Effects of alcohol exposure during early life on neuron numbers in the rat hippocampus. I. Hilus neurons and granule cells

We previously showed that 16-day-old rats exposed to a relatively high dose of ethanol at 10-15 postnatal days of age have fewer neurons in the hilus region of the hippocampus compared with controls. Dentate gyrus granule cell numbers, however, showed no statistically significant changes attributable to the ethanol treatment. It is possible that some of the changes in brain morphology, brought about as a result of the exposure to ethanol during early life, may not be manifested until later in life. This question has been further addressed in an extension to our previous study. Wistar rats were exposed to a relatively high daily dose of ethanol on postnatal days 10-15 by placement in a chamber containing ethanol vapour, for 3 h/day. The blood ethanol concentration was found to be similar to430 mg/dl at the end of the period of exposure. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anaesthetised and killed either at 16 or 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle and the physical disector methods were used to estimate, respectively, the regional volumes and neuron cell numerical densities in the hilus and granule cell regions of the dentate gyrus. The total numbers of neurons in the hilus region and granule cell layer were computed from these estimates. It was found that 16-day-old animals had 398,000-441,000 granule cells, irrespective of group. The numbers of granule cells increased such that by 30 days of age, rats had 487,000-525,500 granule cells. However, there were no significant differences between ethanol-treated rats and their age-matched controls in granule cell numbers. In contrast, ethanol-treated rats had slightly but significantly fewer neurons in the hilus region than did control animals at 16 days of age, but not at 30 days of age. Therefore, it appears that a short period of ethanol exposure during early life can have effects on neuron numbers of some hippocampal neurons, but not others. The effects on hilar neuron numbers, observed as a result of such short periods of ethanol treatment, appeared to be transitory. (C) 2003 Wiley-Liss, Inc.

Effects of age and alcohol exposure during early life on pyramidal cell numbers in the CA1-CA3 region of the rat hippocampus

We have previously shown that exposing rats to a relatively high dose of ethanol during early postnatal life can result in an alteration in spatial learning ability. The hippocampal formation is known to be involved in the control of this ability. The purpose of the present study was to determine whether exposure of rats to ethanol during early postnatal life had either immediate or delayed effects on the numbers of pyramidal cells in the CA1-CA3 subregion of the hippocampus. Wistar rats were exposed to a relatively high daily dose of ethanol at postnatal day 10-15 by placing them for 3 h/day in a chamber containing ethanol vapor. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anesthetized and killed at 16 and 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle was used to determine the volumes of the CA1 and CA2+CA3 regions. The physical disector method was used to estimate the numerical density of neurons in each of the subdivisions. The total number of pyramidal cells was calculated by multiplying the appropriate estimates of the numerical density by the volume. There were significant age-related reductions in the total numbers of pyramidal cells at 16-30 days of age irrespective of the groups examined. Ethanol treated rats were found to have slightly but significantly fewer pyramidal cell neurons than either the MRC or SC groups. These observations indicate that pyramidal cells in the hippocampus may be vulnerable to a relatively high dose of ethanol exposure during this short period of early postnatal life. (C) 2003 Wiley-Liss, Inc.

The origin of the metazoan biphasic life cycle: New insights from an ancient phylum

The biphasic life cycle, characterised by metamorphosis from a pelagic larva to a benthic adult, is found throughout the Metazoa. So is sexual reproduction via eggs and sperm. Amidst a tangled web of hypotheses on the origin of metazoan biphasy, current weight of opinion lies with a simple, larva-like holopelagic ancestor that independently settled multiple times to incorporate a benthic phase into the life cycle. This school of thought derives from Haeckel's interpretation of the gastrula as the recapitulation of a gastrean ancestor that evolved via selection on a simple, planktonic hollow ball-of-cells to develop the capacity to feed. We suggest that a paradigm shift is required to accomodate accumulating evidence of the genomic and developmental complexity of the metazoan last common ancestor, which was likely to have already possessed a biphasic lifecycle. Here we incorporate recent evidence from basal metazoans, in particular poriferans, to argue that a more parsimonious theory of the origin of biphasy is as a direct consequence of sexual reproduction in an ancestral benthic adult form. The metazoan embryo can itself be considered the precursor to a biphasic life cycle, wherein the embryo represents one phase and the adult another. Embryos in the water column are subject to natural selection for longeveity and dispersal, which sets them on the evolutionary trajectory towards the crown metazoan planktonic larvae. This alternate view considers the conserved use of regulatory genes in disparate metazoans as a reflection of both the complexity of the LCA and the antiquity of the biphasic life cycle. It does not require that extant embryogenesis, including gastrulation, recapitulates evolution.

The response of native Australian rodents to predator odours varies seasonally: a by-product of life history variation?

Small mammals are subject to predation from mammalian, avian and reptilian predators. There is an obvious advantage for prey species to detect the presence of predators in their environment, enabling them to make decisions about movement and foraging behaviour based on perceived risk of predation. We examined the effect of faecal odours from marsupial and eutherian predators, and a native reptilian predator, on the behaviour of three endemic Australian rodent species (the fawn-footed melomys, Melomys cervinipes, the bush rat, Rattus fuscipes, and the giant white-tailed rat, Uromys caudimaculatus) in rainforest remnants on the Atherton Tableland, North Queensland, Australia. Infrared camera traps were used to assess visit rates of rodents to odour stations containing faecal and control odours. Rodents avoided odour stations containing predator faeces, but did not avoid herbivore or control odours. The responses of the three prey species differed: in the late wet season U. caudimaculatus avoided predator odours, whereas R. fuscipes and M. cervinipes did not. In contrast, in the late dry season all three species avoided odour stations containing predator odours. We speculate that these different responses may result from variation in life history traits between the species. (c) 2006 The Association for the Study of Animal Behaviour Published by Elsevier Ltd. All rights reserved.