Generation of slow postsynaptic potentials without increases in ionic conductance.

Kobayashi, Haruo; Libet, Benjamin

doi:10.1073/pnas.60.4.1304

Cited by 131 publications

(56 citation statements)

References 22 publications

(2 reference statements)

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“…One of the requirements to be fulfilled by a substance before it can be identified as a given synaptic transmitter is that it must produce the same changes in the post-synaptic membrane as those associated with the orthodromically generated PSP itself. The membrane changes involved in both of these slow PSPs have been found to be different in principle from those involved in the better known, fast PSPs (Kobayashi & Libet, 1968); with the slow PSPs there were no increases in ionic conductance of the membrane, and changes in the initial level of membrane potential altered these responses in ways that are different from those predicted from the ionic mobility hypothesis for the fast PSPs (e.g. Eccles, 1964).…”

Section: Introductionmentioning

confidence: 89%

“…Our primary aim was to detect relative changes in membrane resistance that might be produced during a response rather than to measure absolute values. Earlier studies have shown that sympathetic ganglion cells do not exhibit appreciable rectification with changes in membrane potential over the range employed in this work (Kobayashi & Libet, 1968;Nishi & Koketsu, 1960).…”

Section: Methodsmentioning

confidence: 99%

“…The techniques employed for intracellular study of sympathetic ganglion cells of frog and rabbit have already been described (Tosaka et al 1968; Libet & Tosaka, 1969;Kobayashi & Libet, 1968). Micro-electrodes were generally filled with 0-6 M-K2SO4 and had a resistance of about 100 MQ, as measured with 60 Hz (30-50 MQ when filled with 3 m-KCI).…”

Section: Methodsmentioning

confidence: 99%

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Actions of noradrenaline and acetylcholine on sympathetic ganglion cells

Kobayashi¹,

Libet²

1970

The Journal of Physiology

160

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SUMMARY1. The responses of the post-synaptic membrane of sympathetic ganglion cells to noradrenaline (NA) and to acetylcholine (ACh) were studied in relation to the slow inhibitory post-synaptic potential (S-IPSP) and slow excitatory one (S-EPSP) respectively.2. NA produced an hyperpolarization of about 4 mV in cells of rabbit superior cervical ganglia.3. The hyperpolarizing response to NA was not accompanied by any detectable change in membrane resistance, and it was depressed by conditioning depolarization.4. NA also depressed all the post-synaptic potentials, presumably by an action on presynaptic function.5. ACh produced a large depolarization in ganglion cells of rabbit and of frog (paravertebral) ganglia, which was accompanied by a large decrease in membrane resistance.6. When ACh was applied during nicotinic blockade, achieved with high concentration of nicotine (frog ganglia) or D-tubocurarine (rabbit ganglia), it still produced a considerable depolarization. This response could be blocked by atropine, and is presumably a muscarinic type of action.7. The muscarinic-ACh response was not accompanied by a decrease in membrane resistance. Instead, the frog ganglion cells exhibited increased resistances of up to more than twice the resting value during both the muscarinic-ACh depolarization and the S-EPSP.8. The muscarinic-ACh depolarization and the S-EPSP were both depressed by conditioning hyperpolarization (in nicotinized frog cells). An initial hyperpolarizing phase now appeared in both of these responses. 9. It is concluded that the hyperpolar.zing response to NA and the depolarizing response to muscarinic-ACh action are not generated by * Present address:

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Section: Introductionmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

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Actions of noradrenaline and acetylcholine on sympathetic ganglion cells

Kobayashi¹,

Libet²

1970

The Journal of Physiology

160

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“…The slow e.p.s.p. is quite different: it has been attributed (in substantial part, at least) to the closure of K+-channels (Weight & Votava, 1970;Kuba & Koketsu, 1976; but see Kobayashi & Libet, 1968, for a dissenting view).…”

Section: Introductionmentioning

confidence: 99%

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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“…application ofacetylcholine will mimic both potentials (Takeshige & Volle, 1964a). The inhibition of a resting potassium current probably underlies the depolarization (Kobayashi & Libet, 1968;Weight & Votava, 1970;Brown & Adams, 1980), whereas, in contrast, an increase in potassium permeability appears to be responsible for the hyperpolarization (Dodd & Horn, 1983;Cole & Shinnick-Gallagher, 1984; but see Brown & Selyanko, 1985).…”

Section: Introductionmentioning

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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Generation of slow postsynaptic potentials without increases in ionic conductance.

Cited by 131 publications

References 22 publications

Actions of noradrenaline and acetylcholine on sympathetic ganglion cells

Actions of noradrenaline and acetylcholine on sympathetic ganglion cells

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

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