Neurobehavioral Development Of Rats Research Articles

Prenatal cigarette smoke exposure slightly alters neurobehavioral development in neonatal rats: Implications for developmental origins of health and disease (DoHAD).

Numerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).

Individual and combined effects of manganese, lead and arsenic on neurobehavioral development of rats

Individual and combined effects of manganese, lead and arsenic on neurobehavioral development of rats

Assessing pre/post-weaning neurobehavioral development for perinatal exposure to low doses of methylmercury

Fetuses and neonates are known to be high-risk groups for Methylmercury (MeHg) exposure. MeHg can be transferred to the fetus through the placenta and to newborn offspring through breast milk. The aim of the present study was to investigate the neurotoxic effects of low doses of MeHg (1 and 5μg/mL in drinking water) administration, from gestational day 1 to postnatal day (PND) 21, on the neurobehavioral development of rats. The results showed that the no-observed-effect level of MeHg is somewhere in the range of 1–4μg/mL. Neurobehavioral development analysis revealed a delayed appearance of cliff drop and negative geotaxis reflexes in the 5μg/mL MeHg exposure group. Developmental exposure to MeHg affected locomotor activity functions for the females, but not for the males, implying that the female pups were more vulnerable than the male pups. All pups exposed to 5μg/mL of MeHg showed a significant deficit in motor coordination in the rotarod test compared with controls, and the highest accumulated concentrations of Hg were found in the cerebellum, followed by the hippocampus and cerebral cortex, indicating that the cerebellum is a possible target for MeHg toxicity. We demonstrated adverse effects of developmental exposure to MeHg associated with tissue concentrations very close to the current human body burden of this persistent and bioaccumulative compound.

Effects of the pyridoindole SMe1EC2 on neurobehavioral development in rats: Developmental neurotoxicity study

Effects of the pyridoindole SMe1EC2 on neurobehavioral development in rats: Developmental neurotoxicity study

Effects of butyl benzyl phthalate on neurobehavioral development of rats

To study the effects of butyl benzyl phthalate on neurobehavioral development of rats. Levels of 0 (control), 0.05%, 0.25%, and 0.75% butyl benzyl phthalate (BBP) was given in the diet from 4 weeks of age of female F0 generation to 6 weeks of age of F1 generation in Wistar rats, including the period of the female F0 generation's mating, gestation and lactation and the F1 generation's growth and development. Selected parameters of neurobehavioral development were observed in F1 generation. (1)For the male F(1) generation, surface righting at postnatal (PND) 4 th day was significantly delayed in the low-dose group (P < 0.05) (scoring: 56 vs 61), cliff avoidance at PND 7 was significantly depressed in the high-dose group (P < 0.05) (scoring: 41), air righting at PND 14 was significantly depressed in all treatment groups (P < 0.05). In open field test, low- and high-dose groups moved more than control group (P < 0.05). In Morris water maze test, the escape latency was significantly delayed in the low-dose group at the 5th day of the 5 days' place navigation task (P < 0.05). (2) For the female F1 generation, there were no differences among groups in any parameter in the experiment (P > 0.05). BBP may affect the neurobehavioral development only in male rats in the F1 generation.

Gestational Vitamin B Deficiency Leads to Homocysteine-Associated Brain Apoptosis and Alters Neurobehavioral Development in Rats

Hyperhomocysteinemia has been identified as a risk factor for neurological disorders. To study the influence of early deficiency in nutritional determinants of hyperhomocysteinemia on the developing rat brain, dams were fed a standard diet or a diet lacking methyl groups during gestation and lactation. Homocysteinemia progressively increased in the offspring of the deficient group and at 21 days reached 13.3+/-3.7 micromol/L versus 6.8+/-0.3 micromol/L in controls. Homocysteine accumulated in both neurons and astrocytes of selective brain structures including the hippocampus, the cerebellum, the striatum, and the neurogenic subventricular zone. Most homocysteine-positive cells expressed p53 and displayed fragmented DNA indicative of apoptosis. Righting reflex and negative geotaxis revealed a delay in the onset of integration capacities in the deficient group. Between 19 and 21 days, a poorer success score was recorded in deficient animals in a locomotor coordination test. A switch to normal food after weaning allowed restoration of normal homocysteinemia. Nevertheless, at 80 days of age, the exploratory behavior in the elevated-plus maze and the learning and memory behavior in the eight-arm maze revealed that early vitamin B deprivation is associated with persistent functional disabilities, possibly resulting from the ensuing neurotoxic effects of homocysteine.

Effect of Chemically Induced Propionic Acidemia on Neurobehavioral Development of Rats

High levels of propionic acid (PPA) comparable to those of human propionic acidemia were achieved in blood (1–5 mmol/l) and brain (1 μmol/g) of rats by administering saline-buffered propionate (pH 7.4) subcutaneously twice a day from the 6th to the 28th day of life. PPA doses ranged from 1.44 to 1.92 μmol/g body weight as a function of animal age. Control rats were treated with saline in the same volumes. Growth and development of physical landmarks were assessed by monitoring the following parameters daily: body weight, upper incisor eruption, eye opening, and hair coat. Development of some reflexes was also monitored, and a specific subset of motor skills was evaluated at days 14 and 21 of life by the free-fall righting test and the spontaneous alternation test. Chronic PPA administration had no effect on body weight, cerebral cortex weight, or cerebellum weight, but caused slight but significant delays in the day of appearance of hair coat and eye opening, indicating an effect of PPA on the development of physical parameters. Free-fall righting was impaired in PPA-treated animals. On the other hand, PPA administration had no effect on the performance of the animals in the spontaneous alternation tests. Long-term effects of early PPA administration were investigated by assessing animal performance in an aversive task (two-way shuttle avoidance task) and in a nonaversive (open-field task) behavioral task at 60 days of age. PPA-treated rats did not habituate to the open field, and presented a lack of retention of the shuttle-avoidance task. Our results suggest that early postnatal PPA administration to rats alters normal development and induces long-term behavioral deficits in aversive and nonaversive tasks.

Effect of lead acetate on neurobehavioral development of rats.

We investigated the effects of lead exposure during the pre- and postnatal period on the neurobehavioral development of female Wistar rats (70-75 days of age, 120-150 g) using a protocol of lead intoxication that does not affect weight gain. Wistar rats were submitted to lead acetate intoxication by giving their dams 1.0 mM lead acetate. Control dams received deionized water. Growth and neuromotor development were assessed by monitoring daily the following parameters in 20 litters: body weight, ear unfolding, incisor eruption, eye opening, righting, palmar grasp, negative geotaxis, cliff avoidance and startle reflex. Spontaneous alternation was assessed on postnatal day 17 using a T maze. The animals' ability to equilibrate on a breaker rim was measured on postnatal day 19. Lead intoxication was confirmed by measuring renal, hepatic and cerebral lead concentration in dams and litters. Lead treatment hastened the day of appearance of the following parameters: eye opening (control: 13.5 +/- 0.6, N = 88; lead: 12.9 +/- 0.6, N = 72; P < 0.05), startle reflex (control: 13.0 +/- 0.8, N = 88; lead: 12.0 +/- 0.7, N = 72; P < 0.05) and negative geotaxis. On the other hand, spontaneous alternation performance was hindered in lead-exposed animals (control: 37.6 +/- 19.7; lead: 57.5 +/- 28.3% of alternating animals; P < 0.05). These results suggest that lead exposure without concomitant undernutrition alters rat development, affecting specific subsets of motor skills.

Behavioral effects of prenatal exposure to pulsed-wave ultrasound in unanesthetized rats.

The present experiment examined the developmental neurotoxicity of pulsed-wave (pw) ultrasound in rats, using an exposure system designed to eliminate restraint or anesthesia from the exposure conditions. Pregnant Sprague-Dawley CD rats trained to remain immobile in a water-filled ultrasound exposure tank were scanned with 3-MHz pw ultrasound at spatial peak temporal average intensities (ISPTA) of 0, 2, 20, or 30 W/cm2 on embryonic days 4-20 for approximately 10 min/day. The data showed that such insonation produced no adverse effects on maternal weight gain or reproductive outcome, nor on the postnatal growth or survival of the offspring. No exposure-related alterations in behavioral development were observed in the offspring of rats scanned with pw ultrasound during gestation. In addition, there was no consistent evidence of an ultrasound-associated change in the adult offspring behaviors tested; i.e., no treatment effects were found on measures of locomotor activity, water maze learning, and acoustic startle reactivity. An effect on tactile startle was observed on some trials in the low exposure group male offspring, but this effect was neither dose dependent nor consistent with any other finding. Overall, these results indicate that the neurobehavioral development of rats was not altered by prenatal exposure to pw ultrasound at ISPTA levels of up to 30 W/cm2.