• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.11a
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• pp.171-172
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• 1996

Cocaine is a powerful reinforcer that has become a popular drug of abuse in man. CNS effects that are related to the abuse of cocaine include feeling of well-being and euphoria. Brain dopamine systems are thought to mediate reinforcement and it is often assumed that cocaine's inhibition of dopamine uptake is the mechanism underlying its reinforcing effects. With increase in cocaine use among general population in recent years, adverse effects of the drug have occurred in all social strata and age groups. Therefore, it has been recognized that the epidemic of cocaine abuse is a growing major concerning public health. One of the most troubling aspects of cocaine abuse is its use by pregnant women. Drug abuse during pregnancy puts two lives at risk. Cocaine produces toxic effects on the fetus at concerntrations that are apparently nontoxic to the mother. Not only does cocaine cross the placenta via diffusion and via rapid penetration to mucous membranes, due to its high lipid solubility, but cocaine can also be found in breast milk, the effects of the cocaine can persist long after the child is born. Although it is known that prenatal cocaine exposure is associated with developmental risk to the fetus ana newborn, few studies have been conducted to assess the mechanisms whereby either short-term or long-term administration of cocaine can exert its harmful effects on the mother or the child. Therefore, it was our great interest to investigate the pharmacological and neurobehavioral changes in offspring that are prenatally exposed to cocaine.

• Journal of Nutrition and Health
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• v.31 no.5
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• pp.897-905
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• 1998

Docosahexaenoic acid(DHA), a $\omega$3 series fatty acid and arachidonic acid(AA). a $\omega$6 series fatty acid were found in relatively high concentrations in the phospholipids(PLs) of cell membranes of nerve tissues, and they can be affected by various factors. The present study examined the effects of dietary $\omega$6 and $\omega$3 fatty acid composition on P/M/S and on $\omega$3/$\omega$6 fatty acid ratios in brain PLs of 2nd generation rats. The expeimental diets consisted of 10% fat(by wt), which were computer- searched mixed oil('M') with P/M/S ratio, 1 : 1.4 : 1 and $\omega$6/$\omega$3 ratio, 6 : 1 and safflower oil('S') poor in $\omega$3 fatty acids. The experimental diets were started 3-4 wks prior to conception. During the lactation period, the feeding mothers were switched 1 wk after birth and provided the pups for 2 wks with milk which had compositions different from that of their natural mother. The same diet as their mothers was provided from weaning to 9 wks of age. The 'M'and 'S' rats were again subdivided into MM, MS, SS, SM rats according to diet which their lactating mothers were fed from the begining of the experiment. The relative percentage of P/M/S fatty acids in brain PLs in all experimental groups converged to a very similar value at 9 wks of age, indicating the existence of a control mechanism for the degree of fatty acids, unsaturation. The $\omega$3/$\omega$6 fatty acid ratios of brain PLs converged to about 1.0 in MM & SM groups and to 0.7 in SS & MS groups, suggesting also the existence of some balance between $\omega$3 and $\omega$6 fatty acids in developing rat brain. The concentrations of $\omega$3 fatty acids, especially DHA, in the SM group were increased and became similar to those in MM group at 9 wks of age. The increase in DHA of brain PLs was counterbalanced b)r a decrease in 22 5$\omega$6. Therefore, the ratios of 22 : 6$\omega$6/22 : 5$\omega$6 were higher in both MM & SM groups than those of SS & MS groups at 9 wak of age. Although dietary $\omega$3 and $\omega$6 fatty acids affected 22 : 6$\omega$S and 22 : 5$\omega$6 contained in rat brain PLs reciprocally, the relative percentage of AA did not appear to be significantly influenced by the diet in all groups at 9 wks of age, suggesting that a mechanism for the maintenance of a certain level of AA in brain PLs exists. In conclusion, the $\omega$3/$\omega$6 fatty acid and 22 : 6$\omega$3/22 : 5$\omega$6 ratios, but not P/M/S ratio, of rat brain PLs were affected by the postnatal dietary changes. Futher studies are required to clarify the mechanism(S) of ensuring a certain level of DHA and of maintaining a similar level of AA in rat brain PLs after. weaning(9 wk) regardless of prenatal and postnatal dietary changes. (Korean J Nutrition 31(5) : 897-905, 1998)

• Applied Microscopy
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• v.38 no.3
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• pp.213-219
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• 2008

The plasticity of nervous system is generated not only due to changes in neurons but also due to changes in neuroglial cells. Astrocyte is important for maintaining the normal brain function and controlling the neuronal functions. The amygdala receives an array of important sensory information of danger signals. This information is further transduced and integrated to produce the highly adaptive emotion, fear. In this study, morphometric changes in the cell bodies of astrocytes in the amygdala, induced by prenatal stress and restraint stress were examined. For this purpose. rats were classified into 4 groups; control group (CON), only restraint-stressed (starting on P90 for 3 days) group (CONR), prenatally-stressed group (PNS), and prenatally and restraint (on P90 for 3 days) stressed group (PNSR). Astrocytes were verified with anti-GFAP immunohistochemistry, counter stained with methylene blue/azure II and were examined using the Neurolucida. Results showed that astrocytes in the amygdala of PNS rats had significantly larger cell bodies than did CON rats and this was enhanced further by restraint stress. Thus this data showed that hypertrophy of the astrocytic cell bodies of amygdala complex is induced by prenatal and restraint stress.

• Journal of Preventive Medicine and Public Health
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• v.40 no.2
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• pp.155-161
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• 2007

Objectives : Bisphenol A diglycidyl ether (BADGE) is the major component in commercial liquid epoxy resins, which are manufactured by co-reacting bisphenol A with epichlorohydrin. This study was performed to show the developmental effects of prenatal and postnatal exposures to BADGE in male rat offspring. Methods : Mated female rats were divided into four groups, each containing 12 rats. The dosing solutions were prepared by thoroughly mixing BADGE in corn oil at the 0, 375, 1500 and 3000 mg/kg/day concentrations. Mated females were dosed once daily by oral gavage on gestation day (GD) 6 - 20 and postnatal day (PND) 0 - 21. Pregnant female dams were observed general symptoms and body weight. Also, male pups were observed the general symptoms, body weight, developmental parameters (e.g. anogenital distance, pina detachment, incisor eruption, nipple retention, eye opening, testis descent), organ pathologic changes and hormone levels of plasma. Results : Pregnant rats treated with BADGE died at a rate of about 70% in the 1500 mg/kg/day group and all rats treated with 3000 mg/kg/day died. Body weight, for male pups treated with doses of 375 mg/kg/day, was significantly lower than in the control group at PND 42, 56, and 63 (p<0.05). Evaluation of body characteristics including; separation of auricle, eruption of incisor, separation of eyelid, nipple retention, descent of testis, and separation of the prepuce in the BADGE treated group showed no difference in comparisons with the control group. AGD and adjusted AGD (mm/kg) for general developmental items in BADGE 375 mg/kg/day treated pups tended to be longer than in controls, however, these differences were not statistically significant. Relative weights of adrenal gland, lung (p<0.05), brain, epididymis, prostate, and testis (p<0.01) were heavier than in control in measures at PND 9 weeks. There were no significant changes in comparisons of histological findings of these organs. Loss of spermatids was observed in the seminiferous tubule at PND 9 weeks, but no weight changes were observed. The plasma estrogen levels were similar in the control and treatment groups at PND 3, 6 and 9 weeks. The plasma testosterone levels in the control group tended to increase with age. However, in the BADGE 375 mg/kg/day treated male pups it did not tend to increase. Conclusions : These findings suggest that BADGE is a chemical that has developmental effects consistent with it being an endocrine disruptor.