Spatial Learning Ability of Rats Following Differing Levels of Exposure to Alcohol During Early Postnatal Life

Tomlinson, David; Wilce, Peter A.; Bedi, K. S.

doi:10.1016/s0031-9384(97)00424-1

Cited by 45 publications

(40 citation statements)

References 36 publications

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“…These findings correspond with previous research demonstrating impaired spatial learning and memory in E animals on the Morris water maze (Blanchard et al, 1990;Gianoulakis, 1990;Kim et al, 1997;Blanchard et al, 1987). Deficits in spatial ability also have been shown following neonatal ethanol exposure (Goodlett & Johnson, 1997;Goodlett & Peterson, 1995;Pauli, Wilce, & Bedi, 1995;Tomlinson, Wilce, & Bedi, 1998). Although deficits following prenatal ethanol exposure may not always appear in relatively simple spatial FIGURE 2 Annulus crossings on Day 4 (mean AE SEM) for E, PF, and C males in H and NH treatments at 2 (Young; top panels) or 13 to 14 (Mid-Aged; bottom panels) months of age (ns ¼ 8-10 in each Prenatal Group Â Postnatal Treatment).…”

Section: Discussionsupporting

confidence: 91%

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Gabriel

Johnston

Weinberg

2002

Developmental Psychobiology

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Prenatal ethanol exposure results in spatial navigation deficits in young and mid-aged animals. In contrast, postnatal handling attenuates spatial deficits that emerge with age in animals that are not handled. Therefore, we investigated the ability of handling to attenuate spatial deficits in animals prenatally exposed to ethanol (E). Sprague-Dawley male offspring from E, pair-fed (PF), and control (C) groups were handled (H) or nonhandled (NH) from 1 to 15 days of age and tested on the Morris water maze at 2 or 13 to 14 months of age. In young animals, H-E males had longer latencies to locate the submerged platform, and E animals, across handling conditions, showed altered search patterns compared to their PF and C counterparts. Mid-aged animals had longer latencies than young animals, with no differences among E, PF, and C animals. However, corticosterone levels were higher in mid-aged E than in C males. Handling did not attenuate impairments associated with either prenatal ethanol exposure or aging.

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Section: Discussionsupporting

confidence: 91%

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Gabriel

Johnston

Weinberg

2002

Developmental Psychobiology

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“…The progressive increases in body weight across all groups, is similar to weight growth curves reported in previous studies (Goodlett and Johnson, 1997;Thomas et al, 2003;Tomlinson et al, 1998). The increase in alcohol-treated group was significantly less than in GC and SC groups, which is in agreement with the results of similar studies (Thomas et al, 2003;Tomlinson et al, 1998;Tran et al, 2000).…”

Section: Effects Of Postnatal Alcohol Exposure On Body and Brain Weightssupporting

confidence: 91%

“…The increase in alcohol-treated group was significantly less than in GC and SC groups, which is in agreement with the results of similar studies (Thomas et al, 2003;Tomlinson et al, 1998;Tran et al, 2000). In contrast, other investigators have reported no significant weight loss in rats exposed to alcohol during early postnatal period (Chen et al, 1999;Chen et al, 1998).…”

Section: Effects Of Postnatal Alcohol Exposure On Body and Brain Weightssupporting

confidence: 91%

Early postnatal alcohol exposure reduced the size of vibrissal barrel field in rat somatosensory cortex (SI) but did not disrupt barrel field organization

Oladehin

Margret

Maier

et al. 2007

Alcohol

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Prenatal alcohol exposure (PAE) has been shown to alter the somatosensory cortex in both human and animal studies. In rodents, PAE reduced the size, but not the pattern of the posteromedial barrel subfield (PMBSF) associated with the representation of the whiskers, in newborn, juvenile, and adult rats. However, the PMBSF is not present at birth, but rather first appears in the middle of the first postnatal week during the brain growth spurt period. These findings raise questions whether early postnatal alcohol exposure might disrupt both barrel field pattern and size, questions that were investigated in the present study. Newborn Sprague-Dawley rats were assigned into alcohol (Alc), nutritional gastric control (GC), and suckle control (SC) on P4. Rat pups in Alc and GC were artificially fed with alcohol and maltose-dextrin dissolved in milk respectively, via an implant gastrostomy tube, from postnatal day 4 (P4) to P9. Pups in the Alc group received alcohol (6.0 g/kg) in milk, while the GC controls received isocaloric equivalent maltose-dextrin dissolved in milk. Pups in the SC group remained with their mothers and breast fed throughout the experimental period. On P10, pups in each group were weighed, sacrificed, and their brains removed and weighed. Cortical hemispheres were separated, weighed, flattened, sectioned tangentially, stained with cytochrome oxidase, and PMBSF measured. The sizes of barrels and the interbarrel septal region within PMBSF, as well as body and brain weights were compared between the three groups. The sizes of PMSBF barrel and septal areas were significantly smaller (p < 0.01) in Alc group compared to controls, while the PMBSF barrel pattern remained unaltered. Body, whole brain, forebrain, and hemisphere weights were significantly reduced (p < 0.01) in Alc pups compared to control groups. GC and SC groups did not differ significantly in all dependent variables, except body weight at P9 and P10 (p < 0.01). These results suggest that postnatal alcohol exposure, like prenatal exposure, significantly influenced the size of the barrel field, but not barrel field pattern formation, indicating that barrel field pattern formation consolidated prior to P4. These results are important for understanding sensorimotor deficits reported in children suffering from fetal alcohol spectrum disorder (FASD).

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“…The precise functional consequences (if any) of their loss and subsequent replacement by new cells remain unknown. However, we previously reported (Pauli et al, 1995b;Tomlinson et al, 1998) that exposure of rats to ethanol can have deleterious effects on spatial learning behaviour, as measured in the Morris water maze (Morris, 1981;Morris et al, 1982). Stressful situations have also been shown to impair spatial learning ability (Luine et al, 1994;Diamond et al, 1996).…”

Section: _________________________________________________ Ethanol Exmentioning

confidence: 98%

“…As a consequence, we have been engaged for a number of years in examining both the short-term and long-term effects of exposure to ethanol on the rat brain at various periods of time during the first 2 weeks of postnatal life. For example, we previously reported (Pauli et al, 1995b;Tomlinson et al, 1998) that a high dose of ethanol exposure to rats during early postnatal life can result in long-lasting alterations in spatial learning ability as tested on the Morris water maze (Morris 1981;Morris et al, 1982). The question arises whether such behavioural deficits are accompanied by measurable morphological changes in the brains of these animals.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2003

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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 approximately 430 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.

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Spatial Learning Ability of Rats Following Differing Levels of Exposure to Alcohol During Early Postnatal Life

Cited by 45 publications

References 36 publications

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Early postnatal alcohol exposure reduced the size of vibrissal barrel field in rat somatosensory cortex (SI) but did not disrupt barrel field organization

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

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