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Biomedical subjects

M I Talan

Publications and source records attributed to M I Talan.

At least 55 records · Page 3Linked to original sources

Age-related decline in cold tolerance can be retarded by brain stimulation.

The sharp decline in capacity of old C57BL/6J male mice to maintain body temperature during 3-hr cold exposure can be delayed and even partly restored after 15, 30-min, daily sessions of hypothalamic self-stimulation. In control experiments it was demonstrated that electrical stimulation of "rewarding" areas of hypothalamus itself is sufficient for improvement of the age-related deterioration of thermoregulatory ability.

Acclimatization↗

Analysis of hypothalamic self-stimulation with stimulation of fixed duration.

Correlation between the frequency of bar pressing and the frequency of hypothalamic self-stimulation of fixed duration was studied in cats during changes in strength of the stimulating current. Strong direct correlation was found between the frequency of bar pressing and the frequency of self-stimulation, whereas strong negative correlation was found between the frequency of pressing and the animal's "work effectiveness." It is suggested that the strongest motivation arises in the presence of an optimal strength of self-stimulation, giving rise to maximal frequency of bar pressing.

Animals↗

Metabolic heat production and cold tolerance during cold stress of different intensity of adult and aged male C57BL/6J mice.

Adult and aged male C57BL/6J mice were subjected to a 3-h cold stress test at either 24 degrees C, 18 degrees C, 12 degrees C, or 6 degrees C. Body mass was measured before the test, and colonic temperature, O2 consumption, and CO2 production were measured during the test. The slopes of colonic temperature over time of test and the mean metabolic heat production were calculated for each animal. While adult mice had a relatively small reduction in colonic temperature during the test at all four ambient temperatures, in the aged mice ambient temperatures resulted in steeper reductions of colonic temperature. In adult mice, an increase in metabolic heat production was proportional to ambient cold. The thermogenic response of aged mice at 24 degrees C and at 18 degrees C was similar to adult mice, suggesting that the ability of aged mice to respond to cold by increasing heat production does not diminish with age. However, in aged mice metabolic heat production at 12 degrees C and 6 degrees C was significantly below that of adult mice, which indicated a reduced capacity for thermogenesis.

Aging↗

Oxygen consumption in adult and AGED C57BL/6J mice during acute treadmill exercise of different intensity.

Submaximal and maximal oxygen consumption was determined in untrained adult and aged male C57BL/6J mice during treadmill running. Each of 12-month-old (ADULT) and 24-month-old (AGED) male mice was tested on a motor-driven treadmill once at different speeds. VO2 was measured before, during, and after exercise by means of indirect calorimetry in metabolic treadmill chambers. The resting VO2 averaged 3064.67 +/- 87.71 mL/kg/h for ADULT mice and 2472.95 +/- 69.41 mL/kg/h for AGED mice. During exercise, VO2 increased linearly with work intensity (running speed): ADULT mice--from 5908.06 +/- 422.35 mL/kg/h at 3 m/min to 10861.99 +/- 174.03 mL/kg/h at 25 m/min; AGED mice--from 5217.25 +/- 263.26 mL/kg/h at 3 m/min to 7817.32 +/- 290.28 mL/kg/h at 20 m/min. Further increase of the running speed resulted in a decline of VO2 in ADULT and refusal to run in AGED mice. The results of this study demonstrated that in untrained C57BL/6J mice VO2max and maximal exercise capacity declined with age. At the same absolute and relative workloads, VO2 was lower in AGED mice.

Age Factors↗

Nonshivering thermogenesis during acute cold exposure in adult and aged C57BL/6J mice.

In C57BL/6J adult and aged mice, housed at room temperature (22.5 +/- 1 degrees C), we measured O2 consumption and CO2 production and calculated metabolic heat production under conditions of anesthesia and myorelaxation during acute cold stimulation when body temperature was lowered 7.5 degrees C below control level. An independent group of mice was subjected to a three hour partial physical restraint at 6 degrees C and concentration of uncoupling protein (thermogenin) was measured in interscapular brown adipose tissue mitochondria at different times after cold exposure. Heat production under anesthesia and myorelaxation was about 57-66% lower than in nonanesthetized conditions, but increased significantly during cold stimulation in both age groups. Under anesthesia and myorelaxation before and during cold stimulation aged mice produced about 20% more heat than adult mice. Because in these experiments all sources of facultative thermogenesis, except nonshivering, were suppressed by anesthesia and myorelaxation, and because brown adipose tissue is the major source of nonshivering thermoproduction, we concluded that aged mice housed at room temperature have an increased thermogenesis in brown adipose tissue. This conclusion was also supported by the finding that the concentration of uncoupling protein measured in the mitochondria of brown adipose tissue after single cold exposure was significantly higher in aged than in adult mice. Therefore, we propose that the lower, cold-induced, heat production typically observed in nonanesthetized aged mice may reflect reduced thermogenic capacity of skeletal muscles. While aged mice have less brown adipose tissue than adult animals, the remaining brown adipose tissue may compensate by increasing the concentration of uncoupling protein.

Adipose Tissue, Brown↗

Heat loss during cold exposure in adult and aged C57BL/6J mice.

Metabolic heat production (MHP), colonic temperature (Tco), and nonevaporative (dry) heat loss were measured in ADULT and AGED C57BL/6J male mice during cold exposure. Dry heat loss was assessed as a differential temperature (Td) between incoming and outgoing air through the chamber for indirect calorimetry. The average Td during cold exposure normalized to surface area for ADULT mice was significantly higher than that for the AGED animals (0.0618 +/- 0.0003 degree C/cm2 and 0.0553 +/- 0.0005 degree C/cm2, respectively). Linear regression analysis showed that at the same Tco AGED mice showed lower values of Td normalized to surface area, indicating that at the same body temperature they were losing less heat than ADULT animals. It was concluded that age-related decline in cold tolerance in mice is not due to a lack of ability to reduce heat loss during cold exposure. On the contrary, AGED animals had lower heat loss in comparison with ADULT. We suggest that augmentation of heat conservation mechanisms is an adaptive response to diminishing cold-induced heat production.

Aging↗