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Biomedical subjects

J R Leite

Publications and source records attributed to J R Leite.

At least 19 recordsLinked to original sources
PubMed1994

Effect of valepotriates on the behavior of rats in the elevated plus-maze during diazepam withdrawal.

The effect of a mixture of valepotriates on the elevated plus-maze performance of diazepam withdrawn rats was evaluated. The rats were chronically (28 days) treated with diazepam (doses increased up to 5.0 mg/kg) and then treated with control solution for 3 days to induce a withdrawal syndrome. Chronically vehicle-treated rats were used as control. The abstinent animals treated with vehicle showed a significant decrease in the percentage of time spent in the open arms when compared with the control animals. Diazepam and valerian 12.0 mg/kg reversed this anxiogenic effect. Valerian 6.0 mg/kg did not show any difference in relation to the others group.

Analysis of Variance↗
PubMed1994

The effect of corticosterone in rats submitted to the elevated plus-maze and to to pentylenetetrazol-induced convulsions.

1. In order to examine the effects of corticosterone in the anxiety response, the effect of acute, subchronic and chronic corticosterone (CORT) administration were studied using two animal models to study anxiolytic effects of drugs: the elevated plus-maze and the blockade of pentylenetetrazol (PTZ)-induced clonic convulsion. 2. The results obtained with the plus-maze showed an increase in the percentage of open arm entries and time spent in the open arms after acute treatment with the CORT. These results may be interpreted as an anxiolytic effect of corticosterone. Three days of vehicle treatment followed by an acute CORT administration, produced results that should also indicate anxiolytic effect of the corticosteroid. No effect was seen after 14 days of vehicle treatment followed by an acute CORT injection. Subchronic or chronic CORT treatment did not produce results different from controls. CORT treatment did not affect the PTZ-induced clonic convulsion. 3. In conclusion these results suggest that the acute anxiolytic effect observed in the elevated plus-maze did not occur after repeated CORT administration or mild stressors. Moreover they also suggest that the anxiolytic effect did not involve GABA mechanisms.

Administration, Cutaneous↗
PubMed1994

Evidence against the involvement of ACTH/CRF release or corticosteroid receptors in the anxiolytic effect of corticosterone.

The present study was designed to evaluate the role of ACTH and/or CRF release and corticosteroid receptors (glucocorticoid and mineralocorticoid) in the anxiolytic effect of corticosterone (CORT). Costicosteroid receptor mediation was evaluated using a dose-response analysis of the effect of CORT and by the action of dexamethasone (DEX), which binds to glucocorticoid receptors but not to mineralocorticoid receptors. DEX administration also permits indirect evaluation of the effect of ACTH/CRF release on the anxiolytic effect of CORT. Male Wistar rats (3 months old) weighing 250-350 g were treated sc with vehicle (N = 38), CORT 1.25 (N = 18), 2.5 (N = 13) and 5.0 (N = 24) mg/kg, or DEX 5.0 (N = 19) and 10.0 (N = 17) mg/kg and tested in the elevated plus-maze 2 h later. The group that received the highest dose of CORT (5.0 mg/kg) showed a significant increase in percent open arm entries (38 +/- 2.6, mean +/- SEM) as well as in percent time spent in open arms (27 +/- 4.0) when compared with the vehicle-treated rats (24.3 +/- 2.8 and 12.4 +/- 1.9, respectively; both P < 0.05). There were no other significant differences among groups in the two parameters tested or in total arm entries. These data corroborate previous findings of the anxiolytic effect of CORT and suggest that inhibition of ACTH/CRF release and corticosteroid receptors do not play a major role in the anxiolytic effect of CORT.

Adrenocorticotropic Hormone↗
PubMed1992

Anxiolytic effect of carbamazepine in the elevated plus-maze: possible role of adenosine.

In order to extend previously reported observations with other animal models of anxiety, the effect of carbamazepine (CBZ) was presently measured in rats placed on the elevated plus-maze. Intraperitoneal injection of CBZ (5-40 mg/kg) increased the percentage of open arm entries as well as the percentage of time spent on the open arms of the maze, without affecting the total number of arm entries. This effect is characteristic of anxiolytic drugs. The inhibitor of adenosine neuronal uptake papaverine (5-40 mg/kg) caused a similar anxiolytic effect, whereas the adenosine receptor antagonist aminophylline (1-4 mg/kg) selectively decreased the percentage of open arm entries, indicative of an anxiogenic effect. Furthermore, the combination of an anxiogenic dose (4 mg/kg) of aminophylline with an anxiolytic dose (40 mg/kg) of CBZ resulted in cancellation of each other effects. Since reported neurochemical evidence shows that CBZ interacts with adenosine receptors, the present results provide preliminary support for a participation of this neurotransmitter in the anxiolytic action of CBZ.

Adenosine↗
PubMed1990

Effects of acute or chronic carbamazepine on experimentally-induced conflict in the rat.

The effects of acutely or chronically administered carbamazepine were studied in rats submitted to the modified Geller-Seifter conflict test. Diazepam was used as a standard anxiolytic. The results showed an increase in punished response after carbamazepine, as observed with diazepam, leading to the suggestion of an anti-conflict-effect for this drug. No tolerance to the anti-punishment-effect was seen after chronic carbamazepine administration.

Animals↗
PubMed1990

Daily changes in pentylenetetrazol-induced convulsions and open-field behavior in rats.

Susceptibility to pentylenetetrazol (PTZ)-induced clonic convulsions was measured in rats over the 24-hr light-dark cycle at four-hour intervals. The results showed a higher sensitivity to PTZ around 2200 hr. Other groups of rats were exposed to a four-min open-field session. In the first two min of the session the animals were submitted to open-field environmental stimuli. The next two-min observation occurred with sound and light presented to the animals. Differences through the 24-hr period of the day for both sessions were seen. A reduction in rearing at 2200 hr and increase in defecation at 2200 hr and 0200 hr was observed.

Animals↗
PubMed1989

Anxiolytic effect of carbamazepine measured in the elevated plus-maze.

The anxiolytic effect of carbamazepine was measured in rats placed in an elevated plus-maze. Doses from 5 to 40 mg/kg, ip, of carbamazepine increased the percentage of open arm entries as well as the percentage of time spent in the two open arms of the maze. Both of these measures are interpreted as indexes of anxiety. The total number of entries in either the open or the two enclosed arms, considered as an index of general activity, was not changed by the drug. Therefore, carbamazepine caused a selective anxiolytic effect as measured in the elevated plus-maze, which is predictive of clinical efficacy.

Animal Testing Alternatives↗
PubMed1988

Decreased susceptibility to local anesthetics-induced convulsions after paradoxical sleep deprivation.

The effect of 50% convulsant (CD50) and 50% lethal (LD50) doses of lidocaine, bupivacaine and pentylenetetrazol were determined in mice stressed by paradoxical sleep deprivation (PSD). The results showed a reduced mortality after high doses of local anesthetics and decreased seizure susceptibility induced by bupivacaine after 48 h and 72 h of PSD. On the other hand this stressful manipulation increased the susceptibility to pentylenetetrazol-induced convulsions. These data may suggest a different mechanism of action for these drugs. Possible alterations in drug metabolism or on aminergic transmission after PSD may be involved in the protection to the toxic effect of the local anesthetics.

Anesthetics, Local↗
PubMed1987

The effects of carbamazepine on two animal models of depression.

Some clinical reports on antimanic, antidepressant and prophylactic effects of carbamazepine (CBZ) in manic-depressive illness have appeared since its initial use as an anticonvulsant drug. The present report deals with the effects of CBZ on two animal models of depression, namely the potentiation of amphetamine-induced anorexia, and the behavioral despair model. Carbamazepine (10, 20 or 40 mg/kg) neither modified the methamphetamine anorectic effect, nor induced anorexia when administered alone. Subacute and chronic administration of imipramine (4 or 15 mg/kg) decreased immobility of rats in the behavioral despair model. Subacute and chronic administration of CBZ (40 mg/kg) also decreased immobility, whereas the dose of 10 mg/kg CBZ was effective only after chronic treatment. It was concluded that CBZ is similar to atypical antidepressants, since it did not potentiate the amphetamine-induced behavioral effect, but did have an effect on the behavioral despair model of depression.

Animals↗
PubMed1986

Effects of acute and chronic carbamazepine administration on apomorphine-elicited stereotypy.

Three experiments were performed in order to find if carbamazepine interacts with dopaminergic systems. In the first experiment carbamazepine itself did not induce stereotypy but it potentiated the apomorphine-elicited stereotypy. The potentiation was no longer seen in the second experiment with carbamazepine given chronically. Moreover, stereotyped behaviour was reduced when apomorphine was administered alone after chronic carbamazepine administration. In the third experiment it was shown that carbamazepine together with chronic haloperidol administration or with rapid eye movement-sleep deprivation prevented the development of dopaminergic supersensitivity. These experiments support the hypothesis of a dopaminergic effect of carbamazepine.

Animals↗
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↗
PubMed1983

Aminooxyacetic acid induced accumulation of GABA in the rat brain. Interaction with GABA receptors and distribution in compartments.

The effect of aminooxyacetic acid (AOAA, 90 mg/kg i.v.) on bicuculline, picrotoxin and 3-mercaptopropionic acid (3-MPA) induced convulsions and on GABA concentrations in cerebellum, whole brain and a synaptosomal fraction of whole brain was investigated. At various intervals after AOAA the rats were either injected with one of the convulsive drugs or sacrificed for analysis of the GABA concentration. AOAA caused a rapid initial (0-30 min) and a later slower increase of GABA in cerebellum and whole brain. In the synaptosomal fraction the GABA accumulation was delayed and less pronounced when compared to the whole brain. The bicuculline induced convulsions were markedly potentiated during the first hour but completely blocked from 2-6 h after AOAA. Picrotoxin showed a somewhat different pattern to bicuculline in the interactions with AOAA. The initial strong potentiation was not observed but the later phase of protection was present. In the interactions with 3-MPA, the effect of AOAA was always protective. The time to onset of convulsions was gradually increased during the first 30 min after AOAA. This protective effect remained practically unchanged up to 6 h after AOAA. However, once started, the convulsions were generally of the same duration and intensity. The results can be interpreted as GABA accumulating after AOAA stimulates GABA receptors to a degree more or less proportional to the whole brain GABA concentration and further that GABA synthetized in neurons is liberated, stimulates inhibitory bicuculline sensitive (predominant) and excitatory bicuculline insensitive receptors and is captured to a large extent by non-neuronal cells.

3-Mercaptopropionic Acid↗
PubMed1982

Effects of cannabidiol on behavioral seizures caused by convulsant drugs or current in mice.

In mice, running, clonic and tonic convulsions and lethality were assessed following transcorneal (electroshock) current or convulsant drugs, each administered alone and after cannabidiol (CBD) pretreatment. CBD prevented tonic convulsions caused by a convulsant current (CC) 99.99, and by the convulsant dose (CD) 99.99 values of gamma-aminobutyric acid (GABA) inhibitors, 3-mercaptoproprionic acid (3MPA), picrotoxin (PIC), isonicotinic acid hydrazine (INH), pentylenetetrazol (PTZ) and bicuculline (BIC). Rankorder potencies, based on the antitonic ED50 of CBD, were: 3MPA greater than PIC = current = PTZ = BIC. Further, CBD prevented 3MPA-induced lethality, but failed to prevent the occurrence of the other behavioral endpoints of the above treatments. CBD also failed to prevent convulsions and lethality caused by the CD 99.99 of strychnine, a glycine antagonist. The differential effects of CBD suggest that the cannabinoid acts to inhibit seizure spread in the CNS by an action on GABA, but not glycine, mechanisms.

Animals↗
PubMed1982

Effects of sodium barbitone on learning and memory-storage of an appetitive and an aversive task.

In order to test the effects of sodium barbitone on the acquisition and retention of an appetitively and an aversively reinforced behavior, mice were trained in a spatial discrimination Y-maze task. Learning was observed in both situations, with acquisition unimpaired by the drug. Sodium barbitone did, however, affect retention of both tasks in all groups treated with the drug before training. Results are discussed in light of the various modes of action of this drug, i.e., as an inhibitor of protein synthesis, as a blocker of catecholamine biosynthesis, with regard to its effects on paradoxical sleep and on gamma-amino-butyric acid (GABA).

Animals↗
PubMed1982

Anticonvulsant effects of the (-) and (+)isomers of cannabidiol and their dimethylheptyl homologs.

The anticonvulsant actions of the (-) and (+)isomers of cannabidiol and dimethylheptyl-cannabidiol were studied with the maximal electroconvulsive shock model in mice. The ratio of the times for hindlimb extension and fore limb flexion was recorded as an anticonvulsant index. All the cannabinoids were anticonvulsant. They also potentiated pentobarbitone sleeping time. The (+)isomer was more active than the (-)isomer. Possible mechanisms of actions on receptors or membranes are discussed.

Animals↗
PubMed1978

Effects of chronic ingestion and withdrawal of sodium barbitone on learning in rats.

Rats were submitted to three different manipulations: chronic ingestion of sodium barbitone, which was added to the drinking water; chronic administration of barbitone and subsequent withdrawal of the drug; and drinking water only. Both groups of experimental animals showed deficient acquisition in both shuttle-box avoidance and passive-avoidance response when compared to the control animals. Nevertheless, no impairment was observed in passive avoidance when the period of withdrawal was 15 days. Neither was impairment observed when the animals were tested in a T-maze or in another appetitive task. These results cannot be explained by differences in weight or fluid consumption.

Animals↗