The effect of diffusional barriers upon the pharmacology of cells within the central nervous system

Curtis, D. R.; Eccles, Rosamond M.

doi:10.1113/jphysiol.1958.sp005988

Cited by 121 publications

(34 citation statements)

References 20 publications

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“…Alternatively this phenomenon may be related to the presence of synaptic barriers preventing the efficient access of the blocking agent. Such barriers were proposed by Curtis & Eccles (1958) to explain the failure of cholinergic blocking agents to prevent the first few spikes evoked in a Renshaw cell following ventral root stimulation (Curtis & Eccles, 1958;Eccles, Fatt & Koketsu, 1954). produced depression of firing often within 10 see and ending equally promptly (Fig.…”

Section: Resultsmentioning

confidence: 99%

Cholinergic mechanisms in the rat somatosensory cerebral cortex

Stone¹

1972

The Journal of Physiology

129

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1. The responses of identified cells in the rat cerebral cortex to cholinomimetic and anticholinergic substances has been investigated. 2. Acetylcholine and muscarinic agonists have an excitatory action on 80% of pyramidal tract cells. This response is found especially on cells responding to specific thalamic stimulation and the burst of spikes evoked from this site can sometimes be blocked by the iontophoresis of atropine. This strongly suggests an excitatory transmitter function for acetylcholine in a specific thalamocortical pathway. 3. Experiments on non‐pyramidal tract cells have detected a muscarinic depression of some cells, and a nicotinic excitation of some cells above a depth of 600 μ in the cortex. 4. It is suggested that the increased release of acetylcholine from the cortex produced by atropine administration may be due to an excess of muscarinic inhibitory over excitatory synapses in the cortex.

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Section: Resultsmentioning

confidence: 99%

Cholinergic mechanisms in the rat somatosensory cerebral cortex

Stone¹

1972

The Journal of Physiology

129

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“…which persist with almost unchanged latency and frequency even after very large doses (Eccles, Fatt & Koketsu, 1954;Eccles et al 1956; Curtis & Eccles, 1958b;Brooks & Wilson, 1959). A further indication of an intense iiUtial synaptic excitatory action is provided by the lengthened interval that often disturbs the rhythm between the second and third discharges (Eccles, Fatt & Koketsu, 1954, Fig.…”

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confidence: 99%

Electrophysiological investigations on Renshaw cells

Eccles¹,

Eccles²,

Iggo³

et al. 1961

The Journal of Physiology

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132

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“…Single spike discharges only were observed during and after the application of nicotine. It has been reported that intravenous administration of methacholine, carbamyl choline and succinylcholine had little effect on Renshaw cells, but that the cells were activated when these agents were administered electrophoretically (10,13). This suggests that the compound which has a quarternary ammonium base does not pass through the blood brain barrier.…”

Section: Effects Of S-6 and Other Cholinergic Drugs On Renshaw Cellsmentioning

confidence: 83%

Effects of 1-Methyl-5-Chloroindoline Methylbromide (S-6) on Renshaw Cells of Cats

Irikura

Ohkubo

Hirayama

et al. 1977

Japanese Journal of Pharmacology

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Abstract-Effects of 1-methyl-5-chloroindoline methylbromide (S-6) on Renshaw cells were investigated in cats anesthetized with pentobarbital sodium. S-6 proved to have little effect on spike discharges of Renshaw cells when administered intra venously, but the agent electrophoretically applied revealed excitatory effects which resembled the action of methacholine and such effects were blocked by intravenous administration of atropine. It was concluded that (1) S-6 is impermeant to the blood brain barrier and (2) the excitatory action of S-6 on Renshaw cells is muscarinic in nature.Previous reports from this laboratory have demonstrated that 1-methyl-5-chloroindoline methylbromide (S-6) exerts a remarkable parasympathomimetic effect on various peripheral organs (1, 2), and that i.v. administration revealed little effect on activities of the central nervous system, such as EEG, spinal reflexes and anti-convulsive activity (3). These results suggested that intravenously administered S-6 may not enter the central nervous system.In the present study, the effects of electrophoretically administered S-6 on Renshaw cells were compared with the results seen with intravenous administration.The action of electrophoretically applied S-6 on the electrical activity of the Renshaw cells was also com pared with that of other cholinergic agents. MATERIALS AND METHODSExperiments were carried out on 29 adult cats anesthetized with pentobarbital sodium (35 mg/kg i.p.) and immobilized with gallamine triethiodide. The head and pelvis of the animal were stereotaxically fixed.Laminectomy was performed at levels from Ll to S2. The L7 ventral root was sectioned peripherally and the central end was placed on a bipolar platinum wire electrode for stimu lation by square pulses of 0.1 msec duration at a rate of 1 Hz.Double or triple barrel microelectrodes were used for electrophoretic application of S-6 and other drugs to Renshaw cells. Unitary activities of Renshaw cells were recorded extracellularly with one barrel filled with 4 M NaCI (tip resistance, 1-3 MQ). The other barrels were filled with one or two of the following drugs dissolved in 0.9% saline: S-6 (2 M, pH 3.9), methacholine bromide (Tokyo Kasei) (2 M, pH 3.2), acetylcholine chloride (Daiichi Seiyaku) (1 M, pH 4.1) and nicotine tartrate (Nakarai Kagaku Yakuhin) (1 M, pH 2.9). The tip resistances of drug-containing barrels were kept below 20 MQ to avoid

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The effect of diffusional barriers upon the pharmacology of cells within the central nervous system

Cited by 121 publications

References 20 publications

Cholinergic mechanisms in the rat somatosensory cerebral cortex

Cholinergic mechanisms in the rat somatosensory cerebral cortex

Electrophysiological investigations on Renshaw cells

Effects of 1-Methyl-5-Chloroindoline Methylbromide (S-6) on Renshaw Cells of Cats

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