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Biomedical subjects

G Gianutsos

Publications and source records attributed to G Gianutsos.

At least 73 records · Page 4Linked to original sources
PubMed1977

Possible significance of clozapine-induced increase in brain dopamine.

Clozapine elevates the concentration of dopamine in the brains of mice injected with doses of 5-20 mg/kg while a 40 mg/kg dose has no effect. This biphasic change in dopamine content is seen in both the striatum and olfactory tubercle. The elevated dopamine concentration is dose-dependently antagonized by apomorphine, while a corresponding clozapine-induced reduction in norepinephrine concentrations is unaffected by apomorphine. These results suggest that part of the action of clozapine may be to reduce the release of dopamine.

Animals↗
PubMed1976

Differential actions of dopamine agonists and antagonists on the gamma-butyrolactone-induced in mouse brain dopamine.

gamma-Butyrolactone (GBL) increased the dopamine concentration in the forebrain of the mouse. Apomorphine dose-dependently antagonized the GBL effect, while piribedil was less effective. Haloperidol prevented the antagonism of GBL by apomorphine but pimozide was ineffective in blocking apomorphine. After chronic treatment with haloperidol or pimozide, there was no alteration of the maximum GBL-induced increase in dopamine nor was there any significant change in the antagonism by apomorphine, although a trend toward increased sensitivity to apomorphine was noted in the group withdrawn from haloperidol. These results suggest that in the mouse, haloperidol is a more effective antagonist of presynaptic dopamine autoreceptors than pimozide, while apomorphine is a better presynaptic agonist than piribedil.

4-Butyrolactone↗
PubMed1976

Effects of cholinergic agonists and antagonists on morphine-withdrawal syndrome.

The effects of pilocarpine, atropine and dexetimide were studied on the occurrence and intensity of morphine-withdrawal signs observed after cessation of chronic morphine injections. Pilocarpine was effective in reducing both 'wet-dog' like body shakes and aggression but it increased diarrhea and weight loss. Pretreatment with atropine blocked all of the effects of pilocarpine on withdrawal signs. Methylscopolamine pretreatment blocked only diarrhea. The administration of atropine or dexetimide produced no significant effect on any of the withdrawal signs. These results indicate a role for central cholinergic mechanism in narcotic withdrawal.

Animals↗
PubMed1976

Blockade of apomorphine-induced aggression by morphine or neuroleptics: differential alteration by antimuscarinics and naloxone.

Both morphine and the neuroleptics, haloperidol and oxyperomide, dose-dependently reduce the aggression in rats produced by 20 mg/kg of apomorphine, a dopamine receptor stimulant. The narcotics antagonist, naloxone, prevents this effect of morphine but not the effect of neuroleptics. Dexetimide, a centrally acting antimuscarnic drug, antagonizes the reduction in aggression produced by the neuroleptics, but does not affect morphine's action. The cholinergic agonist, pilocarpine, enhances this action of oxyperomide. These results suggest that a cholinergic component contributes to the anti-agression action of neuroleptics and demonstrates a difference in the mechanism of action between neuroleptics and morphine.

Aggression↗
PubMed1975

Paradoxical absence of aggression during naloxone-precipitated morphine withdrawal.

Aggression, which is normally seen during withdrawal from narcotics, could not be produced in morphine-dependent rats by the administration of naloxone at doses which causes other signs of withdrawal. Apomorphine injected instead of naloxone was capable of producing aggression, without other withdrawal signs. Naturally occurring aggression (72-hr withdrawal) was enhanced by apomorphine and unaffected by naloxone.

Aggression↗
PubMed1975

Effect of loperamide, haloperidol and methadone in rats trained to discriminate morphine from saline.

In an operant procedure of lever pressing at FR10 schedule of food reinforcement, rats were trained to respond differentially in order to discriminate the effects of morphine (10 mg/kg) injections from those of saline injection. These rats learned to press a lever on one side after morphine injection and a lever on the opposite side after saline injection. In subsequent testing, these rats reliably emitted responses on the morphine lever after 10 or 20 mg/kg of morphine IP, 50 mg/kg of morphine given orally or 2 mg/kg methadone. Two mg/kg of morphine (or 10 or 20 mg/kg given orall) was recognized as saline. In contrast, after either loperamide (an antidiarrheal drug) given in doses up to 10 mg/kg or haloperidol (a neuroleptic) given in doses up to 0.32 mg/kg, all responses were made on the saline lever. Higher doses suppressed responding. Since neither the antidiarrheal activity nor the neuroleptic activity was sufficient to provide the discriminable cue associated with morphine, it is suggested that specific central effects produced only by narcotic analgesics are the basis for these morphine cues.

Animals↗
PubMed1975

Aggression in mice after p-chloroamphetamine.

Two or 3 days after a single high-dose (20 mg/Kg) of p-chloroamphetamine (PCA) aggression was reliably observed in male mice. This agression was not produced when the same dose of d-amphetamine was injected or when PCA was injected one hour before testing. However, PCA produced an increase in locomotor activity one hour, but not 24 hours, after injection.

Aggression↗