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Biomedical subjects

A Rabe

Publications and source records attributed to A Rabe.

31 records · Page 2Linked to original sources
PubMed1976

Position reversal deficit in young ferrets.

Young ferrets (6 and 10 weeks old at the start of the experiments) were compared to adult ferrets on learning (1) a Lashley III maze, (2) a left-right discrimination in T-maze with identical choice arms, and (3) a reversal of the left-right discrimination. The young were not inferior to the adults in learning either the Lashley III maze or the initial discrimination in the T-maze. However, the young were markedly (and significantly) inferior to the adults in learning to reverse.

Age Factors↗
PubMedDate not supplied

Visual discrimination by rats with transplacentally induced micrencephaly.

Long-Evans rats with micrencephaly induced by prenatal exposure to methylazoxymethanol acetate and normal controls were trained in a two-choice box to discriminate between stimuli of different brightness (black vs. white) or pattern (horizontal vs. vertical alternating black-and-white stripes). Mild footshock was used to motivate the rats to learn. The micrencephalic rats were impaired in learning the pattern, but not brightness discrimination. These results confirm and extend similar findings with micrencephalic Wistar rats by another laboratory. The visual discrimination performance of micrencephalic rats was similar to that reported for normal rats with lesions in the visual cortical areas.

Animals↗
PubMedDate not supplied

Premature decline in Morris water maze performance of aging micrencephalic rats.

The rat with methylazoxymethanol-induced micrencephaly is a useful animal model of congenital brain defects and associated cognitive impairment. Born with profound morphological and neurochemical alterations in the forebrain, it shows impaired ability to learn mazes. In order to determine how an animal with such a developmentally damaged brain would function in old age, Long-Evans rats 6, 15, and 24 months of age were tested for their ability to learn to locate a hidden platform in the Morris water maze. The performance of micrencephalic rats of all ages was impaired on acquisition, retention, and transfer trials. Moreover, the magnitude of their acquisition deficit increased with age. It remains to be determined whether the premature decline of the micrencephalic rat in learning the task simply reflects a greater impact on an already compromised brain by neuron loss characteristic of aging brains or whether the prenatal insult alters some basic processes resulting in premature aging.

Aging↗
PubMedDate not supplied

Augmented memory loss in aging mice after one embryonic exposure to alcohol.

Prenatal exposure to alcohol can produce behavioral and cognitive deficits even in the absence of dysmorphic facial features. In a mouse model, we tested whether embryonic exposure to alcohol could exacerbate functional loss as animals age. Normal-appearing offspring were selected from litters produced by C57Bl/6J mice that had been gavaged with one teratogenic dose (5.8 g/kg) of ethyl alcohol during organogenesis on the 9th day of gestation. In adulthood, the offspring suffered a deficit in long-term retention, but not acquisition, of a place learning task. Although barely detectable in young adults, the retention deficit was severe in aging mice. These findings demonstrate that the functional deficits resulting from embryonic exposure to alcohol can interact with those of aging.

Aging↗
PubMedDate not supplied

Experimental maternal phenylketonuria: an examination of two animal models.

Two satisfactory rat models of maternal phenylketonuria (PKU) have been developed. Continuous subcutaneous infusion into pregnant rats from the 9th-20th day of gestation of either (1) phenylacetate (PA), to elevate plasma levels of unconjugated PA to 0.25-0.60 mumol/ml, or (2) a nontoxic dose (0.2 mumol/g/day) of p-chlorophenylalanine (pClPhe) with L-phenylalanine (Phe), to elevate plasma Phe levels at least 10-fold (1.7-2.3 mumol/ml) and unconjugated PA to at least 0.2 mumol/ml, produced the syndrome of untreated maternal PKU: spontaneous abortion, mortality rate greater than normal among the newborn, retarded growth of fetal body and brain, and a learning deficit among the progeny. From the plasma of rats infused with only pClPhe, a metabolite was isolated and identified as p-chlorophenylacetic acid. This compound, at a concentration greater than 0.15 mumol/ml plasma was found to retard fetal body and brain growth. In the pregnant rat, plasma levels of unconjugated PA, in the range observed in some PKU individuals on a normal diet, effectively induced a simulation of maternal PKU. The results of this investigation support our contention that PA, which is produced in excessive amounts in clinical PKU, is the primary cause of the brain dysfunction.

Animals↗