Muscle Of Aged Mice Research Articles

O-384 - Neural cell adhesion molecule in aged mouse muscle.

Expression of the neural cell adhesion molecule was compared in endplate and non-endplate regions of skeletal muscles of mature and old CBF-1 mice, in order to determine whether age-related changes in neuromuscular morphology were correlated with age changes in neural cell adhesion molecule expression. Three muscles were examined: two (soleus and sternomastoid) showed age-related regionalization of nerve terminals as one manifestation of increased synaptic remodelling while the third (diaphragm) did not. Relative neural cell adhesion molecule content in these muscles was measured by densitometry of immunoblots after concentration by affinity chromatography. Expression of the major 140,000 mol. wt form of neural cell adhesion molecule, which was most abundant in the endplate region, was increased in sternomastoid and soleus of old compared to adult mouse, but was unchanged with age in diaphragm. A 70,000-80,000 mol. wt presumably proteolytic polypeptide fragment of neural cell adhesion molecule was increased in immunoblots of all old muscles. Immunocytochemical studies of skeletal muscles showed no difference in neural cell adhesion molecule cellular distribution in mature vs old mice, but in motor nerve of sternomastoid, the number of neural cell adhesion molecule-positive nerve fibers was increased in old mice. Several lines of evidence indicated that partial denervation was rare in old CBF-1 mice, and therefore could not account for the findings above. Selective increase of 140,000 mol. wt neural cell adhesion molecule expression in the junctional regions of those muscles of old mice which show neuromuscular remodelling indicates that this adhesion molecule may play a role in the age-related instability of motor nerve terminals.

Choline acetyltransferase and acetylcholinesterase activities in muscles of aged mice

The activities of choline acetyltransferase (CAT) and acetylcholinesterase (AChE) were assayed in intact diaphragm, extensor digitorum longus (EDL), and soleus muscles or their homogenates of young (2–6 months) and aged (24–34 months) mice. CAT activity (per mg of protein) was significantly higher in diaphragm and soleus of old mice in comparison with the young but the age change in EDL was negligible. On the other hand, AChE activity (per mg of protein) was significantly higher in EDL of old mice but in diaphragm and soleus muscles the enzyme activity did not show any significant change statistically. The diaphragm muscle was divided into two fractions, one being neuromuscular (NM) fraction and the other the remainder of the muscle (M fraction). No appreciable change in the ratio of the enzyme activities of NM fraction to the one of M fraction was obtained between the young and aged preparations. Thus, it seems likely that there is an age-related change in CAT and AChE activities which might be affected by the degree to which muscle activity is maintained.

The effects of enforced running on the gastrocnemius muscle in aging mice: An ultrastructural study

C57BL/6J mice (6, 19 and 27 months old) were trained in an electrically driven treadmill for a total period of 10 weeks. The training program started with 5 min. run per day and reached a maximum of 30 min. perday. Light and electron microscopy examinations of the gastrocnemius muscle showed that in young animals endurance training did not evoke any appreciable changes. In contrast, both test animals and their controls in the old group revealed clear signs of muscle cell atrophy which for the most part was accompanied by focal loss of myofilaments, mitochondrial changes and an increase in the amount of endomyseal collagen fibrils. In the old-trained group, the most obvious abnormally comprised of multiplication of both the T-tubules and of the tubules of the sarcoplasmic reticulum. Consequently, most of these animals showed the formation of tubular aggregates in their gastrocnemius muscle. Hence, it appears that endurance training in old animals tends to enhance the regressive changes that accompany the aging process of mammalian skeletal muscle.