Effect of monoamineoxidase inhibitors on 5‐hydroxytryptamine output from perfused cerebral ventricles of anaesthetized cats

Goodrich, Cecilie A.

doi:10.1111/j.1476-5381.1969.tb09525.x

Cited by 19 publications

(4 citation statements)

References 12 publications

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“…A further suggestion of a defect in 5-HT metabolism was obtained by injecting tranylcypromine. Goodrich (1969) reported that a single injection in normal cats of this monoamine oxidase inhibitor, as used in the present study, produces an increase in 5-HT in the cerebral ventricles from .8 to 6.4 ng/ml after 3 hr., but this dosage had no effect on the abnormal behavior in the present study.…”

Section: Anatomysupporting

confidence: 60%

5-hydroxytryptamine metabolism, superior colliculus, and grooming behavior in cats with pontile lesions.

Trulson¹,

Randall²

1973

Journal of Comparative and Physiological Psychology

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Cats with pontile lesions display an abnormal grooming behavior that waxes and wanes during the year. Data are presented indicating that the abnormal behavior is mediated by serotonergic neurons in the superior colliculus. Manipulations of 5-hydroxytryptamine metabolism were made systemically, as well as locally in the superior colliculus, in normal cats and in cats with pontile lesions. 5-hydroxytryptophan administration abolished the abnormal behavior, and p-chlorophenylalanine administration induced the abnormal behavior in cats with pontile lesions; but p-chlorophenylalanine administration to normal cats did not induce the abnormal behavior. The results indicate that the pontile lesion produces at least 2 critical deficits that induce the abnormal behavior. Previous data indicated that another critical deficit is in glucocorticoid function.

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Section: Anatomysupporting

confidence: 60%

5-hydroxytryptamine metabolism, superior colliculus, and grooming behavior in cats with pontile lesions.

Trulson¹,

Randall²

1973

Journal of Comparative and Physiological Psychology

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“…If the MAO inhibitors have first to be absorbed into the blood stream, even when injected intraventricularly, before they can prevent the hypothermia of a halothane anaesthesia, this does not exclude an action on the anterior hypothalamus. In favour of an action on this region of the brain is the finding that MAO inhibitors increase the 5-HT output from the perfused third ventricle of the cat when injected intraperitoneally (El Hawary et al, 1967;Goodrich, 1969). If the effect were solely due to an action on the anterior hypothalamus it would however be difficult to understand why the intraventricular were not more effective than the intraperitoneal injections.…”

Section: Discussionmentioning

confidence: 99%

“…Its inhibition would therefore prevent the destruction of the released 5-HT, which could then overcome the temperature lowering effect of noradrenaline (Feldberg & Lotti, 1967). The ability of intraperitoneal injections of MAO inhibitors to increase the 5-HT output from the perfused cerebral ventricles in cats (El Hawary, Feldberg & Lotti, 1967;Goodrich, 1969) supports this theory.…”

Section: Introductionmentioning

confidence: 90%

Effects of monoamine oxidase inhibitors and amphetamine on hypothermia produced by halothane

Feldberg

Lang

1970

British J Pharmacology

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Summary1. In cats, the effects of tranylcypromine and pheniprazine, two monoamine oxidase (MAO) inhibitors with strong amphetamine-like actions, of pargyline, an inhibitor without amphetamine-like actions, and of amphetamine itself, were examined on the hypothermia produced by a 2 hr period of halothane inhalation. 2. The hypothermia was prevented by intraperitoneal injections of the three MAO inhibitors. Tranylcypromine and pheniprazine acted in doses of a few milligrams, pargyline in doses of over 100 mg. 3. The hypothermia was prevented by injections into the cerebral ventricles of tranylcypromine and pheniprazine, in doses which were effective also on intraperitoneal injection; intraperitoneal injections were sometimes more effective. The large doses of pargyline needed to prevent the hypothermia when injected intraperitoneally were not tested by the intraventricular route, as the injections had to be made in a volume of 01 ml. In smaller doses intraventricular pargyline was not effective. 4. The hypothermia was prevented by an intraperitoneal or intraventricular injection of amphetamine in a dose as little as 1 mg; intraperitoneal injections were sometimes more effective. 5. The effects of tranylcypromine and pargyline given intraperitoneally, and of amphetamine given intraventricularly as well, were also examined on the hypothermia produced by an intraventricular injection of 200 ,g noradrenaline. The two MAO inhibitors and amphetamine prevented the hypothermia, or greatly reduced it. 6. It is concluded (a) that even on intraventricular injection the MAO inhibitors must first be absorbed into the blood stream before they can prevent the hypothermia of a halothane anaesthesia; (b) that their action may not be solely on the anterior hypothalamus ; and (c) that they may not act only through MAO inhibition.

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“…This was first shown by El Hawary, Feldiberg & Lotti (1967) for tranylcypromine. Recently Goodrich (1969) found that, weight for weight, tranylcypromine was twice as potent as pheniprazine, eight times as potent as nialamide and sixty times as potent as pargyline in increasing the 5-HT output. Previous experiments (Funderburk et al, 1962;Schoepke & Wiegand, 1963), in which the increase in the 5-HT level of the cat brain was studied after repeated suibcutaneous or intraperitoneal injections, also show that tranylcypromine and pheniprazine were more potent than nialamide and much more potent than pargyline.…”

Section: Discussionmentioning

confidence: 99%

Effects of monoamine oxidase inhibitors on the hypothermia produced in cats by halothane

Summers

1969

British J Pharmacology

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1. In cats, the effects of intraperitoneal injections of four monoamine oxidase (MAO) inhibitors, tranylcypromine, pheniprazine, pargyline, and nialamide, were examined on rectal temiperature and on the hypothermia during anaesthesia produced by a 2 hr period of halothane inhalation. 2. A 2 hr period of halothane inhalation produced a steady fall in temperature amounting to between 20 and 3.50 C. After discontinuation of halothane inhalation, temperature quickly returned to the pre-anaesthetic level but no pyrexia developed. A peculiar stiffness of the leg muscles occurred in several experiments either at the beginning of the inhalation or after its discontinuation.3. An injection of tranylcypromine (5 mg/kg) caused a rise in rectal temperature and prevented the hypothermia of halothane anaesthesia. This effect lasted for at least 4 hr; 20 hr after the injection, halothane again caused hypothermia.4. An injection of pheniprazine (10 mg/kg) usually caused a small rise in temperature which was not sustained. Pheniprazine not only prevented the hypothermia of halothane anaesthesia during the sulbsequent 20 hr, but during the first few hours after the injection halothane inhalation actually produced a steep rise in temperature.5. An injection of pargyline (50 mg/kg) had no effect on temperature but the hypothermia due to halothane inhalation was prevented 1 hr after the injection and attenuated after 20 hr. Injection of 200 mg/kg caused a steady rise in temperature which was accelerated when halothane was administered 1 hr later.6. An injection of nialamide (10, 25 or 50 mg/kg) had no immediate effect on temperature, but pyrexia developed overnight after the two larger doses. The effect on the hypothermia due to halothane inhalation was greater 20 hr after the injection than it was after 1 to 2 hr. Twenty hours after injection of the two larger doses, halothane no longer produced hypothermia but caused a lethal rise in temperature either during or after its inhalation. 7. In rabbits, the effect on temperature of halothane inhalation varied. Either temperature rose slightly or it fell, but not as much as in cats. In one rabbit in which the inhalation had produced a transient rise, pyrexia developed 40 min after discontinuation of halothane.

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Effect of monoamineoxidase inhibitors on 5‐hydroxytryptamine output from perfused cerebral ventricles of anaesthetized cats

Cited by 19 publications

References 12 publications

5-hydroxytryptamine metabolism, superior colliculus, and grooming behavior in cats with pontile lesions.

5-hydroxytryptamine metabolism, superior colliculus, and grooming behavior in cats with pontile lesions.

Effects of monoamine oxidase inhibitors and amphetamine on hypothermia produced by halothane

Effects of monoamine oxidase inhibitors on the hypothermia produced in cats by halothane

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