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C F Mello

Publications and source records attributed to C F Mello.

27 records · Page 2Linked to original sources

Effects of postnatal methylmalonate administration on neurobehavioral development of rats.

Administration of methylmalonic acid in rats has been used as a model for methylmalonicacidemia in humans. Nestling Wistar rats of both sexes received 5 injections daily at 3-h intervals (starting at 7:30 a.m.) of saline or methylmalonic acid (MMA, 10 mg/ml) in a volume of 9 microliters/g body weight per injection subcutaneously in the lumbar region from the 5th to the 9th day of life and 11 microliters/g from day 10 to 14. Growth and neuromotor development were assessed by monitoring the following parameters daily in 54 rats: body weight, ear unfolding, incisor eruption, eye opening, righting, palmar grasp, negative geotaxis, cliff avoidance, free-fall righting and startle reflex. The only statistically significant effects of MMA administration were on the day of appearance of the free-fall righting reflex: MMA, 12.44 +/- 1.55 vs 11.0 +/- 0.39 days for saline control (P < 0.05, by two-way ANOVA) and a significant decrease in weight (P < 0.05, by ANOVA with repeated measures). The results suggest that chronic MMA administration to rats has a selective effect on neuromotor development.

Animals↗

Undernutrition during suckling has no effect on the rat locomotor activity response to caffeine.

It is known that early malnutrition causes hyposensitivity to serotonergic, gabaergic, catecholaminergic and opioid stimulation. In the present study, we determined whether adult rats undernourished during suckling presented an altered response to caffeine administration in a locomotor activity test. Rats were undernourished during suckling by feeding their dams a 7% casein diet. During the same period, well-nourished dams were fed a 28% casein diet. Animals (90-100 days of age) were habituated to the apparatus. Thereafter, a dose-response curve for caffeine (2.5, 10.0, 20.0, 40.0 and 120.0 mumol/kg, ip) was determined. During handling sessions, undernourished rats presented lower activity scores than well-nourished animals (average values: 44.2 +/- 16.4 vs 57.9 +/- 15.4). Well-nourished and undernourished rats responded in a similar way to caffeine administration by increasing the locomotor activity in a dose-dependent manner. Although undernourished animals present an altered sensitivity to various neuropharmacological compounds, the present results indicate that their sensitivity to the locomotor-activating effect of caffeine is the same as that of rats well-nourished during suckling.

Animals↗

Effects of undernutrition during suckling on footshock escape behavior and of post-training beta-endorphin administration on inhibitory avoidance task test behavior of young rats.

The hypothalamic beta-endorphin system of young Wistar rats of both sexes (21-day-old) responds in a distinct way to behavioral situations when compared to adult rats (90 to 120-day-old). In the present study we investigated whether the post-training amnestic effect of beta-endorphin previously demonstrated in Wistar adult rats is also observed in young (21-day-old) well-nourished and undernourished rats. Rats were undernourished since birth by feeding their dams an 8% casein diet, while well-nourished offspring were fed by dams maintained on a 20% casein diet. beta-endorphin was administered after training in a step-down inhibitory avoidance task using a 0.2- or 0.8-mA footshock. Retention was tested 24 h later. We observed that the dose of beta-endorphin (1 microgram/kg, ip) previously reported to have an amnestic effect on adult rats was ineffective in weanling rats of both nutritional groups. At a higher dose (2 micrograms/kg, ip) and using a 0.2-mA shock, beta-endorphin impaired the retention only of well-nourished rats. Test-to-training difference (in s) in step-down latency for well-nourished beta-endorphin-treated rats was 7 vs 25 s for well-nourished rats treated with saline (P < 0.05). Undernourished rats were hyperreactive to this shock intensity. Footshock escape latency (in s) for undernourished rats was 3.56 vs 5.80 for well-nourished rats (P < 0.05, experiment 1) and 5.01 vs 10.89 (P < 0.05, in experiment 2) and showed better retention than did well-nourished rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Undernutrition during the preweaning period changes calcium ATPase and ADPase activities of synaptosomal fractions of weanling rats.

The presence of activities that hydrolyse externally added ATP to adenosine in synaptosomal preparations from various sources is well demonstrated. The hydrolysis of ATP to AMP can be mediated either by the concerted action of enzymes or by an ATP-diphosphohydrolase (EC 3.6.1.5; apyrase). Undernutrition during the preweaning period can delay the development of several enzymes involved in the metabolism of neurotransmitters or neuronal function. In young rats, the presence of an apyrase in synaptosomal preparations from cerebral cortex was investigated. The results suggested that the hydrolysis of externally added ATP and ADP can be mediated by a single enzyme. The effects of preweaning undernutrition on the hydrolysis of ATP and ADP were also investigated. In weanling rats, previous undernutrition caused a decrease of about 20% in the hydrolysis of both substrates in synaptosomal fractions.

Adenosine Diphosphate↗

Undernutrition during suckling and latent learning ability of rehabilitated adult male rats.

The present report investigates the effects of early undernutrition on the latent learning ability of rehabilitated adult male rats in a simple maze task. Rats were undernourished during suckling by feeding their dams an 8% casein diet. Well-nourished dams received a 25% casein diet during the same period. Rats were weaned at 21 days of age and nutritionally rehabilitated until they became adults, when behavioral task was conducted. Under a nonappetitive condition, rats were exposed either to an open field or to a maze apparatus. They were thereafter deprived of water and tested in the maze apparatus. Both well-nourished and undernourished rats that had been previously exposed to the maze performed better than those exposed to the open field. Nutritional treatment had no effect on performance of either the latent learning or of the open-field groups. These results suggest that rehabilitated adult rats are able to learn about the environment when no immediate reinforcement is involved. The discrepancy between our findings and results reported by others may be due to differences in task complexity and/or perhaps to the fact that nutritional rehabilitation also plays a role in reversing some of the deleterious effects of early undernutrition on learning ability of rats.

Animals↗

Early undernutrition blocks the effect of naltrexone on rat exploratory behavior.

1. Young rats were undernourished by feeding their dams an 8% protein diet (w/w) from birth until weaning (21 days); the dams of control rats were fed a 20% protein diet (w/w) until weaning. All offspring were fed a 20% protein diet from 21 to 120-150 days of age, when they were tested. 2. The involvement of endogenous opioids in the exploratory activity (rearing response and crossing frequency in a 2-compartment open-field test) was evaluated by examining the effects of a single injection of naltrexone (0.75 mg/kg, ip) 6 min prior to testing. 3. Naltrexone decreased exploratory activity (rearing) by approximately 50% in normal rats but had no effect on undernourished rats. 4. These data provide additional evidence for an alteration in the opioid system of undernourished rats.

Animals↗

Effects of undernutrition during suckling and of post-training beta-endorphin administration on avoidance performances of adult rats.

1. The effects of undernutrition during suckling and of post-training beta-endorphin administration on avoidance task were investigated in adult rats. 2. Young rats were undernourished from delivery until weaning (21 days) by feeding their mothers a diet containing 8% protein (w/w). Mothers of well-nourished rats were fed a 20% protein diet. After weaning, both groups of rats were fed a 20% protein diet until 90-120 days of age, when they were subjected to behavioral sessions. 3. Acquisition was measured in training sessions and retention in test sessions 24 h after training. Beta-endorphin or saline (control) was injected ip immediately after training. Rats were subjected to shuttle and step-down inhibitory avoidance sessions using footshock of 0.2 or 0.8 mA intensity. 4. Undernutrition during suckling caused hyperreactivity to 0.2 mA footshocks. Beta-endorphin caused amnesia to shuttle avoidance task only in normal rats trained with 0.8 mA footshocks. In the step-down inhibitory avoidance task, beta-endorphin was amnesic only for normal rats and only for 0.2 mA footshocks. Beta-endorphin was not amnesic in undernourished rats.

Animals↗

Effects of dopaminergic agents on visceral pain measured by the mouse writhing test.

The present study explored the role of the dopaminergic transmission in the mouse writhing test analgesia by examining the relative analgesic activity of indirect dopaminergic agonists (amphetamine and cocaine), a mixed D1/D2 direct agonist (apomorphine), and a direct D1 (SKF38393) and D2 (bromocriptine) dopaminergic agonist. Amphetamine (1, 3 and 10 mg/kg, s.c.), cocaine (3 and 10 mg/kg, s.c.), apomorphine (0.3, 1 and 3 mg/kg, s.c.) and bromocriptine (30 mg/kg, s.c.) induced a significant decrease of the number of writhes. SKF38393 (1, 3, 10 and 30 mg/kg, s.c.) had no effect on writhing. The antinociceptive effect of amphetamine and cocaine was not reversed by naltrexone, haloperidol or SCH23390. The apomorphine- and bromocriptine-induced analgesia was not reduced by naltrexone or SCH23390 but was attenuated by haloperidol; the apomorphine-induced analgesia was not modified by domperidone. The present results suggest an involvement of the dopaminergic transmission in visceral nociception. This dopaminergic component appears to involve exclusively the central D2 receptor system, and does not seem to be influenced by opioid mechanisms.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗