Biomedical subjects

Rodney A Swain

Publications and source records attributed to Rodney A Swain.

4 recordsLinked to original sources

PubMed2004

Effects of exercise on Pavlovian fear conditioning.

Exercise promotes multiple changes in hippocampal morphology and should, as a result, alter behavioral function. The present experiment investigated the effect of exercise on learning using contextual and auditory Pavlovian fear conditioning. Rats remained inactive or voluntarily exercised (VX) for 30 days, after which they received auditory-cued fear conditioning. Twenty-four hours later, rats were tested for learning of the contextual and auditory conditional responses. No differences in freezing behavior to the discrete auditory cue were observed during the training or testing sessions. However, VX rats did freeze significantly more compared to controls when tested in the training context 24 hr after exposure to shock. The enhancement of contextual fear conditioning provides further evidence that exercise alters hippocampal function and learning.

Acoustic Stimulation↗

PubMed2003

Pretraining enhances recovery from visuospatial deficit following cerebellar dentate nucleus lesion.

Following bilateral lesions targeting lateral deep cerebellar nuclei, rats were subjected to a bridge test as a measure of visuomotor coordination and were trained on the Morris water maze (MWM) as a measure of visuospatial processing. Lesioned rats were significantly impaired in visuospatial processing, but not visuomotor coordination, relative to sham rats. In a 2nd experiment, rats were pretrained on a delayed spatial alternation task (T maze) before MWM training. Pretraining reversed the visuospatial deficit caused by the lesions as compared with nonpretrained rats. Results suggest that lateral deep cerebellar nuclei contribute to visuospatial processing with a negligible contribution to visuomotor skills and that visuospatial deficits resulting from lateral nuclei damage can be reversed with pretraining on aspatial working memory task.

Animals↗

PubMed2002

Dendritic spine and dendritic field characteristics of layer V pyramidal neurons in the visual cortex of fragile-X knockout mice.

Fragile-X syndrome is a common form of mental retardation resulting from the inability to produce the fragile-X mental retardation protein. The specific function of this protein is unknown; however, it has been proposed to play a role in developmental synaptic plasticity. Examination of human brain autopsy material has shown that fragile-X patients exhibit abnormalities in dendritic spine structure and number, suggesting a failure of normal developmental dendritic spine maturation and pruning in this syndrome. Similar results using a knockout mouse model have previously been described; however, it was noted in retrospect that the mice used in that study may have carried a mutation for retinal degeneration, which may have affected cell morphology in the visual cortex of those animals. In this study, dendritic spines on layer V pyramidal cells of visual cortices, taken from fragile-X knockout and wild-type control mice without the retinal degeneration mutation and stained using the Golgi-Cox method, were investigated for comparison with the human condition. Quantitative analyses of the lengths, morphologies, and numbers of dendritic spines, as well as amount of dendritic arbor and dendritic branching complexity, were conducted. The fragile-X mice exhibited significantly more long dendritic spines and significantly fewer short dendritic spines than control mice. Similarly, fragile-X mice exhibited significantly more dendritic spines with an immature-like morphology and significantly fewer with a more mature type morphology. However, unlike the human condition, fragile-X mice did not exhibit statistically significant dendritic spine density differences from controls. Fragile-X mice also did not demonstrate any significant differences from controls in dendritic tree complexity or dendritic arbor. Long dendritic spines with immature morphologies are characteristic of early development or a lack of sensory experience. These results are similar to those found in the human condition and further support a role for the fragile-X mental retardation protein specifically in normal dendritic spine developmental processes. They also support the validity of these mice as a model of fragile-X syndrome.

Animals↗

PubMedDate not supplied

Exercise, experience and the aging brain.

While limited research is available, evidence indicates that physical and mental activity influence the aging process. Human data show that executive functions of the type associated with frontal lobe and hippocampal regions of the brain may be selectively maintained or enhanced in humans with higher levels of fitness. Similarly enhanced performance is observed in aged animals exposed to elevated physical and mental demand and it appears that the vascular component of the brain response may be driven by physical activity whereas the neuronal component may reflect learning. Recent results have implicated neurogenesis, at least in the hippocampus, as a component of the brain response to exercise, with learning enhancing survival of these neurons. Non-neuronal tissues also respond to experience in the mature brain, indicating that the brain reflects both its recent and its longer history of experience. Preliminary measures of brain function hold promise of increased interaction between human and animal researchers and a better understanding of the substrates of experience effects on behavioral performance in aging.

Aged↗