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Biomedical subjects

T Baptista

Publications and source records attributed to T Baptista.

50 records · Page 3Linked to original sources
PubMed1993

The attitudes toward psychiatry of physicians and medical students in Venezuela.

Attitudes toward psychiatry were assessed in 490 medical students and 362 physicians from two universities in Venezuela: Universidad de Los Andes (ULA) and Universidad Centro-Occidental Lisandro Alvarado (UCLA). A modified version of the Attitude Toward Psychiatry-30 scale was used. The attitude toward psychiatry of all the students and physicians was moderately positive. Students from ULA displayed a more positive attitude than UCLA students, whereas physicians from UCLA displayed a more positive attitude than ULA physicians. The most negative attitude toward psychiatry was observed in students planning to select obstetrics and gynecology (ULA + UCLA), in physicians working in Surgery, obstetrics and gynecology (ULA + UCLA) and in basic sciences (ULA). Female students tended to display a more positive attitude than male students. The attitude toward psychiatry was similar in students with low and high academic achievement in the courses in psychiatry. A large number of years in the profession did not modify the attitude of the physicians. It is recommended to improve teaching and communication with the students and physicians that displayed the most negative attitudes toward psychiatry.

Adult↗
PubMed1991

Mechanism of the sex-dependent effect of lithium on body weight in rats.

Two experiments are reported here. First, the effect of lithium chloride (1, 2 and 4 mEq/kg IP for 21 days) on body weight was assessed in female and male rats. Food intake was measured in the rats treated with 2 mEq/kg. All the doses tested significantly increased body weight in female rats. A linear relationship between body weight gain and lithium dose was also observed. In contrast, in male rats, the low doses of lithium (1 and 2 mEq/kg) did not affect body weight, whereas the high dose (4 mEq/kg) decreased body weight. These results confirm previous reports on a sex-dependent effect of lithium on body weight in rats. In the second experiment, body weight and food intake were assessed in female rats treated with lithium alone, or in combination with insulin or sulpiride, a D2 dopamine receptor blocker. It was found that the effect of lithium on body weight and feeding was additive to the effects of sulpiride and insulin. These findings are indirect evidence that lithium enhances body weight in rats by a different mechanism than the one described for sulpiride or insulin.

Animals↗
PubMed1991

Hypothalamic sites affecting masticatory neurons in rats.

The effects of hypothalamic electrical stimulation and dl-sulpiride injections on the unit activity of masticatory trigeminal neurons were assessed in rats. Unilateral electrodes or bilateral cannulas were implanted in the perifornical hypothalamus. The animals which exhibited eating to electrical stimulation or to sulpiride injections were selected. Then, under urethane anesthesia, electrical stimuli or sulpiride injections were applied at sites which elicited eating while a passive jaw movement-related neuron was recorded. Electrical stimulation or sulpiride injections affected the basal firing rate of 15 out of 32 (53%), and 13 out of 17 (76%) jaw movement-related neurons, respectively. The basal firing rate of 3 out of 18 (16.6%) was affected by electrical stimulation of noneliciting feeding nearby places. Facilitation was observed in 7 out of those 13 jaw movement-related trigeminal neurons after intrahypothalamic sulpiride injections. When dopamine was injected in the hypothalamus 3 minutes before sulpiride, this drug could only affect the basal firing rate of 1 out of 12 (8%) jaw movement-related neurons. The electrical stimulation and sulpiride injections into the hypothalamus had the same inhibitory or excitatory effect on a given trigeminal neuron as the passive jaw movement did. A similar phenomenon was observed with the sulpiride-induced facilitation. These results suggest that hypothalamic D2 satiety receptors modulate brain stem feeding reflexes.

Animals↗
PubMed1991

Hypothalamic serotonin in treatments for feeding disorders and depression as studied by brain microdialysis.

Microdialysis was used to measure changes in extracellular serotonin in the hypothalamus of rats while they engaged in feeding behavior or received drug treatments used to treat feeding disorders and affective disorders in humans. Hypothalamic serotonin increased significantly relative to controls in response to (1) intraperitoneal tryptophan after food deprivation, (2) the smell of food and eating a meal, (3) a conditioned taste aversion, (4) d-fenfluramine and fluoxetine, and (5) an amphetamine challenge test after chronic low doses of lithium. In some cases, increases correlated with nonspecific behavioral arousal were seen in the hippocampus. The results suggest that diet, drug, and behavioral therapies, alone or combined, can be used to preferentially modify hypothalamic serotonin in the control of behavioral, emotional, and endocrine problems.

Animals↗
PubMed1990

Systemic sulpiride increases dopamine metabolites in the lateral hypothalamus.

In rats with microdialysis probes in the perifornical lateral hypothalamus (PFH) a single injection of the D2 receptor blocker 1-sulpiride (20 mg/kg IP) significantly increased extracellular dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), but not 5-hydroxyindoleacetic acid (5-HIAA). This suggests that sulpiride crosses the blood-brain barrier and blocks D2 dopamine receptors in the PFH leading to increased dopamine turnover reflected in increased extracellular DOPAC and HVA. We conclude that D2 blockade in the hypothalamus could play a role in the hyperphagia and body weight gain observed in female rats under chronic administration of the antipsychotic drug, sulpiride.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Neurochemical effects of chronic haloperidol and lithium assessed by brain microdialysis in rats.

1. Psychotropic drugs ameliorate psychotic symptoms only after repeated administration. 2. To assess the neurochemical effects of chronic haloperidol and lithium administration, microdialysis was performed simultaneously in the prefrontal cortex, the nucleus accumbens, and the striatum after haloperidol, and separately in the lateral hypothalamus and the hippocampus after lithium. 3. Chronic administration of haloperidol decreased dopamine turnover in the prefrontal cortex and the striatum. It did not affect the nucleus accumbens detectably. 4. No tolerance to haloperidol developed in any of the three regions. 5. Lithium enhanced the response of the serotonergic system to amphetamine in the lateral hypothalamus but not in the hippocampus. 6. The antipsychotic effect of haloperidol might be related to dopamine turnover decrease in the prefrontal cortex. 7. The antidepressant effect of lithium might be related to enhancement of serotonin responsiveness in the hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Mechanism of the body weight increase induced by systemic sulpiride.

Long-term intraperitoneal administration of sulpiride induced body weight increase in female but not in male rats. The hypothesis that systemic sulpiride causes an endocrine unbalance which in turn causes body weight gain and hyperphagia was tested in four experiments. First, it was shown that even when they are on a high-fat diet male rats do not show body weight gain induced by systemic sulpiride. Second, sulpiride suppressed the estrous cycle. Third, gonadectomy prevented the body weight gain induced by systemic sulpiride in female rats. Fourth, estradiol simultaneously administered with sulpiride prevented the expected sulpiride-induced body weight gain. These results are discussed in terms of an hypothetical functional castration produced by systemic sulpiride. The well known hyperprolactinemia, induced by the pituitary D2 dopamine receptor blockade, might bring about an impairment of the steroidogenesis with subsequent decrease in estrogens level, which in turn might be responsible for the hyperphagia and body weight increase induced by systemic injections of sulpiride.

Animals↗
PubMed1989

Hypophagia after long-term administration of sulpiride in adult female rats: a model of D2 dopamine receptors supersensitivity?

Sulpiride (20 mg/kg/ip for 21 days) induced in female rats a significant body weight increase and hyperphagia. After drug withdrawal a significant hypophagia was observed. It is hypothesised that this hypophagia might be a spontaneous manifestation of D2 dopamine receptors supersensitivity, either in the perifornical region of the lateral hypothalamus or in the pituitary.

Animals↗
PubMed1988

Puberty modifies sulpiride effects on body weight in rats.

Sulpiride (20 mg/kg, i.p.) for 21 days increased body weight in prepubertal, peripubertal and adult female rats. The increment was higher in the adult group, where a significant hyperphagia was also noted. In males, the same treatment tended to decrease body weight in the peripubertal and adult groups while in the prepubertal animals an increase of body weight without a significant hyperphagia was observed. These results are discussed in terms of an hypothetical sulpiride-induced reduction in serum gonadal steroid levels.

Aging↗
PubMed1987

Long term administration of some antipsychotic drugs increases body weight and feeding in rats. Are D2 dopamine receptors involved?

Long term administration of the antipsychotic drugs thioridazine, trifluoperazine, haloperidol, and sulpiride increased body weight in rats. This effect was found to be sex dependent, that is, while female rats were prone to gain weight, male rats did not. Chlorpromazine and fluphenazine decreased body weight in male rats but did not affect females. The mechanism of body weight gain was investigated with sulpiride. A linear relationship between dose of sulpiride and body weight gain was found. Also, sulpiride increased caloric intake, and both actions were counteracted by bromocriptine, a specific D2 receptor agonist. These results confirm that antipsychotic drugs affect feeding and body weight and suggest that hyperphagia and body weight gain might be mediated by blockade of dopamine receptors of the D2 type.

Animals↗
PubMed1986

Lateral hypothalamic sites eliciting eating affect medullary taste neurons in rats.

A hypothetical functional relationship between the feeding area of the lateral hypothalamus and the medullary and pontine taste areas was assessed in rats. Multiple electrodes were implanted in the lateral hypothalamus and the animals which exhibited eating upon electrical stimulation were selected. Then under pentobarbital anesthesia, the hypothalamus was electrically stimulated while unit activity of medullary and pontine taste areas was recorded. Electrical stimulation of the hypothalamus at sites which elicited eating affected 22% of gustatory neurons, 13% of proprioceptive neurons sensitive to oropharyngeal stimuli but only 0.2% of the remaining nongustatory neurons. Electrical stimulation at nonfeeding sites affected 3% of the gustatory neurons. The electrical stimulation of the hypothalamus had the same inhibitory or excitatory effect on a given gustatory neuron as the sapid stimulation of the tongue did. These results are discussed in terms of the taste pathways and their possible role in electrically elicited feeding.

Action Potentials↗
PubMedDate not supplied

Tamoxifen prevents sulpiride-induced weight gain in female rats.

To evaluate its potential utility in counteracting neuroleptic-induced obesity, the effects of long-term administration of tamoxifen (TAM) on body weight (BW) and food intake (FI) of gonadally intact and sulpiride-treated (SUL) female rats were assessed. In addition, estradiol and prolactin serum levels were measured in rats treated with SUL. SUL plus TAM and SUL plus bromocriptine (BR). TAM, at doses of 10, 50 and 100 micrograms, significantly decreased BW gain: FI was significantly reduced at the doses of 50 and 100 micrograms. In addition, doses of TAM ranging from 5-100 micrograms completely prevented SUL-induced BW gain and hyperphagia. BR also prevented SUL effects on BW and FI. In contrast to BR, concomitant administration of TAM did not prevent SUL-induced hyperprolactinemia. Estradiol levels were not modified by SUL alone or SUL plus BR, but they were significantly increased in the animals treated with TAM plus SUL. Neuroleptic-induced obesity in female rats might be related to an alteration in gonadal steroid balance secondary to hyperprolactinemia. While BR might counteract neuroleptic-induced weight gain by preventing hyperprolactinemia, TAM might directly interact with estrogen receptors, or indirectly increase estradiol levels. The use of TAM in preventing neuroleptic-induced obesity in humans warrants further investigation.

Animals↗
PubMedDate not supplied

[Advances in the molecular treatment of depression].

AIMS: The objective of this study is to survey present and future antidepressant drug therapy based on the progress made in the field of biotechnology. DEVELOPMENT: The simplistic and mistaken view that one single system of neurotransmission is altered in depression and that there is, therefore, just one single treatment has changed. Molecular biology and Genetics have enabled us to determine other possible chemical alterations in the brain, beyond the sole participation of the monoaminergic modulation systems, which is the classical hypothesis. In this paper we describe the evidence for the relations between depression and the therapeutic effect the classical antidepressants have on: 1. The peptidergic system of the corticotropin-releasing hormone, cortisol and the functional state of its receptors; 2. Intracellular signalling systems such as cAMP on transcription factors like CREB and neurotrophins; 3. The immune system and cytosines; 4. Glutamate transmission; and 5. The neuropeptidergic system of substance P, neuroactive steroids and the neuroglia. This has allowed other biochemical hypotheses about depression and the possibility of new treatments to be put forward. CONCLUSIONS: We are still not certain about the exact cause or the processes that determine mental illnesses such as depression or how improvements are achieved with the antidepressants we currently have available. Nevertheless, biotechnology is expected to be a great help in advancing towards a better understanding of the interrelations between the nervous, immune and endocrine systems, with their intracellular cascades and final outcomes in genetic expression and protein function, in depression. This will enable more efficient, more selective and faster-acting drugs to be developed and, in the future and with the help of psychogenomics, even make it possible to produce tailor-made medication for each patient.

Antidepressive Agents↗