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J Palermo-Neto

Publications and source records attributed to J Palermo-Neto.

At least 37 records · Page 2Linked to original sources
PubMed1999

Effects of diazepam on Mycobacterium bovis-induced infection in hamsters.

The in utero exposure of hamsters to low doses of diazepam results in impaired host defense against Mycobacterium bovis during adulthood. Delayed developmental immunotoxicity, however, represents a specific situation that might not be general. The present experiment was undertaken to investigate the effects of diazepam on hamster resistance to M. bovis using adult animals. The effects of diazepam treatment on serum cortisol levels were also studied. Adult hamsters (N = 10 for each group) were treated with diazepam (E1 = 1. 0, E2 = 2.0 or E3 = 3.0 mg kg-1 day-1 subcutaneously) or with control solution (C) for 30 days. Seven days after the beginning of the treatment, the animals received identical inoculum concentrations of M. bovis. Hamsters treated with the higher (2.0 and 3.0 mg kg-1 day-1) doses of diazepam exhibited: 1) increased granuloma areas in the liver (C = 1.81 +/- 1.39, E2 = 10.29 +/- 4.64 and E3 = 15.80 +/- 4.82) and lung (C = 0.54 +/- 0.55, E2 = 6.28 +/- 3.85 and E3 = 6.31 +/- 3.56) and 2) increased scores of M. bovis colony-forming units isolated from liver (C = 2.0, E2 = 3.0 and E3 = 3.5), lung (C = 1.0, E2 = 3.0 and E3 = 3.5) and spleen (C = 1.0, E2 = 2.5 and E3 = 4.0). These effects were dose dependent, and were not detected or were less severe in animals treated with the lowest (1.0 mg/kg) dose of diazepam as well as in those of the control group. Furthermore, diazepam treatment (3.0 mg kg-1 day-1 for 30 days) increased (E3 = 71.32 +/- 2.99; N = 10) the serum levels of cortisol compared to control hamsters (C = 22.61 +/- 2.75; N = 10). The present data, that demonstrate an impaired defense against M. bovis in adult hamsters treated with diazepam, were tentatively explained on the basis of a direct and/or indirect action of diazepam on the cytokine network. The effects may be related to stimulation of peripheral benzodiazepine receptor binding sites (PBR) by macrophages and/or lymphocytes, or they may be mediated by PBR stimulation of the adrenals.

Analysis of Variance↗
PubMed1999

Benzodiazepine receptors and avian macrophage activity: diazepam decreases spreading and phagocytosis.

The complex interrelations between the nervous system and the immune system have led to the creation of a new research area denoted neuroimmunology. The effects of stress on the immune response have long been observed in chickens. Since benzodiazepine receptors are involved in the stress reaction, we proposed to assess the importance of these receptors in the activity of chick peritoneal macrophages. We used 420 viable embryonated eggs of the commercial Hubbard broiler line treated through the chorioallantoid membrane on the 11th day of incubation: falsely manipulated (Sham group), with 40% propyleneglycol (PG) in simple Ringer solution (Vehicle group), and treated with diazepam (DZ), 8 mg/kg (DZ group). After hatching, the chicks were housed in metal rearing cages of the "battery" type for 5 weeks. At 36 days of age, 24 chicks from each treated group were divided at random into two groups of 12 animals each which were treated with DZ (2 mg/kg) or with 40% PPG in an equal volume once a day by the oral route for 4 days. Peritoneal macrophages were collected and submitted to the spreading an phagocytosis tests. Data were analyzed statistically using the SAS software (p < 0.05). Administration of DZ in ovo did not cause a significant decrease in egg hatchability, birth weight or performance parameters during the 5 weeks of assessment. However, the rate of macrophage spreading and phagocytosis was reduced. When administered at 40 days of age, DZ did not change the spreading rate but reduced the phagocytosis rate. There was no interaction between treatments. These results indicate that benzodiazepine receptors seem to be important for macrophage activity also in birds, as previously observed in rodents and primates. Since benzodiazepine receptors are involved in the response to stress, it is possible that the effects of stress on avian immunity may be mediated in part by these receptors.

Animals↗
PubMed1999

Developmental, neuro and immunotoxic effects of perinatal diazepam treatment in rats.

In utero exposure of rats to low dosages of diazepam (1.0-2.0 mg/kg) has been found to result in depression of the cellular and humoral immune responses during adulthood. Behavioral dysfunctions were also reported in infants from mothers with high benzodiazepine (BDZ) intake during pregnancy. The present experiment was undertaken to reconsider the potential action of diazepam during ontogeny in order to obtain further information about developmental processes using a refined methodology. Time-pregnant rats were treated subcutaneously with diazepam (2.0 mg/kg/day,: group E1) or with diazepam vehicle (group C1) from gestational day 14 to 20. Other dams (group E2) received the same BDZ dose from the 1st to the 21st day of lactation (weaning) or were not treated, remaining undisturbed in their home cages (group C2). The following results were obtained for animals perinatally treated with diazepam compared to groups C1 and C2: 1--increased time for testis descent and decreased time for vaginal opening (group E2); 2--no changes in the dates for ear end eye opening, or incisor tooth eruption (groups E1 and E2); 3--increased locomotor activity in the open-field (group E2) and/or in the plus maze (groups E1 and E2); 4--decreased levels of anxiety measured in the plus maze (groups E1 and E2); 5--decreased macrophage spreading and phagocytosis (groups E1 and E2). These results, which occurred in the absence of overt signs of maternal or fetal toxicity, demonstrate developmental, neuro- and immunotoxic effects of perinatal diazepam treatment in rats.

Animals↗
PubMed1998

Effects of haloperidol and GM1 ganglioside treatment on striatal D2 receptor binding and dopamine turnover.

Previous studies have shown that whereas exogenous GM1 ganglioside co-administration leads to an increase of haloperidol-induced behavioral supersensitivity, GM1 significantly attenuates the behavioral parameters of dopaminergic supersensitivity when administered after abrupt haloperidol withdrawal. In the present study, the effects of GM1 and haloperidol co-administration (5 mg/kg GM1 i.p. and 1 mg/kg haloperidol i.p., twice daily, for 30 days) as well as the effects of a 3 day treatment with GM1 were investigated in rats withdrawn from haloperidol administration by measuring striatal D2 dopamine receptor binding and dopamine turnover. The results showed that under these two experimental conditions GM1 modified neither the haloperidol-induced striatal D2 dopamine receptor up regulation nor the decrease in dopamine turnover produced by haloperidol withdrawal. These results suggest that the effects of GM1 on behavioral supersensitivity are not related to modifications in dopamine receptor number or affinity and in the synaptic availability of this catecholamine.

Animals↗
PubMed1998

Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks.

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1997

Repeated monosialoganglioside administration attenuates behavioral sensitization to amphetamine.

The effects of repeated monosialoganglioside (GM1) administration on amphetamine-induced behavioral sensitization were studied using locomotion frequency of mice observed in an open-field as an experimental parameter. GM1 (30 mg/kg, once a day for 7 days) did not modify mouse behavior per se but decreased the hyperlocomotion of mice repeatedly treated with amphetamine (3.0 mg/kg, once a day for 7 days, 30 min after GM1 injection). GM1 acutely administered 30 min before amphetamine did not modify the increase in locomotion frequency induced by acute amphetamine administration. These results agree with previous reports that gangliosides treatment may affect synaptic-plasticity, modifying the induction of the adaptive changes following drug-treatment.

Animals↗
PubMed1997

Dopaminergic systems. Dopamine receptors.

This article describes D1 and D2 receptor subfamilies, their neuroanatomic localizations and the possibility of their neuronal co-localization and relation to the other dopamine autoreceptors and those coupled to G-proteins as well as the actions of antipsychotic drugs on D1 and D2 receptor subfamilies are also analyzed.

Animals↗
PubMed1997

Effects of monosialoganglioside on a new model of tardive dyskinesia.

1- The effects of monosialoganglioside GM1 were studied on a new model of tardive dyskinesia, i.e., the frequency of spontaneous tongue protrusions in rats repeatedly treated with reserpine. 2- Rats were co-treated with vehicle (VEH) or reserpine (RES) (0.1 mg/kg, s.c., every other day) and saline (SAL) or GM1 (5 mg/kg, i.p., every day) for 30 days and observed for tongue protrusions on days 10, 20 and 30. 3- During each test day animals of the RES + SAL group exhibited an increase in tongue protrusions relative to rats of the VEH + SAL group. However, rats of the RES + GM1 group showed an increased frequency of tongue protrusions only on day 10, when compared to animals of the VEH + SAL group. There were no significant differences in tongue protrusion frequency between the VEH + GM1 and the VEH + SAL groups. 4- These results differ from previous studies which reported a facilitatory effect of GM1 co-administration on conventional behavioral animal models of tardive dyskinesia. The possibility is raised that GM1 attenuates the reserpine-induced increase in tongue protrusions through its protective effect on glutamate/oxidative stress neurotoxicity.

Animals↗
PubMed1997

Behavioural subsensitivity induced by long-term administration of a low dose of haloperidol to rats.

This study examines the effects on open-field and stereotyped behaviour of rats of abrupt withdrawal from repeated treatment with a low (0.03 mg kg-1) dose of haloperidol. Single administration of this low dose of haloperidol significantly increased open-field locomotion without modifying apomorphine (0.5 or 2.0 mg kg-1)-induced stereotyped behaviour. Forty-eight hours after abrupt withdrawal from 0.03 mg kg-1 haloperidol (twice daily for 15 days) a significant decrease in locomotion frequency was observed, but no change was observed in apomorphine-induced stereotypy. Our results suggest that dopamine autoreceptor supersensitivity might be evaluated in a behavioural situation of absence of postsynaptic dopamine receptor supersensitivity.

Administration, Oral↗
PubMed1997

Developmental and behavioral effects of postnatal amitraz exposure in rats.

The effects of postnatal amitraz exposure on physical and behavioral parameters were studied in Wistar rats, whose lactating dams received the pesticide (10 mg/kg) orally on days 1, 4, 7, 10, 13, 16 and 19 of lactation; control dams received distilled water (1 ml/kg) on the same days. A total of 18 different litters (9 of them control and 9 experimental) born after a 21-day gestation were used. The results showed that the median effective time (ET50) for fur development, eye opening, testis descent and onset of the startle response were increased in rats postnatally exposed to amitraz (2.7, 15.1, 21.6 and 15.3 days, respectively) compared to those of the control pups (1.8, 14.0, 19.9 and 12.9 days, respectively). The ages of incisor eruption, total unfolding of the external ears, vaginal and ear opening and the time taken to perform the grasping hindlimb reflex were not affected by amitraz exposure. Pups from dams treated with amitraz during lactation took more time (in seconds) to perform the surface righting reflex on postnatal days (PND) 3 (25.0 +/- 2.0), 4 (12.3 +/- 1.2) and 5 (8.7 +/- 0.9) in relation to controls (10.6 +/- 1.2; 4.5 +/- 0.6 and 3.4 +/- 0.4, respectively); the climbing response was not changed by amitraz. Postnatal amitraz exposure increased spontaneous motor activity of male and female pups in the open-field on PND 16 (140 +/- 11) and 17 (124 +/- 12), and 16 (104 +/- 9), 17 (137 +/- 9) and 18 (106 +/- 8), respectively. Data on spontaneous motor activity of the control male and female pups were 59 +/- 11 and 69 +/- 10 for days 16 and 17 and 49 +/- 9, 48 +/- 7 and 56 +/- 7 for days 16, 17 and 18, respectively. Some qualitative differences were also observed in spontaneous motor behavior; thus, raising the head, shoulder and pelvis matured one or two days later in the amitraz-treated offspring. Postnatal amitraz exposure did not change locomotion and rearing frequencies or immobility time in the open-field on PND 30, 60 and 90. The present findings indicate that postnatal exposure to amitraz caused transient developmental and behavioral changes in the exposed offspring and suggest that further investigation of the potential health risk of amitraz exposure to developing human and animal offsprings may be warranted.

Animals↗
PubMed1996

Monosialoganglioside attenuates the excitatory and behavioural sensitization effects of ethanol.

The effects of long-term monosialoganglioside GM1 treatment on the acute excitatory effects of ethanol and behavioural sensitization to this effect were studied, using locomotion frequency of mice observed in an open field as an experimental parameter. GM1 (30 mg/kg, once a day, for 21 days) did not modify mouse behaviour but decreased both the acute excitatory (1.8 g/kg) and the behavioural sensitization effects of ethanol (1.8 g/kg, once a day for 21 days, 30 min after GM1 injections). GM1 administered acutely 30 min or 24 h before ethanol did not modify the ethanol-induced increase in locomotion frequency. These results agree with previous reports in which ganglioside treatment modified both dopaminergic plasticity and other behavioural and biochemical effects of ethanol.

Animals↗
PubMed1996

Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats.

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1996

Effects of high doses of diazepam on carrageenin-induced paw edema in rats.

Benzodiazepine (BDZ) receptor sites play a relevant role in immune/inflammatory reactions. Acute BDZ treatments were shown not only to suppress cell proliferation in rat thymus but also to decrease TNF-alpha, IL-1 and IL-6 release from adult mouse macrophages. In the present investigation the effects of acute (10.0 and 20.0 mg/kg) and long-term (10.0 mg kg-1 day-1, for 21 days) diazepam treatment on carrageenin-induced paw edema were studied in rats. The results showed that acute treatment with high doses of diazepam decreased paw edema volume in a dose-dependent manner, and this effect was observed as early as 1 h after the administration of the 20.0 mg/kg dose and continued until the last measurement was performed (8 h). In contrast, long-term diazepam administration did not modify the phlogistic-induced edema. Taken together, these data show that 1) acute diazepam treatment with high doses decreases the volume of the acute inflammatory paw edema developed by the organism as a response to carrageenin-induced injury, and 2) long-term diazepam treatment induces tolerance to this effect. These results are discussed in the light of a possible effect of diazepam on the components of the rat cellular and humoral immune/inflammatory reaction such as T lymphocytes and/or interleukins.

Animals↗
PubMed1995

Effects of monosialoganglioside on dopaminergic supersensitivity.

The effects of monosialoganglioside (GMl) treatment on dopaminergic supersensitivity induced by long-term haloperidol administration were studied; both general activity of rats observed in an open-field and apomorphine-induced stereotyped behavior were used as experimental parameters. GMl per se (5.0 mg/kg, twice daily, for 30 days) did not modify rat behavior, but when given in combination with haloperidol (1.0 mg/kg, twice daily, for 30 days) it increased neuroleptic withdrawal symptoms as detected in both models. When GMl (5.0 mg/kg, twice daily) was administered after abrupt withdrawal from haloperidol (1.0 mg/kg, twice daily, for 30 days), it attenuated the increases in both general activity of rats observed in the open-field and apomorphine-induced stereotyped behavior. These results suggest that GMl may affect synaptic plasticity, facilitating the induction of the adaptative changes in receptor function (up and down-regulation), following long-term haloperidol treatment and withdrawal.

Animals↗
PubMed1995

Effect of manipulation of the GABA system on dopamine-related behaviors.

The interaction between GABAergic and dopaminergic systems within the central nervous system was investigated in rats using the open-field apparatus and apomorphine-induced stereotypy, and in mice using haloperidol-induced catalepsy. The single intraperitoneal administration of baclofen 3.0 mg/kg, 4,5,6,7-tetrahydroisoxasolo-(5,4-c) piridin-3-ol (THIP) 10.0 mg/kg and picrotoxin 2.0 mg/kg decreased both ambulation and rearing frequencies of the rats in the open-field; only the GABA agonists increased the duration of animal immobility. THIP (10.0 mg/kg) increased the duration of haloperidol-induced catalepsy. For apomorphine-induced stereotypy, baclofen 3.0 mg/kg and picrotoxin 1.0 mg/kg induced a significant leftward displacement of the control dose-response curve constructed for apomorphine (0.1-10 mg/kg) in relation to the control. In addition, baclofen, THIP, picrotoxin and 3-mercaptopropionic acid (3-MPA) 10.0 mg/kg decreased both rearing and sniffing behaviors elicited by apomorphine and increased licking and/or gnawing. Different mechanisms seem to be involved in the similar effects induced by GABA agonists and antagonists. Picrotoxin induced stereotyped movements per se with a dose-dependent effect, but baclofen and THIP did not. The present data suggest that GABA manipulation facilitates the progressive activation of the different dopaminergic pathways involved in stereotyped behaviors, thus increasing those stereotyped components (gnawing and licking) that appear after a high level of activation of dopaminergic pathways.

3-Mercaptopropionic Acid↗
PubMed1995

Intracerebroventricular administration of cholecystokinin reduces stereotypy in dopamine-supersensitive rats.

Cholecystokinin (CCK-8) coexists with dopamine in some neurons and modulates dopaminergic neurotransmission. In the present study we determined the effect of CCK-8 on stereotyped behavior in supersensitive dopaminergic system. Adult male Wistar rats, weighing 200-250 g, were used. Dopaminergic supersensitivity was induced by long-term haloperidol (HAL) treatment (30 days: 1.0 mg/kg twice a day). Seventy-two hours after HAL withdrawal animals received CCK-8 (14.5 nmol/5 microliters) or saline intracerebroventricularly (icv) before being tested for apomorphine (APO, 0.6 mg/kg, sc)-induced stereotyped behavior. Experimental groups were: long-term HAL-treated rats that received saline (HSAL, N = 9) or CCK-8 (HCCK, N = 11) icv and long-term saline-treated rats that received CCK-8 (SCCK, N = 9) or saline (SSAL, N = 8) icv. As expected, HSAL rats showed statistically significant higher stereotypy scores than SSAL rats (42 +/- 1.7 vs 31 +/- 1.6; P < 0.05) and CCK-8 significantly reduced stereotyped behavior in supersensitive rats (42 +/- 1.7 vs 37 +/- 1.5; P < 0.05). These results show that CCK-8 icv reduces stereotypy in dopaminergic-supersensitive rats, and suggest that the dopamine supersensitivity phenomenon can be modulated by CCK-8.

Analysis of Variance↗
PubMed1995

Effects of acute 2,4-dichlorophenoxyacetic acid on cattle serum components and enzyme activities.

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D) was studied in cattle. Steers were dosed po with 100, 300 or 600 mg 2,4-D/kg bw. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), O-glutamyl transferase (O-GT), creatine kinase (CK), lactate dehydrogenase (LDH) activities and urea, creatinine, glucose, total proteins and albumin levels were determined at intervals after dosing. The lowest 2,4-D dose did not change the biochemical parameters studied; the 300 mg/kg dose decreased AST, O-GT and CK activities and increased urea and glucose levels; the highest dose of 2,4-D increased LDH and CK activities and protein, urea, creatinine and glucose levels. These changes were time and dose-dependent and completely reversible. Acute 2,4-D intoxication disrupted the serum levels of several enzymes and blood components which mainly reflect kidney and muscle damage induced by the herbicide.

2,4-Dichlorophenoxyacetic Acid↗