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Brain postnatal

Figure 2. Changes in the rate of in vitro microtubule assembly during brain development. Hiese rates were measuored for the guinea-pig a species v ch has a mature brain at birth and the rat and mouse vMch develop their brain postnatally. Hie figure also shows that the changes in the rates of microtubule assembly is delayed for the hypothyroid rat brain. Figure 2. Changes in the rate of in vitro microtubule assembly during brain development. Hiese rates were measuored for the guinea-pig a species v ch has a mature brain at birth and the rat and mouse vMch develop their brain postnatally. Hie figure also shows that the changes in the rates of microtubule assembly is delayed for the hypothyroid rat brain.
An additional study reported age-dependent effects. Lakshmana and Raju (1994) found that oral treatment of rat pups with endosulfan from postnatal days 2-10 resulted in changes in the concentration of noradrenalin, dopamine, and serotonin in various brain areas that differed either in magnitude or direction from changes seen in pups treated from postnatal days 2-23. While the results from this study do not necessarily indicate that neonates are more sensitive to the toxic effects of endosulfan, they do show that the duration of exposure in neonates is an important parameter to consider. [Pg.174]

Noland-Gerbec EA, Pfohl RJ, Taylor DH, et al. 1986. 2-Deoxyglucose uptake in the developing rat brain upon pre- and postnatal exposure to trichloroethylene. Neurotoxicology 7 157-164. [Pg.282]

Valencia A., Collado P., Cales J.M., et al. (1992). Postnatal administration of dihydrotestosterone to the male rat abolishes sexual dimorphism in the accessory olfactory bulb a volumetric study. Dev Brain Res 68, 132-135. [Pg.254]

Decreased numbers of dendritic spines and malformed spines in brain parietal cortex were observed at postnatal day 30 in rat pups whose mothers were administered 256-480 mg lead/kg/day as lead acetate in drinking water during gestation and lactation (Murray et al. 1978). PbB levels were not reported. [Pg.206]

Campbell JB, Woolley DE, Vijayan VK, et al. 1982. Morphometric effects of postnatal lead exposure on hippocampal development of the 15-day-old rat. Dev Brain Res 3 595-612. [Pg.498]

Chandra SV, Murthy RC, Saxena DK, et al. 1983. Effects of pre- and postnatal combined exposure to Pb and Mn on brain development in rats. Ind Health 21 273-279. [Pg.500]

Cory-Slechta DA, Pokora MJ, Widzowski DV. 1992. Postnatal lead exposure induces supersensitivity to the stimulus properties of a D2-D3 agonist. Brain Res 598 162-172. [Pg.505]

Urade, Y., et al. (1987a). Postnatal changes in the localization of prostaglandin D synthetase from neurons to oligodendrocytes in the rat brain./. Biol Chem. 262, 15132-6. [Pg.385]

Comparison of hypocretm/orexin and melanin-concentrating hormone neurons and axonal projections in the embryonic and postnatal rat brain. J. Chem. Neuroanat. 27, 165-81. [Pg.431]

Homung, J. P and Fritschy, J. M. (1996) Developmental profile of GABAA-receptors in the marmoset monkey expression of distinct subtypes in pre- and postnatal brain. J. Comp. Neurol. 367,413-130. [Pg.106]

To confirm their results and check for methodological problems, some studies have been carried out. As there was a probability that hypothermic conditions during temporary removal from dam may have affected the results, Pauluhn and Schmuck administered S-bioallethrin and deltamethrin to neonatal mice from postnatal day 10 to 16 under a hypo-, normo-, or hyperthermic environment, and measured the MAChR density at the age of 17 days [51]. Increase in MAChR in Cortex at PND 17 in animals treated with S-bioallethrin was observed. Meanwhile, no changes were observed in animals treated with deltamethrin. In addition, an enormous influence of environmental temperature on the density of MAChR receptors in the crude synaptosomal fraction of the cerebral cortex was ascertained. Tsuji et al. exposed mouse dams with their litters to D-allethrin by inhalation for 6 h from postnatal day 10 to 16. The inhalation administration method is the most relevant route of exposure for humans, including babies and infants, after indoor use of D-allethrin. The neonatal exposure to D-allethrin by inhalation did not induce effects either on the brain MAChR density or motor activity at 17 days and 4 months of age, or on performance in the leaming/memory test at 11 months of age [52]. Other unpublished studies with D-allethrin, S -bioallethrin, or deltamethrin were examined to confirm the results of Eriksson et al. and showed inconsistent results [53]. The reasons for discrepancy among these findings are unknown. [Pg.91]

Also, harmala alkaloids create effects on monoamine turnover. Postnatal rats administered harmaline (shortly before birth) have elevations in brain levels of the norepinephrine metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG), but decreases in the dopamine and serotonin metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5-HIAA) (Okonmah et al. [Pg.367]

Tsuruo Y, Ishimura K, Fujita H, Osawa Y. 1994. Immunocy-tochemical localization of aromatase-containing neurons in the rat brain during pre- and postnatal development. Cell Tissue Res 278 29-39. [Pg.90]


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