could be evoked in a portion of neurones of the rabbit superior cervical ganglia; however, PTD was not detected in neurones of the rat superior cervical ganglia.8. Decentralization of the guinea-pig and rabbit superior cervical ganglia for 14 d did not alter the number of neurones in which PTD could be elicited, its amplitude, or its time course. 9. Our results suggest that a chemical substances) is responsible for the generation of PTD; it may be released from the soma and/or dendrites and acts in an auto-receptive manner on the cells in question. The nature and origin of the second hyperpolarization remain to be clarified.

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“…Isolation of the ganglion and recording of intracellular potentials have been described in previous papers (Nishi & Koketsu, 1960;Christ & Nishi, 1970). The ganglion was perfused with an oxygenated Tyrode solution which was maintained at a constant temperature between 360 and 380 C.…”

Section: Methodsmentioning

confidence: 99%

“…in the superior cervical ganglion by decreasing the release of transmitter from the presynaptic nerves (Christ & Nishi, 1970); however, little is known about the presynaptic mechanism of action. This investigation was undertaken to clarify the mechanism by which adrenaline decreases the release of transmitter.…”

Section: Introductionmentioning

confidence: 99%

Effects of adrenaline on nerve terminals in the superior cervical ganglion of the rabbit

Christ

Nishi

1971

British J Pharmacology

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Summary1. Adrenaline decreases the release of transmitter from the presynaptic nerves in the superior cervical ganglion of the rabbit. The presynaptic mechanism of adrenaline action was investigated with micro-electrode techniques. 2. Adrenaline (10-1M) did not change the threshold of the presynaptic nerve terminals to a current stimulus.3. The effect of adrenaline on the excitatory postsynaptic potential (e.p.s.p.) was decreased when the calcium concentration of the perfusing solution was increased to 10 mM. 4. The effect of adrenaline on a train of e.p.s.ps (30-50 Hz) was analysed. Adrenaline decreased the readily available stores of transmitter, but only slightly changed the probability of release. 5. The probability of release was increased when the calcium concentration was increased to 5 mM. 6. It was concluded that adrenaline acts directly on excitation release coupling in the presynaptic terminals.

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Site of adrenaline blockade in the superior cervical ganglion of the rabbit

Cited by 105 publications

References 20 publications

Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Post‐tetanic depolarization in sympathetic neurones of the guinea‐pig

Effects of adrenaline on nerve terminals in the superior cervical ganglion of the rabbit

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