A Golgi study of mouse hippocampal CA1 pyramidal neurons following perinatal ethanol exposure

Davies, David; Smith, David

doi:10.1016/0304-3940(81)90424-9

Cited by 129 publications

(45 citation statements)

References 17 publications

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“…For example, developmental exposure of rats to lead can result in ultrastructural changes in the hippocampus associated with decreased axonal and dendritic outgrowth (Alfano and Petit, 1982), and inhibitory effects of lead on neurite outgrowth have been observed in primary cultures of rat hippocampal neurons (Kern and Audesirk, 1995;Kern et al, 1993). A similar correlation was observed between the inhibitory effects of ethanol on dendritic arbor size in the hippocampus in vivo (Davies and Smith, 1981) and in primary hippocampal neurons in vitro (Yanni and Lindsley, 2000).…”

Section: Primary Culturessupporting

confidence: 59%

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

2008

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Section: Primary Culturessupporting

confidence: 59%

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

2008

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“…The developing hippocampus is a brain region which has been shown to be highly susceptible to EtOH-induced neurotoxicity [Barnes and Walker, 1981;Davies and Smith, 1981;West and Pierce, 1986], and this structure produces high levels of neurotrophic factors and their receptors [Maisonpierre et al, 1990;Roback et al, 1992;Fryer et al, 1996]. Reductions in critical neurotrophic support in neuronal populations has been hypothesized to exacerbate direct EtOH-induced toxicity .…”

Section: Discussionmentioning

confidence: 99%

“…Direct EtOH-induced neurotoxicity may be exacerbated by reductions in critical neurotrophic support in target central nervous system (CNS) regions, such as the hippocampus . The hippocampus was chosen, for the present study, since it has been shown to produce significantly high levels of neurotrophic factors and their receptors [Maisonpierre et al, 1990;Cellerino, 1996;Fryer et al, 1996] coupled with this brain region's inherent selective vulnerability to EtOH [Riley and Walker, 1978;Walker et al, 1980;Davies and Smith, 1981;Sulik et al, 1984;West and Pierce, 1986;West et al, 1986]. Additionally, it appears likely that many of the cognitive and behavioral deficits seen in FAE and FAS may involve the compromised function of the septohippocampal system [Abel 1982a, b;West, 1986;West et al, 1994].…”

Section: Introductionmentioning

confidence: 99%

BDNF and NGF Afford in vitro Neuroprotection against Ethanol Combined with Acute Ischemia and Chronic Hypoglycemia

et al. 1999

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Consumption of alcohol during pregnancy can result in central nervous system deficits in infants ranging from fetal alcohol effects to fetal alcohol syndrome. Changes in cerebral metabolism causing ischemic in utero conditions can also result from ethanol (EtOH). Growth factors have been shown to ameliorate ischemic damage and EtOH-induced neurotoxicity. However, using an in vitro model system of fetal alcohol effects/fetal alcohol syndrome, this study examines the neuroprotective effects of nerve growth factor, brain-derived neurotrophic factor, or glial cell line derived neurotrophic factor against EtOH treatment (0, 200, 400, 800, or 1,600 mg/dl) combined with acute ischemia (2-hour hypoxia in EtOH-containing glucose-free media) followed by chronic hypoglycemia (16-hour glucose deprivation in EtOH-containing media). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assays assessed relative neurotoxicity. Glial cell derived neurotrophic factor was not neuroprotective. Nerve growth factor protected against ischemia/hypoglycemia combined with 0–1,600 mg/dl EtOH. Brain-derived neurotrophic factor protected against ischemia/hypoglycemia combined with 0–800 mg/dl EtOH. These studies demonstrate marked growth factor neuroprotection against a myriad of conditions encountered by developing EtOH-exposed fetuses.

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“…Tel : j61-7-3365-3058 ; fax : j61-7-3365-1299 ; e-mail : k.bedi!mailbox.uq.edu.au. maturation (Davies & Smith, 1981 ;StoltenburgDidinger & Spohr, 1983) and synapses (Kjellstrom & Conradi, 1995) as well as the organisation of neural circuitry (West et al 1981(West et al , 1984.…”

Section: mentioning

confidence: 99%

Exposure of rats to a high but not low dose of ethanol during early postnatal life increases the rate of loss of optic nerve axons and decreases the rate of myelination

2000

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Visual system abnormalities are commonly encountered in the fetal alcohol syndrome although the level of exposure at which they become manifest is uncertain. In this study we have examined the effects of either low (ETLD) or high dose (ETHD) ethanol, given between postnatal days 4-9, on the axons of the rat optic nerve. Rats were exposed to ethanol vapour in a special chamber for a period of 3 h per day during the treatment period. The blood alcohol concentration in the ETLD animals averaged " 171 mg\dl and in the ETHD animals " 430 mg\dl at the end of the treatment on any given day. Groups of 10 and 30-d-old mother-reared control (MRC), separation control (SC), ETLD and ETHD rats were anaesthetised with an intraperitoneal injection of ketamine and xylazine, and killed by intracardiac perfusion with phosphatebuffered glutaraldehyde. In the 10-d-old rat optic nerves there was a total of " 145 000-165 000 axons in MRC, SC and ETLD animals. About 4 % of these fibres were myelinated. The differences between these groups were not statistically significant. However, the 10-d-old ETHD animals had only about 75 000 optic nerve axons (P 0n05) of which about 2n8 % were myelinated. By 30 d of age there was a total of between 75 000-90 000 optic nerve axons, irrespective of the group examined. The proportion of axons which were myelinated at this age was still significantly lower (P 0n001) in the ETHD animals (" 77 %) than in the other groups (about 98 %). It is concluded that the normal stages of development and maturation of the rat optic nerve axons, as assessed in this study, can be severely compromised by exposure to a relatively high (but not low) dose of ethanol between postnatal d 4 and 9.

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A Golgi study of mouse hippocampal CA1 pyramidal neurons following perinatal ethanol exposure

Cited by 129 publications

References 17 publications

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

BDNF and NGF Afford in vitro Neuroprotection against Ethanol Combined with Acute Ischemia and Chronic Hypoglycemia

Exposure of rats to a high but not low dose of ethanol during early postnatal life increases the rate of loss of optic nerve axons and decreases the rate of myelination

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