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Biomedical subjects

S Tufik

Publications and source records attributed to S Tufik.

At least 109 records · Page 6Linked to original sources
PubMed1988

Reversal of the increase in apomorphine-induced stereotypy and aggression in REM sleep deprived rats by dopamine agonist pretreatments.

REM sleep deprivation (REMSD) induces augmented responses to dopaminergic agonists. Prolonged administration of neuroleptics induces a similar state, probably by the production of supersensitivity of dopaminergic receptors. Such a supersensitive state could be induced by REMSD as a result of impairment of dopamine neurotransmission. In order to test this hypothesis, bromocriptine, nomifensine, amphetamine, L-dopa, imipramine and electroconvulsive shock (ECS) were administered to rats during REMSD, and aggressive and stereotyped behaviors were measured. Amphetamine and L-dopa pretreatment attenuated the increases in apomorphine-induced stereotypy and aggression in REMSD rats, but ECS selectively reduced apomorphine-induced aggression. The other drugs tested were ineffective on both behavioral tests. Such a selective action may reflect different effects of ECS on different dopaminergic systems such as those involved with stereotypy and aggression. The results suggest that REMSD induces an increase in dopaminergic sensitivity which may be reversed by pretreatment with some dopaminergic agonists.

Aggression↗
PubMed1987

Does REM sleep deprivation induce subsensitivity of presynaptic dopamine or postsynaptic acetylcholine receptors in the rat brain?

Yawning behavior was used to evaluate the sensitivity of presynaptic dopamine receptors and postsynaptic acetylcholine receptors of normal and REM sleep-deprived (REMSD) rats. The results show a lowering of the dose-response curve obtained with apomorphine and pilocarpine, as well as a shift to the right in the curve obtained with physostigmine. These results suggest that REMSD induces subsensitization of presynaptic dopamine receptors and/or postsynaptic acetylcholine receptors with different characteristics related to the mechanism of action of the cholinomimetic agent employed.

Animals↗
PubMed1987

Rem sleep deprivation in an experimental model of Parkinson's disease.

Previous investigations have shown that REM sleep deprived (REM SD) rats display an enhanced response to dopamine agonists. This action seems to be mediated through a supersensitivity of dopamine post-synaptic receptors. Accordingly, REM SD was performed on rats with an experimental model of Parkinson's disease. The animals were bilaterally lesioned in the nigrostriatal pathway through a stereotaxically directed electrical current. Seven days after the surgery the animals were REM SD for 72 hours and immediately after the end of this period were observed in an open field for ambulation, rearing, grooming, and latency. In comparison with non-deprived rats there was a significant increase in ambulation and rearing, a response that appeared again after a second REM SD period on day 21th after the surgery. These data of improvement of two parameters of an experimental model of Parkinson's disease suggest that SD may be useful in this condition.

Animals↗
PubMed1986

REM sleep deprivation induces a decrease in norepinephrine-stimulated 3H-cyclic AMP accumulation in slices from rat brain.

Beta adrenergic sites in rat brain are reduced after repeated treatment with antidepressant drugs, with REM sleep deprivation (REMSd) having the same effect. This paper reports the effects of REMSd in the production of 3H-cyclic AMP in frontal cortical slices by NE challenge. Data presented in this paper report a marked decrease in 3H-cyclic AMP synthesis after REMSd, which is in accordance with previous results showing adrenergic receptor down-regulation following REMSd. Results are discussed in view of possible interaction with dopaminergic systems and depression management.

Adenylyl Cyclases↗
PubMed1986

Pharmacology of lemongrass (Cymbopogon citratus Stapf). III. Assessment of eventual toxic, hypnotic and anxiolytic effects on humans.

A herbal tea (called an abafado in Brazil) prepared from the dried leaves of lemongrass was administered to healthy volunteers. Following a single dose or 2 weeks of daily oral administration, the abafado produced no changes in serum glucose, urea, creatinine, cholesterol, triglycerides, lipids, total bilirubin, indirect bilirubin, GOT, GPT, alkaline phosphatase, total protein, albumin, LDH and CPK. Urine analysis (proteins, glucose, ketones, bilirubins, occult blood and urobilinogen) as well as EEG and EKG showed no abnormalities. There were slight elevations of direct bilirubin and of amylase in some of the volunteers, but without any clinical manifestation. These results taken together indicate that lemongrass as used in Brazilian folk medicine is not toxic for humans. The eventual hypnotic effect of lemongrass was investigated in 50 volunteers who ingested samples of lemongrass and a placebo under double-blind conditions. The parameters (i.e. sleep induction, sleep quality, dream recall and rewakening) did not show any effect of lemongrass as compared to the placebo. Eighteen subjects with high scores of trait-anxiety were submitted to an anxiety-inducing test following taking lemongrass or placebo under double-blind conditions. Their anxiety levels were similar, indicating that the abafado of the plant does not have anxiolytic properties. It is concluded that lemongrass, one of the most popular Brazilian herbal medicines, used for its alleged CNS-depressant effects, is atoxic but lacks hypnotic or anxiolytic properties.

Administration, Oral↗
PubMed1981

Changes of response to dopaminergic drugs in rats submitted to REM-sleep deprivation.

Three experiments were performed in order to add further support to the hypothesis that the exaggerated aggressiveness elicited by apomorphine in REM sleep deprived rats was due to a state of supersensitivity of post-synaptic dopaminergic receptors in brain. In the first experiment, REM deprived rats displayed much aggressiveness when challenged with 10 and 20 mg/kg of bromocriptine and piribedil. Thus, the intensification of responses by REM sleep deprivation is not restricted to apomorphine, as it was also obtained with two other dopaminergic agonists. In the second experiment, the association of REM deprivation with an injection of haloperidol 24 h before apomorphine administration induced still more aggressive behavior when compared to the rats that were only sleep deprived. It has been claimed that 24 h after haloperidol a state of supersensitivity to dopamine agonists occurs in the brain; therefore, it is probable that REM deprivation could also act similarly. The third experiment showed that haloperidol administered 2 h before apomorphine administration blocked the aggressive behavior in rats either submitted to REM deprivation alone or to REM deprivation plus a previous injection of haloperidol 24 h before. This also favors the proposed hypothesis. Alternative possibilities for explaining the observed hyperresponsiveness of REM deprived rats to apomorphine and other dopaminergic agonists are also analysed.

Adrenergic Agonists↗
PubMed1981

Inhibition of central angiotensin I conversion by oral captopril.

1. The central action of captopril (D-3-mercapto-methylpropanoyl-L-proline, SQ 14225) in the rat was evaluated by measuring the effect of the orally administered drug on responses to angiotensin I given intracerebroventricularly. 2. The pressor and dipsogenic effects of angiotensin I (20 ng) injected into the third ventricle were reduced by about 50% for 4 h following the oral administration of captopril, 20mg/kg. Both responses returned to pretreatment control values 8 h after captopril administration. 3. Orally administered captopril affects the action of angiotensin I on the central nervous system thus providing an alternative explanation for the hypotensive effect of captopril. This effect if probably due to the direct passage of captopril through the blood brain barrier.

Administration, Oral↗
PubMed1980

Sex differences in the response to apomorphine in rats.

The response of male and female rats to the hypothermic and verticalization effect (climbing behavior) induced by different doses of apomorphine was studied. A clear sex difference was observed, males showing more verticalization than females. Conversely the females showed a greater decrease in body temperature than males. The verticalization response was also studied in rats of both sexes at seven different ages, varying from 15 to 100 days. At the earlier ages, both groups presented low levels of verticalization. Mature males (60-100 days of age) increased the verticalization response to apomorphine.

Aging↗
PubMed1978

Does REM sleep deprivation induce a supersensitivity of dopaminergic receptors in the rat brain?

The possibility that REM sleep deprivation induces increased sensitivity of rats to the effects of apomorphine was investigated. Rats were deprived of REM sleep by placing them on 6.0 cm platforms for 3 days. Stress control groups consisting of rats placed on 14 cm platforms (control rats) and groups of nonmanipulated animals (normal rats) were used for comparison purposes. Several doses of apomorphine were administered to these 3 groups of animals, and aggressive behavior, stereotyped behavior, verticalization and body temperature were recorded. All measures indicated that REM-deprived rats were more responsive to apomorphine than the normal and control animals, with the exception of verticalization effect, in which both REM-deprived and control animals reacted similarly. These results suggest that REM deprivation induced supersensitivity in brain dopamine receptors. Other possible interpretations are also discussed.

Aggression↗
PubMed1977

Cannabis, catecholamines, rapid eye movement sleep and aggressive behaviour.

1. Previous work from our laboratory has shown that cannabis induces aggressive behaviour in rats that have been deprived of rapid eye movement (REM) sleep. It was suggested that this effect was related to brain catecholamines, with dopamine playing an agonist role and noradrenaline an inhibitory one. The present paper describes new experiments dealing with this subject. 2. Previous REM sleep-deprivation enhanced both delta9-tetrahydrocannabinol (THC)-induced hypothermia and nomifensine effects on aggressive behaviour. 3. A marihuana extract decreased brain dopamine turnover in REM sleep-deprived rats, an effect not observed in non-deprived rats. Noradrenaline metabolism was not altered. 4. Fighting behaviour was elicited in REM sleep-deprived rats treated with 4 different dopamine-beta-hydroxylase inhibitors. 5. Apomorphine, nomifensine and delta9-THC administered to non-deprived rats pretreated with bis(4-methyl-1-homopiperanzinyl-thiocarbonyl) disulphide (Fla-63), induced fighting behaviour. 6. Nomifensine and apomorphine induced fighting in non-deprived rats pretreated with delta9-THC. 7. Clonidine inhibited the fighting elicited in REM sleep-deprived rats by either delta9-THC or Fla-63 pretreatment. 8. The data are discussed in terms of the influence of REM sleep-deprivation (or the stress associated with deprivation) on the response to dopaminergic drugs and cannabis. Taken together they emphasize the participation of brain dopamine and noradrenaline systems in the aggressive behaviour studied.

Aggression↗
PubMedDate not supplied

Treatment with dexamethasone alters yawning behavior induced by cholinergic but not dopaminergic agonist.

Because stressful manipulations have been reported to modify drug-induced yawning, the present study investigated the effects of single and repeated treatment with a synthetic glucocorticoid, dexamethasone (DEXA) on apomorphine- and pilocarpine-induced yawning in male rats. Neither single nor repeated treatment with DEXA altered apomorphine-induced yawning. Single administration of DEXA, however, resulted in an increased number of yawns induced by pilocarpine. Conversely, repeated administration of DEXA led to a decreased number of yawns induced by pilocarpine. In conclusion, the present findings show that dopaminergic and cholinergic are distinctly altered by DEXA, in terms of yawning behavior when animals received DEXA.

Animals↗
PubMedDate not supplied

Role of the anteroventral third ventricle region and the renin angiotensin system in methylprednisolone hypertension.

Methylprednisolone (M, 10 mg/kg/week subcutaneously) was administered to cause hypertension in rats, and the role of AV3V region was assessed before and after development of the hypertensive state. Participation of the renin angiotensin system (RAS) was evaluated by changes in mean arterial pressure (MAP) induced by administration of saralasin (S, 10 micron g/kg/min i.v.) or captopril (C, 20 mg/kg/p.o).aAnaAV3V lesion before M administration partially prevented and delayed the beginning appearance of M hypertension. Furthermore, a prior AV3V lesion abolished an angiotensin II (AII)-dependent pressor component normally identified by S and C administration in this type of hypertension. During the maintenance phase of the hypertension, an AV3V lesion caused a partial reduction in blood pressure. A spontaneous disappearance of a vasoconstrictor component mediated by AII was observed in the late phases of M hypertension. It is concluded that the AV3V region is essential to the full development and maintenance of M hypertension in the rat. Also in this model, integrity of the AV3V area is essential to the expression of the AII-mediated pressor component. Finally it is apparent tha M can cause hypertension even in the absence of the AV3V area or during chronic renin angiotensin blockade, indicating multiple pathogenetic mechanisms in this experimental model.

Angiotensin II↗
PubMedDate not supplied

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

To test the peripheral mechanisms of prevention and reversal of two-kidney, one clip (2K1C) hypertension in the rat by lesion of the anteroventral third ventricle (AV3V) region, we studied blood pressure responses in rats to AV3V lesion produced before (n = 8) or after (n = 8) clipping the left renal artery. Two groups of sham-lesioned, clipped rats (n = 9 each) served as controls. At the end of the experiments, saralasin and captopril were given to evaluate the angiotensin-dependent component of blood pressure. To study the influence of the procedures on plasma renin activity (PRA), two parallel groups of rats (n = 26 and 24, respectively) were submitted to similar surgical protocols. We observed that increases in blood pressure were significantly smaller in the previously lesioned compared to previously sham-lesioned animals (delta BP = 21.5 +/- 3.7 vs. 32.9 +/- 2.5 mm Hg, p less than 0.01); also, AV3V lesion almost completely reversed hypertension (BP from 167.5 +/- 2.9 to 136.0 +/- 4.1 mm Hg, p less than 0.001), which was not observed in the sham-lesioned animals (BP from 172.0 +/- 2.8 to 168 +/- 2.7 mm Hg, NS). Saralasin produced a significantly smaller decrease in BP in the lesioned animals compared to those with sham lesions during both prevention and reversal experiments. Similar results were observed with captopril. Previous AV3V lesion did not significantly affect PRA with clipping of the renal artery, but AV3V destruction after hypertension had been established resulted in significantly lower PRA compared to sham-lesioned animals (4.58 +/- 0.72 vs 8.38 +/- 1.79, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMedDate not supplied

A study of the pharmacological actions of Dioclea grandiflora Martius ex Bentham.

Dioclea grandiflora Mart. ex Bent., known as Mucuna or Mucuna of stone, is a member of the Leguminosae family, popularly used for its possible effects on the Central Nervous System (CNS). Reports mention sedative, tonic, and also antiepileptic properties for this plant. In this paper a screening for CNS action was done with aqueous extracts of the seeds. This study was carried out using some animal models for the study of sedative, hypnotic, anxiolytic, anticonvulsive and neuroleptic activity. The results showed that Dioclea grandiflora Mart. ex Bent. demonstrates the general profile of a CNS depressant drug. However, the extract did not exhibit any of the specific profiles tested. Moreover, the results suggest a possible toxicity stemming from the popular or folk use of this plant.

Analysis of Variance↗