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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2004.9
- 수록면
- 67 - 77 (11page)
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초록· 키워드
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A large number of chemical pollutants including phthalates, alkylphenolic compounds
and organochlorine pesticides have the ability to disrupt endocrine function in animals, and alter cognitive
function. Because hormone mediated events play an important role in central nervous system
development and function, the changes in cognitive function seem to be mediated by the endocrinelike
action of these chemicals. The present study therefore was designed to investigate effect of
bisphenol A (BPA), an endocrine disrupting chemical on neuro-behavial patterns, and expression of
estrogen receptors and tyrosine hydroxylase, a limiting enzyme of dopamine synthesis pathway. BPA
was treated orally for 3 weeks into 3 week old mice, and then the neuro-behavial patterns (stereotype
behaviors such as jumping rearing and forepaw tremor, climbing behavior, tail flick, rotarod and
locomotor activity), and the expression of estrogen receptors and tyrosine hydroxylase were determined
every 3 week for 9 weeks. During the treatment of BPA, the food uptake and body weight
increase were not significantly changed. BPA resulted in the increased stereotype behaviors (jumping,
rearing and forepaw tremor) 6 or 9 weeks after treatment. The time response to tail flick and
locomotor activity were decreased by the treatment of BPA, whereas the time for rotarod was
increased by the treatment of BPA. The expression of estrogen receptor alpha and beta was
increased in the brain and pituitary gland. Maximum expression was found in the brain after 9 week
of 100 mg/kg BPA treatment and in the pituitary gland after 6 week of 100 mg/kg BPA treatment.
Tyrosine hydroxylase was increased in dose and time dependent manners in the brain but no change
was found in the pituitary gland. The present data show that exposure of BPA in the young mice
could alter expression of estrogen receptors and dopamine synthesis pathway, thereby modulate
neuro-behavial patterns (increase of stereotype behaviors but decrease locomotor activity).
and organochlorine pesticides have the ability to disrupt endocrine function in animals, and alter cognitive
function. Because hormone mediated events play an important role in central nervous system
development and function, the changes in cognitive function seem to be mediated by the endocrinelike
action of these chemicals. The present study therefore was designed to investigate effect of
bisphenol A (BPA), an endocrine disrupting chemical on neuro-behavial patterns, and expression of
estrogen receptors and tyrosine hydroxylase, a limiting enzyme of dopamine synthesis pathway. BPA
was treated orally for 3 weeks into 3 week old mice, and then the neuro-behavial patterns (stereotype
behaviors such as jumping rearing and forepaw tremor, climbing behavior, tail flick, rotarod and
locomotor activity), and the expression of estrogen receptors and tyrosine hydroxylase were determined
every 3 week for 9 weeks. During the treatment of BPA, the food uptake and body weight
increase were not significantly changed. BPA resulted in the increased stereotype behaviors (jumping,
rearing and forepaw tremor) 6 or 9 weeks after treatment. The time response to tail flick and
locomotor activity were decreased by the treatment of BPA, whereas the time for rotarod was
increased by the treatment of BPA. The expression of estrogen receptor alpha and beta was
increased in the brain and pituitary gland. Maximum expression was found in the brain after 9 week
of 100 mg/kg BPA treatment and in the pituitary gland after 6 week of 100 mg/kg BPA treatment.
Tyrosine hydroxylase was increased in dose and time dependent manners in the brain but no change
was found in the pituitary gland. The present data show that exposure of BPA in the young mice
could alter expression of estrogen receptors and dopamine synthesis pathway, thereby modulate
neuro-behavial patterns (increase of stereotype behaviors but decrease locomotor activity).
목차
ABSTRACT
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UCI(KEPA) : I410-ECN-0101-2009-513-014287293