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PubMed1995

Factors influencing the repair and adaptation of muscles in aged individuals: satellite cells and innervation.

From the standpoint of structure, the loss of muscle mass could be attributed to the loss of muscle fibers, the reduction of volume of persisting muscle fibers, or both. This review will concentrate upon factors that could contribute to the presence of thin muscle fibers in old muscles. One mechanism that could account for the presence of a population of thin muscle fibers is the loss of innervation due to the death or the remodeling of motor units in aging muscles. If the denervated muscle fibers fail to become reinnervated, or if they are unable to respond to reinnervation by new nerve terminals, they would undergo a progressive atrophy. If muscle fibers are damaged through exercise, direct trauma or other causes, they would degenerate and regenerate. Early regenerating muscle fibers are thinner than normal. If the regenerating muscle fibers are non-innervated, regeneration will not be complete; instead the regenerating muscle fibers will atrophy. All of the above mechanisms could contribute to an overall reduction in muscle mass. This review ends with an enumeration of outstanding questions concerning muscle atrophy and its reversal in old individuals.

Adaptation, Physiological↗
PubMed1996

Cosmetic denervation of the muscles of facial expression with botulinum toxin. A dose-response study.

BACKGROUND: Botulinum toxin has been used for facial hemispasm, strabismus, and blepharospasm. Recently it has been advocated to treat the frown lines. We have extended this program to treatment of other muscles of facial expression. METHODS: Botulinum toxin is injected into the muscles of facial expression in two or three sessions to produce a temporary loss of muscle tone. A standard method of cooling, injection, and compression was developed to minimize pain and bruising. OBJECTIVE: To complete a dose-response study to document the optimum timing and amount of toxin needed for each muscle group. RESULTS: Two to five Botulinum toxin units per muscle was as adequate as higher doses. Toxin that was reconstituted 30 days earlier produced the same loss of muscle tone as freshly mixed toxin. With two or three injection sessions loss of muscle tone lasted for up to 1 year. CONCLUSION: Botulinum toxin is highly effective as an adjuvant therapy for facial rejuvenation. This minor surgical procedure can temporarily reduce the lines on the upper face and produce a pleasing effect. With proper dosing and dilution this rejuvenation program becomes cost effective.

Adult↗
PubMed2001

Maturation of muscle properties and its hormonal control in an adult insect.

The oviposition of female locusts requires longitudinal muscles to tolerate remarkable lengthening. Whether this ability together with concomitant properties develops during maturation or is present throughout life was investigated. The properties of the locust abdominal muscles involved in oviposition behaviour were investigated with respect to their maturation, segment- and gender-specificity and regulation by juvenile hormone (JH). Muscles from the sixth abdominal segment (an oviposition segment) of mature females (>18 days old) were able to tolerate large extensions (>8 mm). At this length, muscles were still able to generate considerable neurally evoked twitch tension. In contrast, muscle fibres from females less than 5 days old did not tolerate extension of more than 4 mm. At this length, tension generation was negligible. The maximum tension generated at different stimulus frequencies was significantly higher in muscles of females more than 18 days old than in females less than 5 days old. Furthermore, the cross-sectional area of muscle fibres increased significantly during reproductive development. Current-clamp recordings from denervated muscle fibres of females more than 18 days old revealed their ability to generate overshooting action potentials. The potentials were tetrodotoxin (TTX)-insensitive (0.5 micromol l(-1) TTX), but were blocked by Cd(2+) (50 micromol l(-1)) or nifedipine (50 micromol l(-1)), which suggests the involvement of L-type Ca(2+) channels. Action potentials recorded from females less than 5 days old differed considerably in amplitude and shape from those recorded from females more than 18 days old, suggesting their maturation during the first 2 weeks of adult life. Inactivation of the corpora allata (CA) by precocene inhibited the maturation of these muscle properties, whereas injection of JH into precocene-treated females reversed this effect. Homologous muscles from the third abdominal segment (a non-oviposition segment, M169) and muscles from males (M214) revealed no comparable changes, although some minor changes occurred during reproductive development. The results suggest a gender- and segment-specific maturation of muscle properties that is related to reproductive behaviour and controlled by JH.

Abdominal Muscles↗
PubMed1984

[Non-quantum release of acetylcholine from motor nerve endings and denervation changes in muscle fiber membranes in the rat following blockade of axonal transport].

On the 5th day after blockade of axonal transport with colchicine in rat the resting potential of diaphragm muscle fibre decreased, input resistance increased and the difference between postsynaptic and extrasynaptic membrane in this respect disappeared; extrasynaptic sensitivity to acetylcholine, anode breakdown and tetrodotoxin-resistant action potentials appeared almost in the same form as after nerve section. Application of colchicine to motor nerve, in contrast to nerve section, did not disrupt quantal and non-quantal acetylcholine secretion in motor nerve endings and did not stop muscle contractile activity. The size of non-quantal acetylcholine secretion was estimated by the amplitude of muscle membrane hyperpolarisation in the presence of curare in solution after preliminary acetylcholinesterase inhibition with armin. The data confirm the suggestion that the neurotrophic control of skeletal muscle fibre membrane in mammals is carried out by substances transported to muscle by axonal flow with participation of impulse activity. Synaptic acetylcholine secretion from motor nerve endings in non-quantal form does not play a marked role in neurotrophic control of muscle fibre membrane.

Acetylcholine↗
PubMed1978

Reinnervation of partially denervated rat soleus muscle.

The reinnervation of partially denervated rat soleus muscles by their interrupted, regenerating motor axons has been examined in adult white rats. If reinnervation occurred after the remaining, intact motor axons had sprouted to their full, maximal extent, then the regenerating axons formed synapses preferentially with denervated muscle fibers and not with fibers innervated by sprouts. The sprouted motor units retained their size as if no reinnervation had occurred. On the other hand, if reinnervation occurred early during the sprouting process, the sprouting motor units were never able to attain their maximal size. Further, some muscle fibers became innervated by both sprouted and regenerating axons. These "hyperinnervated" fibers lost their dual innervation within a few weeks. The sprouted axons seemed to be the nerve fibers preferentially eliminated from these hyperinnervated fibers, since during the loss of hyperinnervation the sprouted motor units decreased in size while the motor units formed by the regenerating axons did not change in size. It is proposed that the occurrence of hyperinnervation is influenced by the amount of time sprouting axons have to consolidate their synapses with muscle fibers. Further, it is proposed that on muscle fibers which can become hyperinnervated, the sprouted motor neurons are at a disadvantage in the competition for maintenance because of their larger unit sizes.

Animals↗
PubMed1975

Contractile repriming of single muscle fibers: inactivation and tubular diffusion.

Following maximal potassium contractures of isolated single fibers from Rana pipiens, a brief recovery period is required to restore the ability to produce maximal tension by subsequent depolarization. At normal potassium concentration (2.5 mM), there is a minimal lag time of 5 s before any tension is produced by a second exposure to elevated K+; half-maximal tension can be produced in 13 s. The rate of repriming is directly related to the square of the fiber radius and is slowed by lowering external calcium concentration (1.5-0.4 mM). There is no significant difference in any of these respects between normal fibers and fibers dissected from semitendinosus muscles which had been chronically denervated for periods of up to 8 wk. Increased potassium concentration (5-20 mM) in the recovery solution decreased the steady-state repriming level, affecting denervated fibers more than controls. No repriming occurred at concentrations above 20 mM (-48 mV membrane potential.) At these intermediate concentrations, repriming was less complete in denervated muscle, reflecting the increased speed of delayed contractile inactivation. From the times to 50% repriming, which were proportional to the square of fiber radius, we estimated an upper limit for the diffusion coefficient for K+ in the transverse tubular system of 0.3 X 10(-6) cm2/s for both control and chronically denervated fibers.

Animals↗
PubMed2001

Reinnervation of the biceps brachii muscle following cotransplantation of fetal spinal cord and autologous peripheral nerve into the injured cervical spinal cord of the adult rat.

In order to compensate the loss of motoneurons resulting from severe spinal cord injury and to reestablish peripheral motor connectivity, solid pieces of fetal spinal cord, taken from embryonic day 14 rat embryos, were transplanted into unilateral aspiration lesions of the cervical spinal cord of adult rats. Concomitantly, one end of a 3.5-cm autologous peripheral nerve graft was put in close contact with the embryonic graft; the other end was sutured to the distal stump of the musculocutaneous nerve which innervate the biceps brachii muscle. The animals were examined 3 and 6 months after surgery. Following intramuscular injection of horseradish peroxidase, retrograde axonal labeling studies indicated that both transplanted and host spinal neurons were able to extend axons all the way through the peripheral nerve graft and nerve stump, up to the reconnected muscles. The labeled cells in the transplant were generally observed close to the intraspinal tip of the peripheral nerve graft. Retrograde axonal tracing, as well as electrophysiological and histological data, demonstrated the sensory and motor reinnervation of the reconnected muscles. This muscular reinnervation was able to reverse the atrophic changes observed in the denervated muscle. In control experiments, the extraspinal end of the peripheral nerve graft was ligatured in order to compare the differentiation of the transplanted neurons and the survival of their growing axons with or without their muscular targets. Six months after both types of surgery, large-size grafted neurons, identified as motoneurons by immunocytochemistry for peripherine and calcitonin gene-related peptide, were only observed in fetal spinal cord transplants which were connected to denervated muscles, thus demonstrating the trophic influence of the muscle target on the survival and differentiation of the transplanted neurons and on the maintenance of the axons they had grown into the peripheral nerve graft.

Animals↗
PubMed1989

Expression of cytotactin in the normal and regenerating neuromuscular system.

Cytotactin is an extracellular glycoprotein found in a highly specialized distribution during embryonic development. In the brain, it is synthesized by glia, not neurons. It is involved in neuron-glia adhesion in vitro and affects neuronal migration in the developing cerebellum. In an attempt to extend these observations to the peripheral nervous system, we have examined the distribution and localization of cytotactin in different parts of the normal and regenerating neuromuscular system. In the normal neuromuscular system, cytotactin accumulated at critical sites of cell-cell interactions, specifically at the neuromuscular junction and the myotendinous junction, as well at the node of Ranvier (Rieger, F., J. K. Daniloff, M. Pinçon-Raymond, K. L. Crossin, M. Grumet, and G. M. Edelman. 1986. J. Cell Biol. 103:379-391). At the neuromuscular junction, cytotactin was located in terminal nonmyelinating Schwann cells. Cytotactin was also detected near the insertion points of the muscle fibers to tendinous structures in both the proximal and distal endomysial regions of the myotendinous junctions. This was in striking contrast to staining for the neural cell adhesion molecule, N-CAM, which was accumulated near the extreme ends of the muscle fiber. Peripheral nerve damage resulted in modulation of expression of cytotactin in both nerve and muscle, particularly among the interacting tissues during regeneration and reinnervation. In denervated muscle, cytotactin accumulated in interstitial spaces and near the previous synaptic sites. Cytotactin levels were elevated and remained high along the endoneurial tubes and in the perineurium as long as muscle remained denervated. Reinnervation led to a return to normal levels of cytotactin both in inner surfaces of the nerve fascicles and in the perineurium. In dorsal root ganglia, the processes surrounding ganglionic neurons became intensely stained by anticytotactin antibodies after the nerve was cut, and returned to normal by 30 d after injury. These data suggest that local signals between neurons, glia, and supporting cells may regulate cytotactin expression in the neuromuscular system in a fashion coordinate with other cell adhesion molecules. Moreover, innervation may regulate the relative amount and distribution of cytotactin both in muscle and in Schwann cells.

Animals↗
PubMed1998

Fast to slow transformation of denervated and electrically stimulated rat muscle.

1. Denervated fast extensor digitorum longus (EDL) muscles of adult rats were stimulated electrically for up to 4 months with a slow pattern resembling the activity in soleus (Sol) motor units and examined with antibodies against myosin heavy chains (MHCs). 2. The normal EDL contained, on average, 45% type IIB, 29% type IIX, 23% type IIA and 3% type I fibres. All type IIB and almost all type IIX fibres disappeared during the first 3 weeks of stimulation. They were replaced by type IIA and type I fibres, whose percentages increased to about 75 and 15, respectively. Type IIA fibres remained at 75% for nearly 2 months and were then gradually replaced by type I fibres during the next 2 months. The transformation occurred sequentially in the order IIB/IIX-->IIA-->I, the first step (IIB/IIX-->IIA) occurring after a short delay (2 weeks) and the last step (IIA-->I in originally IIB or IIX fibres) after a long delay (> 2 months). During the transformation coexpression of MHCs occurred. 3. It appears that the transformation to type I fibres occurred in pre-existing type II fibres since no signs of fibre damage or regeneration were observed. 4. Normal EDL was also stimulated through an intact nerve with the same pattern for up to 37 days. The effects on fibre type distributions were identical to those observed in the denervated EDL. The result indicated that the Sol-like pattern of evoked muscle activity, rather than nerve-derived trophic influences or denervation per se, was primarily responsible for the fast to slow transformation.

Animals↗
PubMed1993

Congruity of acetylcholine receptor, acetylcholinesterase, and Dolichos biflorus lectin binding glycoprotein in postsynaptic-like sarcolemmal specializations in noninnervated regenerating rat muscles.

Noninnervated regenerating muscles are able to form focal postsynaptic-like sarcolemmal specializations either in places of the former motor endplates ("junctional" specializations) or elsewhere along the muscle fibers (extrajunctional specializations). The triple labeling histochemical method was introduced to analyse the congruity of focalization in such specializations of 3 synaptic components: acetylcholinesterase (AChE), acetylcholine receptor (AChR), and a specific synaptic glycoprotein which binds Dolichos biflorus lectin (DBAR). Noninnervated regenerating soleus and extensor digitorum longus (EDL) muscles of the rat were examined and compared with denervated muscles of neonatal and adult rats. All junctional sarcolemmal specializations in noninnervated regenerating muscles accumulated AChE and AChR. Localization of the 2 components was identical within the limits of resolution of the method. DBAR could not be demonstrated in junctional specializations in 17-day-old regenerating muscles. It seems that an agrin-like inducing substance in the former junctional basal lamina invariably triggers the accumulation of both AChE and AChR in the underlying sarcolemma of the regenerating muscle fiber. However, accumulation of DBAR would probably require the presence of the motor nerve. In most of the extrajunctional sarcolemmal specializations in 8-day-old regenerating soleus and EDL muscles, both AChE and AChR accumulated. However, about 10 percent of AChE accumulations lacked AChR and about 35% of AChR accumulations lacked AChE. Even greater variability was observed in 17-day-old regenerating muscles. The presence of DBAR in the extrajunctional postsynaptic-like sarcolemmal specializations could not be demonstrated. Similar extrajunctional sarcolemmal specializations were observed in denervated postnatal rat muscles. About 70% contained both AChE and AChR, and 30% contained only AChR, but none contained DBAR. In denervated mature muscles, sparse extrajunctional AChR accumulations did not contain detectable amounts of AChE. The ability to form complex postsynaptic-like sarcolemmal specializations in the absence of nerve, which is probably inherent to noninnervated immature muscle fibers, may be reduced with muscle maturation. Variable accumulation of individual components in the postsynaptic-like specializations indicates that different triggering factors may be involved in their accumulation or, at least, the mechanisms of their accumulation can function relatively independently.

Acetylcholinesterase↗
PubMed1993

Immunohistochemical identification of muscle fiber types in normal and degenerated muscles.

Myosin ATPase reactions are generally used to differentiate between muscle fibers. However, those reactions have disadvantages including the need for delicate pH control and preincubation under non-physiological pH. Furthermore enzyme activity is only an indirect reflection of myofilament characteristics. In this study, an immunohistochemical method with anti-slow and anti-fast myosin heavy chain antibodies was used to observe: 1) whether muscle fiber types could be distinguished in degenerated muscles, 2) immunoreactivity of type 2C fibers in denervated muscles, and 3) discrepancies in structural disorders. Thirty one muscle biopsies which included neurogenic, myogenic, and control muscles were examined. Muscle fiber types were recognized in normal and in severely degenerated muscles. Type 2C muscle fibers were not necessarily constantly immunoreactive to both anti-slow and anti-fast myosin antibodies. In some targetoid fibers sites with absence of myosin ATPase activity had the same or rather higher immunoreactivity. Some muscle fibers undergoing fiber-type transformation showed discrepancies in reactivity between enzyme- and immuno-reactivity. This immunohistochemical method is capable of observing changes of muscle fibers during denervation, reinnervation, and also sports activity.

Adolescent↗
PubMed1990

Role of different proteolytic systems in the degradation of muscle proteins during denervation atrophy.

In order to clarify the cellular mechanisms of denervation atrophy of skeletal muscle, we have studied protein turnover in denervated and control rat soleus muscles in vitro under different conditions. By 24 h after cutting the sciatic nerve, overall protein breakdown was greater in the denervated soleus than in the contralateral control muscle, and by 3 days, net proteolysis had increased about 3-fold. Since protein synthesis increased slightly following denervation, the rise in proteolysis must be responsible for the muscle atrophy and the differential loss of contractile proteins. Like overall proteolysis, the breakdown of actin (as shown by 3-methyl-histidine production by the muscles) increased each day after denervation and by 3 days was 2.5 times faster than in controls. Treatments that block the lysosomal and Ca2(+)-dependent proteolytic systems did not reduce the increase in overall protein degradation and actin breakdown in the denervated muscles (maintained in complete medium at resting length). However, the content of the lysosomal protease, cathepsin B, increased about 2-fold by 3 days after denervation. Furthermore, conditions that activate intralysosomal proteolysis (incubation without insulin or amino acids) stimulated proteolysis 2-3-fold more in the denervated muscles than in controls. Also, incubation conditions that activate the Ca2(+)-dependent pathway (incubation with Ca2+ ionophores or allowing muscles to shorten) were 2-3 times more effective in enhancing overall proteolysis in the denervated muscle. None of these treatments affected 3-methylhistidine production. Thus, multiple proteolytic systems increase in parallel in the denervated muscle, but a nonlysosomal process (independent of Ca2+) appears mainly responsible for the rapid loss of cell proteins, especially of myofibrillar components.

Actins↗