Intracellular analysis of slow inhibitors and excitatory postsynaptic potentials in sympathetic ganglia of the frog.

Tosaka, Tsuneo; Chichibu, Shiko; Libet, Benjamin

doi:10.1152/jn.1968.31.3.396

Cited by 103 publications

(38 citation statements)

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“…without contaminating slow i.p.s.p. Tosaka et al 1968;Skok, 1973 and Nishi & Koketsu (1968). However, and in contrast to these earlier reports, it should be noted that repetitive preganglionic stimulation was not necessary to elicit a slow e.p.s.p: as shown in Fig.…”

Section: Methodsmentioning

confidence: 60%

Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

Adams¹,

Brown²

1982

The Journal of Physiology

145

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1. Slow muscarinic excitatory post‐synaptic currents (slow e.p.s.c.s) generated by preganglionic nerve stimuli were recorded in voltage‐clamped bullfrog sympathetic neurones. 2. IM‐‐an outward, voltage‐dependent, K+‐current‐‐was inhibited during the slow e.p.s.c., and membrane conductance was reduced in a voltage‐dependent manner. 3. The slow e.p.s.c. was associated with reduced outward rectification in the steady‐state current‐‐voltage (I/V) curve at membrane potentials more positive than‐‐60 m V, with no change in the shape of the non‐rectifying part of the I/V curve at more negative potential. 4. The amplitude of the slow e.p.s.c. was reduced by membrane hyperpolarization, to zero at membrane potentials equal to, or more negative than, ‐60 m V. The voltage sensitivity of the slow e.p.s.c. accorded with that of IM. 5. It is concluded that the slow e.p.s.c. results from a selective inhibition of IM.

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Section: Methodsmentioning

confidence: 60%

Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

Adams¹,

Brown²

1982

The Journal of Physiology

145

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“…It seems unlikely that the muscarinic hyperpolarization ofthe rat superior cervical ganglion was due to the secondary, extracellular calcium-dependent release of catecholamines (Tosaka et al, 1968) for several reasons: (1) 0.1 mM CaCl2 abolished the postsynaptic compound action potential recorded from the internal carotid nerve following the stimulation of the cervical sympathetic trunk (our unpublished observations), whereas the amplitude of the muscarinic hyperpolarization was enhanced in this medium; (2) the hyperpolarization was resistant to tetrodotoxin (0.1-I AM); and (3) idazoxan (0.1-1 .0 JM) antagonized noradrenaline (1 JM)-and dopamine (10 jAM)-induced hyperpolarizations of the ganglion (n = 4 ganglia, for each catecholamine) but not the muscarine-induced hyperpolarization (n = 8, Figure 7). …”

Section: Muscarinic Hyperpolarizationmentioning

confidence: 99%

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

Newberry

Priestley

1987

British J Pharmacology

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1Pharmacological differences have been observed between the muscarinic agonist-induced depolarizing and hyperpolarizing responses of the rat isolated superior cervical ganglion. 2 Pirenzepine (0.3 AM) selectively reduced the depolarizing response and unmasked the hyperpolarizing response. No such selectivity was observed with a concentration of N-methylatropine which was equipotent with pirenzepine in antagonizing the depolarizing response. 3 The neuromuscular blocking agents gallamine (1O tM) and pancuronium (3 jM) exhibited the oppositive selectivity to pirenzepine, both dramatically reduced the hyperpolarization but only slightly antagonized the depolarization. 4 The potencies of a range ofagonists in evoking the depolarizing and hyperpolarizing responses, the latter in the presence of 0.3 tAM pirenzepine, have been determined. Methylfurmethide failed to hyperpolarize the ganglion at concentrations which evoked maximal depolarizations. 5 The muscannic hyperpolarization did not appear to be mediated by the secondary release of catecholamines. 6 It was concluded that the two muscarinic responses on the rat superior cervical ganglion, the slow depolarization and faster hyperpolarization, are mediated by different muscarinic receptor subtypes.

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“…The functional significance of these cells was also discussed in reference to electrophysiological studies on the transmission mechanism in the sympathetic ganglia (NISHI et al, 1967;TOSAKA et al, 1968;KOKETSU, 1969;LIBET, 1970;NISHI, 1974).…”

Section: Ultrastructurementioning

confidence: 99%

“…Several physiologists have claimed that s-EPSP occurs in the B-neuron (TOSAKA et al, 1968;LIBET, 1970) and s-IPSP in the C-neuron (TOSAKA et al, 1968;WEIGHT and PADJEN, 1973a, b). Morphologically, these two types of neuron are equipped with distinctive postsynaptic apparatuses:…”

Section: Fine Structure Of the Gc Cellsmentioning

confidence: 99%

Ultrastructure and Function of the Granule-Containing Cells in the Anuran Sympathetic Ganglia

Watanabe

1977

Arch. Histol. Jap., Arch. Histol. Jpn

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Intracellular analysis of slow inhibitors and excitatory postsynaptic potentials in sympathetic ganglia of the frog.

Cited by 103 publications

References 0 publications

Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

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

Ultrastructure and Function of the Granule-Containing Cells in the Anuran Sympathetic Ganglia

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