The influence of chlorpromazine upon the cerebello-cortical and cerebello-spinal circuits

Kreindler, A; Steriade, Mircea; Zuckermann, Emil C.; Chimion, D.

doi:10.1016/0013-4694(58)90010-5

Cited by 13 publications

(3 citation statements)

References 3 publications

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“…Gellhorn (6) has shown, however, that for small doses largactil and barbiturate spindle-bursts appear in cortical leads and spread to profound leads only after the doses are increased; this may suggest that these substances exert a primary action on the cortex. Besides, the same conclusions were reached by Kreindler, Steriade, Zuckerman and Chimion (7) when studying the, effect of chlorpromazine on cerebelloreticulocortical circuits. In addition, during our experiments, slow phenomena in spindle bursts elicited by quinidine appear exclusively in cortical leads and are absent from diencephalic ones.…”

Section: Discussionsupporting

confidence: 72%

On the Anticonvulsive Effect of Quinidine I. Experimental investigation of somatomotor, vegetative and bioelectrical aspects of convulsive seizures elicited by electroshocks

Steriade¹,

Stoica²

1959

Epilepsia

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In spite of widespread therapeutic use of quinidine in humtps, there has been practically no report on the effects of this drug on the central nervous system.Classical experiments have shown toxic action on the protoplasm and inhibition of cell-respiration, achieved by quinine and its dextrogyrous isomer, quinidine. Datta and Basu (3) recently demonstrated that quinidine inhibits a certain chain of webs' cycle (the step from cetoglutarate to succinate), while Uyeki, Geiling and Dubois (15) reported inhibition of ATP-ase due to this drug. On the other hand, other studies revealed the enhancing effects of quinine on certain hypnotical and analgesic drugs (Orahovats, Lehman and Chapin, 13). Taking into account the importance of intermediary metabolism of carbohydrates in brain activity, as well as the preceding data showing that quinidine acts by inhibiting certain stages of this metabolism, we undertook to study the effects of this drug on one of the most violent manifestations of brain excitability: the epileptic seizure. This is the first of a series of notes concerning experimental work on the inhibitory influence of quinidine on epileptic seizures and is intended to convey information related to various aspects of the convulsive seizure induced by transcerebral electroshock. METHODInvestigations were performed on 61 cats.At the beginning of each experiment, a constant threshold of stimulation by transcerebral electroshock was established for each animal. Progressive doses of a solution of 1 yo quinidine sulphate (540 mg/kg) were then injected intravenously and the influence of this treatment on the electro-convulsive seizure was carefully observed. In a number of animals, the potentiation of the effect of intravenously injected quinidine by intra-muscular administration of certain doses of phenobarbital was studied; these doses were, in themselves, incapable of inhibiting convulsive seizures induced, by electroshocks.Fifty-two animals were clinically studied by analyzing somatomotor aspects of References p . 274

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Section: Discussionsupporting

confidence: 72%

On the Anticonvulsive Effect of Quinidine I. Experimental investigation of somatomotor, vegetative and bioelectrical aspects of convulsive seizures elicited by electroshocks

Steriade¹,

Stoica²

1959

Epilepsia

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“…BASMAJI/,X and SZ.aV,~IARI (1955 b) suggested that the skeletal muscle relaxant effects of CPZ may be due to a depressant effect on facilitatory areas of the brainstem. KREINDLER et al (1958), KmJGLOV (1958) and VALDMAN (1962) offered evidence to support the hypothesis that CPZ acts on descending motor systems ol'the brainstem reticular formation.…”

Section: Introductionmentioning

confidence: 91%

“…MANY investigators have shown that CPZ reduces skeletal muscle tone in experimental animals (DAsGUPTA andWERNER, 1955: SHI~ATZ, 1955;and KREINDLER et al, 1958) and in certain human hyperkinetic states (Lt~:H~vIANY and HANRAHAN, 1954;SZATMARL 1955 a, b: andCOLE andR(~BI~RTSON, 1955). The neural mechanisms of CPZ reduction of skeletal muscle tone appear to be very complex.…”

Section: Introductionmentioning

confidence: 99%

Effects of chlorpromazine on some motor reflexes

Hudson

Domino

1963

International Journal of Neuropharmacology

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The effects of chlorpromazine (CPZ) on the patellar reflex and segmentally evoked spinal cord potentials were determined in various cat preparations. CPZ in doses of I-8 mg/kg given intravenously (as an accumulative dose) produced a signiticant depression of the patellar reflex and segmentally evoked potentials in animals with an intact central nervous system. Hypotension, potentiation of anesthesia, depression of nerve conduction in afferent and efferent nerves, an effect at the neuromuscular junction, or an effect directly on skeletal muscle or muscle spindle were ruled out as p~.~ssible mechanisms of reflex depression.Studies in high spinal and decerebrate animals (Sherrington, Pollock-Davis)and decerebellate suggested a supraspinal sight of CPZ action. CPZ was shown to cause a significant depression of facilitation and inhibition of the patellar reflex produced by electrical stimulation of the mesencephalic facilitatory and medullary inhibitory areas of the reticular formation. The linguomandibular reflex (LMR) was also elicited in several preparations. This reflex was significantly depressed in intact and high spinal animals while the patellar reflex was depressed only in the former. CPZ-induced depression of segmentally evoked potentials was demonstrated to be dependent upon the intensity of electrical stimulation. CPZ was much less effective in depressing potentials elicited by supramaximal than by submaximal stimuli (80 per cent of maximum). The mean arterial blood pressure was depressed by CPZ in all preparations with an intact medullary vasomotor outflow.The site of CPZ depression of these motor reflexes is probably on neurons in portions of the bulbar facilitatory (BF) reticular area as well as a lesser depression of neurons in portions of the bulbar inhibitory reticular area. The possibility that CPZ may also act at a spinal level is discussed.

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Supraspinal and Drug Modulation of the Alpha Motor System

Stern¹,

Ward²

1962

Arch Neurol

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The influence of chlorpromazine upon the cerebello-cortical and cerebello-spinal circuits

Cited by 13 publications

References 3 publications

On the Anticonvulsive Effect of Quinidine I. Experimental investigation of somatomotor, vegetative and bioelectrical aspects of convulsive seizures elicited by electroshocks

On the Anticonvulsive Effect of Quinidine I. Experimental investigation of somatomotor, vegetative and bioelectrical aspects of convulsive seizures elicited by electroshocks

Effects of chlorpromazine on some motor reflexes

Supraspinal and Drug Modulation of the Alpha Motor System

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