ABSTRACT
The aim of the present study was to observe how the exposition of pregnant rats to an electromagnetic field (EMF), with frequency of 60 Hz, and a magnetic field of 3 µT for 2 hours per day and/or using the so-called Regional Basic Diet (RBD), influenced the somatic maturation in their offspring. Four groups were formed: Group A (casein), B (casein and EMF), C (RBD) and D (RBD and EMF). The diet manipulation occurred during pregnancy. The somatic maturation indexes - assessed daily between 12:00 AM and 2:00 PM - were: Eye Opening (EO), Auricle Opening (AO), Auditory Canal Opening (ACO), Low Incisor Eruption (LIE), and Upper Incisor Eruption (UIE). The association between EMF and deficient diet caused a delay in all Somatic Maturation Indexes (SMI) and the RBD caused delay only in the AO. Furthermore, the EMF caused delay in AO, ACO, LIE. In relation to the body weight, the EMF associated with the deficient diet caused change in the twenty-first day of life. The RBD, during pregnancy, caused lower body weight in the offspring in the first and third day of life. The body weight of the offspring whose mothers were fed casein and exposed to the EMF during pregnancy was lower in the third and sixth day of life. In conclusion, the EMF associated with under-nutrition caused delay in all SMI. In relation to the body weight, the EMF associated with under-nutrition caused a decrease in the body weight at the sixth day of life.
O objetivo deste estudo foi observar a influência do campo eletromagnético (CEM), com freqüência de 60Hz, campo magnético de 3 µT, durante 2 horas por dia, associado ou não à dieta básica regional (DBR) no desenvolvimento somático da prole. Quatro grupos foram formados: Grupo A (caseína), B (caseína e CEM), C (DBR) e D (DBR e CEM). A manipulação dietética ocorreu durante a prenhez. Os índices de maturação somática - Abertura dos Olhos (AO), Abertura do Pavilhão Auditivo (APA), Abertura do Conduto Auditivo (ACA), Erupção do Incisivo Inferior (EII), e Erupção do Incisivo Superior (EIS) - foram avaliados diariamente entre 12 e 14 horas. A associação entre o CEM e a dieta deficiente causou retardo em todos os índices de maturação somática (IMS) e a DBR causou retardo somente na APA. O CEM causou retardo na APA, ACA, EII. Em relação ao peso corporal, o CEM associado à dieta deficiente causou mudanças no 21º dia de vida. A DBR, durante a prenhez, causou diminuição do peso corporal dos filhotes no 1º e no 3º dia de vida. O peso corporal dos filhotes, cujas mães foram alimentadas pela caseína e expostas ao CEM, durante a prenhez, apresentaram uma diminuição no 3º e 6º dia de vida. Conclusão: o CEM, associado com a desnutrição, causou retardo em todos os IMS. Em relação ao peso corporal, o CEM, associado à desnutrição, causou uma diminuição no peso corporal no 6º dia de vida.
Subject(s)
Animals , Female , Male , Pregnancy , Rats , Electromagnetic Fields/adverse effects , Protein-Energy Malnutrition/complications , Somatosensory Disorders/etiology , Prenatal Exposure Delayed Effects , Rats, Wistar , Time FactorsABSTRACT
We investigated the somatic maturation of neonate rats treated during the suckling period with citalopram, a selective serotonin reuptake inhibitor. Groups with 6 male neonates were randomly assigned to different treatments 24 h after birth. Each litter was suckled by one of the dams until the 21st postnatal day. Body weight, head axis and tail length were measured daily from the 1st to the 21st postnatal day. Time of ear unfolding, auditory conduit opening, incisor eruption, and eye opening was determined. Pups received 5 mg (Cit5), 10 mg (Cit10) or 20 mg/kg (Cit20) citalopram sc, or saline (0.9 percent NaCl, w/v, sc). Compared to saline, body weight was lower (24.04 percent, P < 0.01) for Cit10 from the 10th to the 21st day and for Cit20 from the 6th to the 21st day (38.19 percent, P < 0.01). Tail length was reduced in the Cit20 group (15.48 percent, P < 0.001) from the 8th to the 21st day. A reduction in mediolateral head axis (10.53 percent, P < 0.05) was observed from the 11th to the 21st day in Cit10 and from the 6th to the 21st day in Cit20 (13.16 percent, P < 0.001). A reduction in anteroposterior head axis was also observed in the Cit20 group (5.28 percent, P < 0.05) from the 13th to the 21stday. Conversely, this axis showed accelerated growth from the 12th to the 21stday in the Cit5 group (13.05 percent, P < 0.05). Auditory conduit opening was delayed in the Cit5 and Cit20 groups and incisor eruption was delayed in all citalopram groups. These findings show that citalopram injected during suckling to rats induces body alterations and suggest that the activity of the serotoninergic system participates in growth mechanisms.
Subject(s)
Animals , Male , Female , Rats , Animals, Newborn , Animals, Suckling , Citalopram , Selective Serotonin Reuptake Inhibitors , Weight Gain , Rats, Wistar , Tail/growth & development , Time FactorsABSTRACT
Most studies suggest that serotonin exerts an inhibitory control on the aggression process. According to experimental evidence, this amine also influences growth and development of the nervous tissue including serotoninergic neurons. Thus, the possibility exists that increased serotonin availability in young animals facilitates a long-lasting effect on aggressive responses. The present study aimed to investigate the aggressive behavior of adult rats (90-120 days) treated from the 1st to the 19th postnatal day with citalopram (CIT), a selective serotonin reuptake inhibitor (20 mg/kg, sc, every 3 days). Aggressive behavior was induced by placing a pair of rats (matched by weight) in a box (20 x 20 x 20 cm), and submitting them to a 20-min session of electric footshocks (five 1.6-mA - 2-s current pulses, separated by a 4-min intershock interval). When compared to the control group (rats treated for the same period with equivalent volumes of saline solution), the CIT group presented a 41.4 percent reduction in the duration of aggressive response. The results indicate that the repeated administration of CIT early in life reduces the aggressive behavior in adulthood and suggest that the increased brain serotoninergic activity could play a role in this effect
Subject(s)
Animals , Male , Rats , Aggression/drug effects , Citalopram/pharmacology , Selective Serotonin Reuptake Inhibitors/pharmacology , Animals, Newborn , Body Weight , Random Allocation , Rats, Wistar , Time FactorsABSTRACT
A patogênese da doença alcoolica cardíaca não é completamente conhecida. Segundo uma das hipóteses, as lesões miocárdicas resultariam de alterações na parede dos vasos. Para avaliar possíveis alterações vaculares parietais, foi realizado estudo morfométrico de arteíolas miocárdica em doze alcoolistas crônicos (nove homens e três mulheres, com idade variando de 24 a 45 anos) e em oito controles (três homens e cinco mulheres, com idade variando entre 20 e 39 anos). Cortes histólogicos de seções transversais, longitudinais e oblíquas da parede livre do ventrículo esuerdo foram analisados em sistema semi-automático de análise de imagem. Não se obseervaram diferenças estatisticamente significativas na espessura da parede articular entre os dois grupos. É possível, portanto, que alteraçõess vasculares, pelo nenos no que se refere a rede arteriolar miocárdica, não contribuam significativamente para a doença alcoólica cardíaca
Subject(s)
Humans , Male , Female , Adult , Arterioles/physiopathology , Histological Techniques , Cardiomyopathy, Alcoholic/physiopathology , Alcoholism/complicationsABSTRACT
We investigated the effect of a single ip injection of ed-fenfluramine (d-fen; 5-10 mg/kg), a serotinin reuptake blocker, on cortical spreading depression (SD) in 17 male Wistar rats (300-360 g body weight). SD was elicited at the right frontal cortex by 1-min application of 2 percent KCl at 20-min intervals. SD propagation was monitored (electrocorticogram and DC-recording) at 2 points on the right parietal surface for 3 h. After a "baseline" recording period (1 h), d-fen was injected and the recording session was continued for 2 h. When compared to the predrug SD velocities (t = 0 min) the values measured after d-fen decreased significantly at t = 20 min (3.44 + or - 0.63 vs 2.66 + or - 0.51 mm/min; N = 17, P<0.001), at t = 40 min (3.32 + or - 0.58 vs 2.53 + or - 0.52 mm/min; N = 14, P<0.001), att=60 min (3.68 + or - 0.63 vs 2.92 + or - 0.72 mm/min; N = 11, P<0.001) and at t = 80 min (3.57 + or - 0.61 vs 3.03 + or - 0.83 mm/min; N = 12, P<0.05) but not at t = 100 min (3.47 + or - 0.72 vs 3.31 + or - 0.88 mm/min; N = 12) nor at t = 120 min (3.44 + or - 0.67 vs 3.37 + or - 0.76 mm/min; N = 11). Furthermore, in 19 of 48 KCl stimulations (40 percent) performed ...
Subject(s)
Animals , Male , Rats , Cortical Spreading Depression , Fenfluramine/pharmacology , Selective Serotonin Reuptake Inhibitors/pharmacology , Cortical Spreading Depression/physiology , Electrophysiology , Fenfluramine/administration & dosage , Selective Serotonin Reuptake Inhibitors/administration & dosage , Rats, WistarABSTRACT
The effect of treatment with naloxone early in life on pain responsiveness was studied in Wistar rats. Litters of six rats were divided equally into groups of 3 pups receiving daily naloxone (50 mg/kg, sc) and 3 pups receiving saline from the 3rd to 18th day of life. On days 30, 50, 70 and 90, one group of animals previously injected during suckling with naloxone (N = 21) and another with saline (N = 21) were submitted to the hot-plate test to measure the latency to paw licking. Other groups of rats also treated during suckling with naloxone (N = 13) and saline (N = 14) were assessed for the antinociceptive effect of morphine (10 mg/kg,sc). The naloxone group displayed a lower latency than the saline group in all test sessions and a diminished analgesic response to morphine. The results indicate that the use of naloxone (an antagonist opioid) during suckling, the brain growth spurt period, facilitates a long-lasting increased pain responsiveness and alters antialgesic mechanisms. In this respect, the opioid and non-opioid effects of naloxone on the ontogeny of neural systems should be taken into account
Subject(s)
Animals , Male , Rats , Hyperalgesia/physiopathology , Naloxone/pharmacology , Animals, Newborn , Animals, Suckling , Hyperalgesia/chemically induced , Morphine/pharmacology , Nociceptors/drug effects , Reaction TimeABSTRACT
The propagation of cortical spreading depression (SD) and the incidence of "spontaneous" SD were enhanced in rats after rapid-eye-movement sleep deprivation (REMD) as compared to control animals. Pseudo-deprived rats were similar to controls, suggesting that the facilitatory effect on SD is due to REMD rather than to the stress accompanying deprivation. In control rats, apomorphine (0.5 to 8 mg/kg) failed to reproduce the effects of REMD and also failed to enhance the REMD effects in deprived rats, suggesting that the dopaminergic system does not play an important role in propagation of cortical SD