The later development of the brain and its vulnerability

Dobbing, John

doi:10.1007/bf01805569

Cited by 203 publications

(237 citation statements)

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“…It is estimated that the rat brain at postnatal days (PN) 1-10 equates to the 3 rd trimester in humans, or that rat neurodevelopment at PN 7 is equivalent to that of the human brain at birth (Andrews and Fitzgerald, 1997;Dobbing and Sands, 1979). It is interesting to note that many of the studies upon which these approximations are based are decades old (Dobbing, 1972;Dobbing, 1974b;Dobbing and Sands, 1979), and some estimate neural development without direct empirical evidence (Dobbing, 1981;Dobbing and Smart, 1974).…”

Section: Rules Of Thumbmentioning

confidence: 99%

“…He expanded on interspecies comparisons of brain growth (Donaldson, 1918), neural-related enzymes (Farooqui and Bachhawat, 1971) and ganglioside concentrations (glycolipids used as an indirect measure of white matter) (Vanier et al, 1971). Dobbing identified growth spurts using DNA to estimate cell numbers, and cholesterol levels to approximate the degree of myelination (Dobbing, 1970), later including brain weights and water content (Dobbing, 1981). Sands and Dobbing produced comparative velocity curves for timing vulnerability periods that occur during growth spurts (Dobbing, 1974b;Dobbing and Sands, 1979;Dobbing and Smart, 1974).…”

Section: Vulnerability Patterns and Growth Spurtsmentioning

confidence: 99%

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Extrapolating brain development from experimental species to humans

et al. 2007

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To better understand the neurotoxic effects of diverse hazards on the developing human nervous system, researchers and clinicians rely on data collected from a number of model species that develop and mature at varying rates. We review the methods commonly used to extrapolate the timing of brain development from experimental mammalian species to humans, including morphological comparisons, "rules of thumb" and "event-based" analyses. Most are unavoidably limited in range or detail, many are necessarily restricted to rat/human comparisons, and few can identify brain regions that develop at different rates. We suggest this issue is best addressed using "neuroinformatics", an analysis that combines neuroscience, evolutionary science, statistical modeling and computer science. A current use of this approach relates numeric values assigned to ten mammalian species and hundreds of empirically derived developing neural events, including specific evolutionary advances in primates. The result is an accessible, online resource (http:// www.translatingtime.net/) that can be used to equate dates in the neurodevelopmental literature across laboratory species to humans, predict neurodevelopmental events for which data are lacking in humans, and help to develop clinically relevant experimental models.

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Section: Rules Of Thumbmentioning

confidence: 99%

Section: Vulnerability Patterns and Growth Spurtsmentioning

confidence: 99%

Extrapolating brain development from experimental species to humans

et al. 2007

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“…EtOH rats received one daily administration of 1.5g, 2.25g, 4.0g, or 6.0g ethanol/Kg body weight using a 25% w/v solution of ethanol in double-distilled water on G1-20, the time approximating trimesters 1 and 2 in human gestation (Bayer et al, 1993;Dobbing, 1981;Dobbing and Sands, 1973;1979). Pair-fed rats were weight-matched to an EtOH female.…”

Section: Alcohol Protocolmentioning

confidence: 99%

“…Alcohol exposure consisted of a range of doses to determine possible threshold levels for causing effects. The timing of alcohol exposure coincided with the first two trimesters-equivalent to human gestation (Bayer et al, 1993;Dobbing, 1981;Dobbing and Sands, 1973;1979), a period of time before and during the generation of neocortical neurons (Fukumitsu et al, 2006;Kennedy and Elliot, 1985;Miller, 1986;1987;. Morphological analyses were carried out in offspring during the time period shown previously to have transitory CC axons (Elberger 1994a,b).…”

Section: Introductionmentioning

confidence: 99%

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Livy

Elberger

2008

Alcohol

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Children exposed prenatally to alcohol can display a variety of neural deficits, including an altered development of the corpus callosum (CC), the largest interhemispheric axon pathway in the brain. Furthermore, these children show functional abnormalities that are related to brain regions with significant numbers of CC connections. Little is known about how alcohol imparts influence on CC development, but one possible mechanism is by affecting the corpus callosum projection neurons (CCpn) directly. The purpose of this study was to quantify the effects of prenatal alcohol exposure on the number, size and distribution of CCpn within the visual cortex. The visual cortex was selected specifically due to the many vision-related deficits noted in fetal alcohol exposed children and because the critical role of the CC in visual cortex development is well documented. Sprague-Dawley rat pups received one of four alcohol dosages during gestational days (G) 1-20, or reared as nutritional or untreated control animals. Each litter was categorized according to the peak blood alcohol concentration (BAC) experienced. Pups were removed from each litter on days equivalent to G29, G36, G43, and G50, for histology and measurement. Callosal axons were labelled retrogradely to their CCpn using DiI and the CCpn were then examined using confocal laser scanning microscopy. Differences between alcohol-exposed and control animals were observed in CCpn cell body size, number, and location with the cortex. This was particularly true of animals exposed to high doses of alcohol. In addition, some trends of CCpn development were found to be unchanged as a result of prenatal alcohol exposure. The results demonstrate clear differences in the development of CCpn in the visual cortex between alcohol-exposed and control animals and suggest that this development is particularly affected in those animals exposed to high doses of alcohol.

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“…By comparison, human brain growth begins antenatally, peaks at birth and continues beyond 30 months postnatally (Dobbing, 1974). In addition to simple increases in brain mass, synaptogenesis and glial proliferation begin during late antenatal periods and continue through postnatal day (PN)40 in the rat (4-6 years old in humans).…”

Section: Introductionmentioning

confidence: 99%

Neonatal Antidepressant Exposure has Lasting Effects on Behavior and Serotonin Circuitry

Maciąg

Simpson

Coppinger

et al. 2005

Neuropsychopharmacol

274

275

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A significant fraction of infants born to mothers taking selective serotonin reuptake inhibitors (SSRIs) during late pregnancy display clear signs of antidepressant withdrawal indicating that these drugs can penetrate fetal brain in utero at biologically significant levels. Previous studies in rodents have demonstrated that early exposure to some antidepressants can result in persistent abnormalities in adult behavior and indices of monoaminergic activity. Here, we show that chronic neonatal (postnatal days 8-21) exposure to citalopram (5 mg/kg, twice daily, s.c.), a potent and highly selective SSRI, results in profound reductions in both the rate-limiting serotonin synthetic enzyme (tryptophan hydroxylase) in dorsal raphe and in serotonin transporter expression in cortex that persist into adulthood. Furthermore, neonatal exposure to citalopram produces selective changes in behavior in adult rats including increased locomotor activity and decreased sexual behavior similar to that previously reported for antidepressants that are nonselective monoamine transport inhibitors. These data indicate that the previously reported neurobehavioral effects of antidepressants are a consequence of their effects on the serotonin transporter. Moreover, these data argue that exposure to SSRIs at an early age can disrupt the normal maturation of the serotonin system and alter serotonin-dependent neuronal processes. It is not known whether this effect of SSRIs is paralleled in humans; however, these data suggest that in utero, exposure to SSRIs may have unforeseen long-term neurobehavioral consequences.

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The later development of the brain and its vulnerability

Cited by 203 publications

References 1 publication

Extrapolating brain development from experimental species to humans

Extrapolating brain development from experimental species to humans

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Neonatal Antidepressant Exposure has Lasting Effects on Behavior and Serotonin Circuitry

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