The Role of Peroxide in the Biological Effects of Irradiated Broth.
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Biomedical subjects
Publications and source records attributed to W S Stone.
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Considerable evidence indicates that epinephrine regulates memory storage processing in young animals. Recent findings suggest that hyperglycemia subsequent to epinephrine release or injection may mediate the hormone's effects on memory. This paper reviews findings demonstrating that epinephrine and glucose treatments attenuate age-related memory impairments in rodents and humans. Additional results suggest that, in aged human and animal subjects, poor glucose regulation predicts memory performance of individual subjects.
Age-related changes in sleep are observed in many species, including rats and humans. Old rats often exhibit less total and paradoxical sleep, shorter sleep bouts and more random sleep-wake periods across 24 hours, than young rats. This paper evaluates recent evidence that deterioration of selected sleep parameters, usually involving levels of paradoxical sleep or durations of sleep bouts, may be related to deterioration of memory in old rats. Similar findings are reviewed with respect to young animals with different forms of experimentally-induced amnesia. Furthermore, a drug that enhances memory in rats and old humans, glucose, also enhances paradoxical sleep in old rats. These data suggest the utility of sleep measures as neurobiological markers of memory dysfunction in old rats.
The goal of this experiment was to determine the correlations among different behavioral and neurobiological measures in aged rats. Aged Sprague-Dawley rats were given a battery of cognitive and sensorimotor tests, followed by electrophysiological assessment of sleep and biochemical measurements of various neurotransmitter systems. The behavioral tests included the following: Activity level in an open field; short-term and long-term memory of a spatial environment as assessed by habituation: spatial navigation, discrimination reversal, and cue learning in the Morris water pool; spatial memory in a T-maze motivated by escape from water; spatial memory and reversal on the Barnes circular platform task; passive avoidance; motor skills. Sleep was assessed by electrographic cortical records. The following neurotransmitter markers were examined: Choline acetyltransferase; the density of nicotinic, benzodiazepine and glutamine receptors in the cortex and caudate nucleus; endogenous levels of norepinephrine, dopamine, and serotonin in the cortex and hippocampus. The duration of bouts of paradoxical sleep was strongly correlated with several cognitive measures and selected serotonergic markers. This finding suggests that changes in sleep patterns and brain biochemistry contribute directly to deficits in learning and memory, or that the same neurobiological defect contributes to age-related impairments in sleep and in learning and memory.
Age-related deficits in memory are correlated with deficits in paradoxical sleep and poor glucose tolerance in rats. The present experiment used a longitudinal design to determine whether memory or glucose tolerance in middle-aged rats could predict deficits in memory, sleep, and glucose tolerance in old age. Correlations were obtained between spontaneous alternation scores and glucose tolerance levels in middle age (14 months) and inhibitory avoidance, daytime sleep, and glucose tolerance levels in old age (24 months). Spontaneous alternation scores, but not glucose tolerance levels, predicted performance on all 3 behavioral and biological measures in old age. Measures of functional integrity, such as memory, may be sensitive predictors of subsequent age-related change in specific cognitive and neurobiological systems.
Despite the complexities of schizophrenia, notable progress has been achieved in its diagnosis and treatment over the last 25 years. In this article we review the genetic research that provides the foundation for continued advances. One of the bases of our current understanding involves the observation that schizophrenia often runs in families. The development and utilization of stringent, reliable diagnostic criteria, together with the advent of modern family, twin, and adoption paradigms, demonstrate the importance of genetic factors in understanding the familial basis of the disorder. Refinements in diagnostic criteria have also enabled advances in understanding the likely mode--or modes--of genetic transmission of both schizophrenia and related disorders. After reviewing representative studies in these areas, we examine genetic linkage studies and our progress toward identifying the genes that cause schizophrenia. Although consistent results have been difficult to obtain and much work remains to be done, evidence for areas of vulnerability has been converging at particular chromosomal sites (e.g., 6p, 8p, and 22q), allowing for cautious optimism. Finally, we discuss challenges and prospects for the new millennium, including the clinical and ethical implications of genetic investigations.