Effects of in utero ethanol exposure on the development of LHRH neurons in the mouse

Scott, Heather; Paull, Willis K.; Rudeen, P. K.

doi:10.1016/0165-3806(92)90147-o

Cited by 11 publications

(1 citation statement)

References 32 publications

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“…Vários trabalhos demonstram as ações nocivas do álcool nas etapas do processo de diferenciação celular, observando-se bloqueio de receptores para neurotransmissores (9,13) , interferência no processo de mielinização (22,31) e na formação e modelamento do axônio e dendrito (26) . Porém o estudo do neurópilo é praticamente ignorado.…”

Section: Introductionunclassified

Efeitos da exposição pré-natal e pós-natal ao etanol no córtex cerebral de ratos: um estudo do neurópilo

Jerônimo¹,

Filho²,

Júnior³

2008

J. Bras. Patol. Med. Lab.

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Primeira submissão em 13/04/07 Última submissão em 21/11/07 Aceito para publicação em 10/12/07 Publicado em 20/02/08 Efeitos da exposição pré-natal e pós-natal ao etanol no córtex cerebral de ratos: um estudo do neurópilo Effects of prenatal and postnatal ethanol exposure in the cerebral cortex of rats: a study of neuropil Márcio Sousa Jerônimo 1 ; Nicodemos Teles de Pontes Filho 2 ; Mário Ribeiro de Melo Júnior 3

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Section: Introductionunclassified

Efeitos da exposição pré-natal e pós-natal ao etanol no córtex cerebral de ratos: um estudo do neurópilo

Jerônimo¹,

Filho²,

Júnior³

2008

J. Bras. Patol. Med. Lab.

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Changes in the reproductive system following acute prenatal exposure to ethanol or methylazoxymethanol in the rat: I. Effects on immunoreactive LHRH cell number

et al. 1994

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It has long been recognized that ethanol (EtOH) interferes with the hypothalamo-pituitary-gonad axis in adults of many species, and recent studies have provided evidence for similar effects after prenatal EtOH exposure. Since EtOH is capable of injuring dividing cells, we investigated the possibility that a single acute in utero EtOH exposure during the period of LHRH neuron formation might change the number of immunoreactive LHRH cells in the hypothalamus. Final LHRH cell division in Long-Evans rats was determined by [3H]thymidine autoradiography to take place over a short period between gestation days 12 and 13. Subsequently, pregnant rats were treated acutely with either EtOH or methylazoxymethanol (MAM), a known neuroteratogen, and the numbers of immunoreactive LHRH cells were counted. On gestation day 22, LHRH-positive cell numbers were significantly fewer than control numbers in both EtOH- and MAM-exposed offspring. On postnatal day 60, cell numbers in EtOH-exposed offspring did not differ from control numbers, whereas cells in MAM-exposed offspring remained significantly reduced. In controls, there were 40% fewer LHRH-positive cells on postnatal day 4 than in late gestation or at maturity. We conclude that 1) acute exposure to a high dose of EtOH at a critical time in early gestation can alter the expression of LHRH in late gestation; 2) exposure to MAM in the same period alters LHRH expression before birth and in the adult; and 3) in the early postnatal period, LHRH expression decreases profoundly.

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Patterns of growth deficiency in rats exposed in utero to undernutrition, ethanol, or the neuroteratogen methylazoxymethanol (MAM)

et al. 1994

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Children and experimental animals exposed to ethanol (EtOH) in utero commonly have low birthweights, and many remain small at maturity. Low body weight or small stature in adulthood may reflect an inability to recover from in utero growth retardation, or it may reflect a separate, postnatal growth deficiency. In this study, daily body weights (postnatal days 1 to 60) were compared among the offspring of the following groups of Long Evans rats: dams fed liquid diet containing 35% EtOH-derived calories; their pair-fed and chow-fed controls; and dams exposed to methylazoxymethanol (MAM) in two previous studies, in which offspring exhibited reduced numbers of growth hormone releasing factor (GRF) neurons. All treatments produced a number of offspring with weight deficits beginning after birth and persisting into maturity. Three distinct patterns of growth deficiency were observed: (1) weight loss relative to controls in the first weeks of life, seen in offspring exposed to EtOH, pair feeding, or MAM on gestation day 13 (G13); (2) a delay in the onset of the prepubertal growth spurt, seen in all EtOH-exposed offspring and in G13 MAM-exposed dwarfs; and (3) failure to sustain the prepubertal growth spurt, seen only after exposure to MAM on G14. The results of this study support the view that prenatal EtOH exposure is capable of affecting postnatal growth specifically; moreover, the pattern of growth deficiency seen in EtOH-exposed offspring was distinct from that of the undernourished offspring of pair-fed dams.

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Effects of in utero ethanol exposure on the development of LHRH neurons in the mouse

Cited by 11 publications

References 32 publications

Efeitos da exposição pré-natal e pós-natal ao etanol no córtex cerebral de ratos: um estudo do neurópilo

Efeitos da exposição pré-natal e pós-natal ao etanol no córtex cerebral de ratos: um estudo do neurópilo

Changes in the reproductive system following acute prenatal exposure to ethanol or methylazoxymethanol in the rat: I. Effects on immunoreactive LHRH cell number

Patterns of growth deficiency in rats exposed in utero to undernutrition, ethanol, or the neuroteratogen methylazoxymethanol (MAM)

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