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M J Forster

Publications and source records attributed to M J Forster.

42 records · Page 3Linked to original sources
PubMed1982

Development of serotonin-mediated behavioral inhibition in the hyperthyroid mouse.

Experimental hyperthyroidism was induced in neonatal mice by thyroxine injections at 1-3 days of age. Control and thyroxine-treated mice were subsequently tested daily for locomotor activity following injections of methysergide, a serotonin antagonist, or saline from 10 through 15 days of age. Although thyroxine-treated mice were more active than controls, the ontogeny of methysergide-induced disinhibition of locomotor activity was similar for both thyroxine-treated and control mice. The results suggest that the early maturation of serotonin-mediated inhibition of behavioral arousal is not affected by thyroxine-accelerated development. Results are discussed in terms of the specificity of the pharmacological agent, methysergide.

Aging↗
PubMedDate not supplied

The benzodiazepine receptor inverse agonist RO 15-3505 reverses recent memory deficits in aged mice.

The benzodiazepine receptor partial inverse agonist RO 15-3505 was tested for its ability to improve impaired recent memory of aged mice. All mice successfully acquired a learning set for accurate identification of the correct arm of a T-maze and could perform with nearly 100% accuracy after 1-min delays. However, performance of the aged mice approached chance levels after 2-h delays. When injected just before testing on a series of 2-h retention tests, RO 15-3505 (from 2.5-3505 (from 2.5-10.0 mg/kg) resulted in a marked improvement of response accuracy. These results confirm the role of benzodiazepine receptor mechanisms in the modulation of memory processes, and suggest that the memory-facilitating effects RO 15-3505 or similar benzodiazepine receptor ligands may be generalized to aged rodents with impaired memory function.

Aging↗
PubMedDate not supplied

Exercise does not modify spatial memory, brain autoimmunity, or antibody response in aged F-344 rats.

Old F-344 rats were given endurance training over a 10-week period on a motorized treadmill. This treatment resulted in substantial heart-to-body weight ratio increases, indicative of effective training. To determine whether endurance training might alter some of the known immune system and cognitive changes observed during aging, exercised old rats were compared to nonexercised old and young controls on three variables: in vivo antigen-specific immune activity, brain-reactive antibody formation, and spatial memory. The exercise training did not influence any of these measures in the old rats. Both groups of old rats showed poorer antibody response to a specific antigen, more brain-reactive antibody formation, and poorer spatial memory than the young controls. There was, however, a significant relationship between brain-reactive antibody formation and spatial memory performance, regardless of training condition.

Aging↗
PubMedDate not supplied

Autoimmunity and age-associated cognitive decline.

It is suggested that the immune system may play a role in the etiology of age-associated cognitive decline and/or Alzheimer's disease. The relationship between brain-reactive antibodies (BRA) and age-associated cognitive dysfunction is reviewed and discussed. A parallel relationship between BRA increases with age and decline of avoidance learning capacity is described in mouse models. Transfer of immunity from old to young mice was found to accelerate both age-related formation of brain-reactive antibodies and age-related decline of avoidance learning capacity. Short-lived mouse genotypes with accelerated autoimmunity were found to show accelerated age-related declines in their ability to acquire an avoidance response when compared with nonautoimmune mice. Overall, these findings suggest that the immune system could be an important target for development of intervention strategies aimed at extending the intellectually competent period of life. Mice in which autoimmunity is accelerated may be useful as models for the development of such interventions.

Aging↗
PubMedDate not supplied

Estimating age-related changes in psychomotor function: influence of practice and of level of caloric intake in different genotypes.

This article presents a discussion of some key considerations in the measurement of age-related changes in psychomotor function of mice. We illustrate that "standard" measures of psychomotor performance, such as running speed on a rotorod task, are highly sensitive to practice effects. Examples are cited in which failure to assess practice effects can influence conclusions regarding the magnitude and rate of change in psychomotor capacity as a function of age. A second set of examples is focused on estimating the effect of an experimental intervention, caloric restriction, on age-related changes in psychomotor performance. These examples show that psychomotor performance at a given age may vary directly, and reversibly, with the level of caloric intake. Independent of such reversible effects, the level of caloric intake can also modulate the rate of change in capacity as a function of age. It is concluded that reversible, short-term effects must be considered in estimating the effect of an experimental intervention on the rate of age-associated change in psychomotor function.

Aging↗