Muscle, Skeletal
Sciatic Nerve
Autonomic Denervation
Muscle Proteins
Muscle, Smooth
Sympathectomy
Muscle Fibers, Skeletal
Muscle Contraction
Muscle Development
Muscle Fibers, Fast-Twitch
The effect of denervation and dystrophy on the adaptation of sarcomere number to the functional length of the muscle in young and adult mice. (1/810)
In young animals the elongation of the limb bones increases the functional lengths of the muscles. In adult animals the functional length of a muscle can be increased by immobilizing it in the lengthened position. In both cases the muscle adapts by adding on more sarcomeres in series. The role of the nerve supply in this adaptation has been investigated using denervated muscles and muscles from dystrophic animals where there is thought to be an abnormality of the nerve supply. Postnatal sarcomere addition in denervated muscles falls short of that of controls. Although this might mean that the nerve supply is necessary for normal addition of sarcomeres, it is just as likely that there is a change in gait resulting from denervation, which affects the sarcomere number. Sarcomere number in fully grown mice is not affected by denervation, nor is the ability of the muscle to adapt to immobilization in the lengthened position. This is true for fast-twitch as well as slow-twitch muscles. In dystrophic muscles postnatal sarcomere addition is normal, although the presence of a few short fibres in the muscle may mean that some muscle fibres cannot adapt to an increase in the functional length of the muscle accompanying bone growth. Adult dystrophic muscle is capable of adapting to immobilization in the lengthened position. However, although the total number of additional sarcomeres is the same as in normal immobilized muscle, they are added on at a slower rate. The experiments show that although denervated and dystrophic muscle fibres are in a state of atrophy they are still capable of adding on sarcomeres in series when the functional length of the muscle is increased. It would appear that the mechanism which enables the muscle to respond in this way to an increased functional length does not involve the nerve supply. This work was supported by a grant from the National Fund for Research into Crippling Diseases. (+info)Specific and innervation-regulated expression of the intermediate filament protein nestin at neuromuscular and myotendinous junctions in skeletal muscle. (2/810)
The intermediate filament proteins nestin, vimentin, and desmin show a specific temporal expression pattern during the development of myofibers from myogenic precursor cells. Nestin and vimentin are actively expressed during early developmental stages to be later down-regulated, vimentin completely and nestin to minimal levels, whereas desmin expression begins later and is maintained in mature myofibers, in which desmin participates in maintaining structural integrity. In this study we have analyzed the expression levels and distribution pattern of nestin in intact and denervated muscle in rat and in human. Nestin immunoreactivity was specifically and focally localized in the sarcoplasm underneath neuromuscular junctions (NMJs) and in the vicinity of the myotendinous junctions (MTJs), ie, in regions associated with acetylcholine receptors (AChRs). This association prompted us to analyze nestin in neurogenically and myogenically denervated muscle. Immunoblot analysis disclosed a marked overall increase of accumulated nestin protein. Similar to the extrajunctional redistribution of AChRs in denervated myofibers, nestin immunoreactivity extended widely beyond the NMJ region. Re-innervation caused complete reversion of these changes. Our study demonstrates that the expression levels and distribution pattern of nestin are regulated by innervation, ie, signal transduction into myofibers. (+info)M2 receptors in genito-urinary smooth muscle pathology. (3/810)
In vitro bladder contractions in response to cumulative carbachol doses were measured in the presence of selective muscarinic antagonists from rats which had their major pelvic ganglion bilaterally removed (denervation, DEN) or from rats in which the spinal cord was injured (SCI) via compression. DEN induced both hypertrophy (505+/-51 mg bladder weight) and a supersensitivity of the bladders to carbachol (EC50=0.7+/-0.1 uM). Some of the SCI rats regained the ability to void spontaneously (SPV). The bladders of these animals weighed 184+/-17 mg, significantly less than the bladders of non voiding rats (NV, 644+/-92 mg). The potency of carbachol was greater in bladder strips from NV SCI animals (EC50=0.54+/-0.1 uM) than either bladder strips from SPV SCI (EC50=0.93+/-0.3 microM), DEN or control (EC50=1.2+/-0.1 microM) animals. Antagonist affinities in control bladders for antagonism of carbachol induced contractions were consistent with M3 mediated contractions. Antagonist affinities in DEN bladders for 4-diphenlacetoxy-N-methylpiperidine methiodide (4-DAMP, 8.5) and para fluoro hexahydrosilodifenidol (p-F-HHSiD, 6.6); were consistent with M2 mediated contractions, although the methoctramine affinity (6.5) was consistent with M3 mediated contractions. p-F-HHSiD inhibited carbachol induced contraction with an affinity consistent with M2 receptors in bladders from NV SCI (pKb=6.4) animals and M3 receptors in bladders from SPV SCI animals (pKb=7.9). Subtype selective immunoprecipitation of muscarinic receptors revealed an increase in total and an increase in M2 receptor density with no change in M3 receptor density in bladders from DEN and NV SCI animals compared to normal or sham operated controls. M3 receptor density was lower in bladders from SPV SCI animals while the M2 receptor density was not different from control. This increase in M2 receptor density is consistent with the change in affinity of the antagonists for inhibition of carbachol induced contractions and may indicate that M2 receptors or a combination of M2 and M3 receptors directly mediate smooth muscle contraction in bladders from DEN and NV SCI rats. (+info)The observation of transplanted embryonic motoneurons in the denervated muscles of adult rats. (4/810)
OBJECTIVE: To observe the survival of embryonic motoneurons after they were transplanted into the denervated skeletal muscles and to find a new method to retard the atrophy of denervated muscles. METHODS: Dissociated embryonic motoneurons prelabled with 5-bromo-2'-deoxyuridine (Brdur) on the embryonic days 12 were injected into the denervated gastrocnemius muscles of adult rats. Then gastrocnemius muscles were processed with Nissl staining, acetylcholinesterase staining and Brdur immunocytochemical staining to show the implanted motoneurons at 9 and 22 weeks post-transplantation. Myofibrillar ATPase staining was used to show the morphology of muscle fibers. The rats in experimental group were implanted with embryonic motoneurons in the predenervation muscles, while the rats in control group were injected with just culture medium without motoneurons. RESULTS: Embryonic motoneurons survived, developed and extended long axons to form neuromuscular junctions with the denervated muscles. The differentiation of muscle fibers and fiber type grouping occurred among bigger fibers in experimental group. The transverse area was smaller and there was no apparent fiber type grouping in control group. CONCLUSIONS: Embryonic motoneurons can survive, develop and reinnervate denervated muscles after being transplanted into denervated muscles. It is worth further investigating on ameliorating the atrophy of denervated muscle. (+info)Cytosolic citrate and malonyl-CoA regulation in rat muscle in vivo. (5/810)
In liver, insulin and glucose acutely increase the concentration of malonyl-CoA by dephosphorylating and activating acetyl-CoA carboxylase (ACC). In contrast, in incubated rat skeletal muscle, they appear to act by increasing the cytosolic concentration of citrate, an allosteric activator of ACC, as reflected by increases in the whole cell concentrations of citrate and malate [Saha, A. K., D. Vavvas, T. G. Kurowski, A. Apazidis, L. A. Witters, E. Shafrir, and N. B. Ruderman. Am. J. Physiol. 272 (Endocrinol. Metab. 35): E641-E648, 1997]. We report here that sustained increases in plasma insulin and glucose may also increase the concentration of malonyl-CoA in rat skeletal muscle in vivo by this mechanism. Thus 70 and 125% increases in malonyl-CoA induced in skeletal muscle by infusions of glucose for 1 and 4 days, respectively, and a twofold increase in its concentration during a 90-min euglycemic-hyperinsulinemic clamp were all associated with significant increases in the sum of whole cell concentrations of citrate and/or malate. Similar correlations were observed in muscle of the hyperinsulinemic fa/fa rat, in denervated muscle, and in muscle of rats infused with insulin for 5 h. In muscle of 48-h-starved rats 3 and 24 h after refeeding, increases in malonyl-CoA were not accompanied by consistent increases in the concentrations of malate or citrate. However, they were associated with a decrease in the whole cell concentration of long-chain fatty acyl-CoA (LCFA-CoA), an allosteric inhibitor of ACC. The results suggest that increases in the concentration of malonyl-CoA, caused in rat muscle in vivo by sustained increases in plasma insulin and glucose or denervation, may be due to increases in the cytosolic concentration of citrate. In contrast, during refeeding after starvation, the increase in malonyl-CoA in muscle is probably due to another mechanism. (+info)Adaptive changes in motor activity associated with functional recovery following muscle denervation in walking cats. (6/810)
In this investigation we examined the changes in the pattern of activity in the medial gastrocnemius (MG) muscle in walking cats following transection of the nerves innervating synergist muscles (lateral gastrocnemius, soleus, and plantaris). Immediately following the nerve transections, there was a large increase in ankle flexion during early stance (from approximately 10 to approximately 30 degrees ) and a marked increase in the magnitude of the MG bursts during stance. We attribute this increase in the magnitude of the MG bursts to an increase in afferent feedback from the abnormally stretched MG muscle. During the week after the nerve transections, there was a progressive decrease in ankle yield. This improvement in ankle function was correlated with an increase in magnitude of two components of the MG bursts; the initial component starting during late swing and ending approximately 40 ms after ground contact, and a late component associated with stance. The time courses of the increases in the initial and late components of the MG bursts were different. Large and significant increases in the late component occurred the day after the nerve transections, whereas increases in the initial component occurred more gradually. This difference in time course was reflected in the kinematics of ankle movement. Over the first few days after the nerve transections, improvement in ankle movement occurred primarily late in the stance phase, and there was little change in ankle yield during early stance. At 1 wk, however, there was a significant reduction in ankle yield during early stance. This decreased yield was most likely due to an increase in stiffness of the MG muscle at the time of ground contact resulting from the increase in magnitude of the initial component of the MG bursts. The increases in the magnitude of the initial and late components of the MG bursts, as well as the improvement in ankle function, depended on use of the leg. All these changes were delayed by immobilizing the leg for 6 days in an extended position. We discuss possible mechanisms underlying the increase in the magnitude of the MG bursts and propose that proprioceptive signals from the stretched MG muscles provide an error signal for rescaling the magnitude of the centrally generated initial component. Our data support the concept that proprioceptive feedback functions to scale the magnitude of feed-forward motor commands to ensure they are appropriate for the biomechanical properties of the musculoskeletal system. (+info)Loss of distal axons and sensory Merkel cells and features indicative of muscle denervation in hindlimbs of P0-deficient mice. (7/810)
Mice lacking the major Schwann cell myelin component P0 show a severe dysmyelination with pathological features reminiscent of the Dejerine-Sottas syndrome in humans. Previous morphological and electrophysiological studies on these mice did not only demonstrate a compromised myelination and myelin maintenance, but were suggestive of an impairment of axons as well. Here, we studied the axonal pathology in P0-deficient mice by quantitative electron microscopy. In addition, we investigated epidermal receptor end organs by immunocytochemistry and muscle pathology by histochemistry. In proximal sections of facial and femoral nerves, axon calibers were significantly reduced, whereas the number of myelin-competent axons was not diminished in 5- and 17-month-old P0-deficient mice. However, in distal branches of the femoral and sciatic nerve (digital nerves innervating the skin of the first toe) the numbers of myelin-competent axons were reduced by 70% in 6-month-old P0-deficient mice. Immunolabeling of foot pads revealed a corresponding loss of Merkel cells by 75%, suggesting that survival of these cells is dependent on the presence or maintenance of their innervating myelinated axons. In addition, quadriceps and gastrocnemius muscles showed pathological features indicative of denervation and axonal sprouting. These findings demonstrate that loss of an important myelin component can initiate degenerative mechanisms not only in the Schwann cell but also in the distal portions of myelinated axons, leading to the degeneration of specialized receptor end organs and impairment of muscle innervation. (+info)Anatomical study of the neural ganglionated plexus in the canine right atrium: implications for selective denervation and electrophysiology of the sinoatrial node in dog. (8/810)
The aim of the present study was to elucidate the topography and architecture of the intrinsic neural plexus (INP) in the canine right atrium because of its importance for selective denervation of the sinoatrial node (SAN). The morphology of the intrinsic INP was revealed by a histochemical method for acetylcholinesterase in whole hearts of 36 mongrel dogs and examined by stereoscopic, contact, and electron microscopes. At the hilum of the heart, nerves forming a right atrial INP were detected in five sites adjacent to the right superior pulmonary veins and superior vena cava (SVC). Nerves entered the epicardium and formed a INP, the ganglia of which, as a wide ganglionated field, were continuously distributed on the sides of the root of the SVC (RSVC). The epicardiac ganglia located on the RSVC were differentially involved in the innervation of the sinoatrial node, as revealed by epicardiac nerves emanating from its lower ganglia that proceed also into the atrial walls and right auricle. The INP on the RSVC (INP-RSVC) varied from animal to animal and in relation to the age of the animal. The INP-RSVC of juvenile dogs contained more small ganglia than that of adult animals. Generally, the canine INP-RSVC included 434+/-29 small, 17+/-4 medium-sized, and 3+/-1 large epicardiac ganglia that contained an estimated 44,700, 6,400, and 2,800 neurons, respectively. Therefore, the canine right atrium, including the SAN, may be innervated by more than 54,000 intracardiac neurons residing mostly in the INP-RSVC. In conclusion, the present study indicates that epicardiac ganglia that project to the SA-node are distributed more widely and are more abundant than was previously thought. Therefore, both selective and total denervation of the canine SAN should involve the whole region of the RSVC containing the INP-RSVC. (+info)Muscle denervation is a medical term that refers to the loss of nerve supply to a muscle or group of muscles. This can occur due to various reasons, such as injury to the nerves, nerve compression, or certain medical conditions like neuromuscular disorders. When the nerve supply to the muscle is interrupted, it can lead to muscle weakness, atrophy (wasting), and ultimately, paralysis.
In denervation, the communication between the nervous system and the muscle is disrupted, which means that the muscle no longer receives signals from the brain to contract and move. Over time, this can result in significant muscle wasting and disability, depending on the severity and extent of the denervation.
Denervation may be treated with various therapies, including physical therapy, medication, or surgical intervention, such as nerve grafting or muscle transfers, to restore function and prevent further muscle wasting. The specific treatment approach will depend on the underlying cause and severity of the denervation.
Denervation is a medical term that refers to the loss or removal of nerve supply to an organ or body part. This can occur as a result of surgical intervention, injury, or disease processes that damage the nerves leading to the affected area. The consequences of denervation depend on the specific organ or tissue involved, but generally, it can lead to changes in function, sensation, and muscle tone. For example, denervation of a skeletal muscle can cause weakness, atrophy, and altered reflexes. Similarly, denervation of an organ such as the heart can lead to abnormalities in heart rate and rhythm. In some cases, denervation may be intentional, such as during surgical procedures aimed at treating chronic pain or spasticity.
Skeletal muscle, also known as striated or voluntary muscle, is a type of muscle that is attached to bones by tendons or aponeuroses and functions to produce movements and support the posture of the body. It is composed of long, multinucleated fibers that are arranged in parallel bundles and are characterized by alternating light and dark bands, giving them a striped appearance under a microscope. Skeletal muscle is under voluntary control, meaning that it is consciously activated through signals from the nervous system. It is responsible for activities such as walking, running, jumping, and lifting objects.
A muscle is a soft tissue in our body that contracts to produce force and motion. It is composed mainly of specialized cells called muscle fibers, which are bound together by connective tissue. There are three types of muscles: skeletal (voluntary), smooth (involuntary), and cardiac. Skeletal muscles attach to bones and help in movement, while smooth muscles are found within the walls of organs and blood vessels, helping with functions like digestion and circulation. Cardiac muscle is the specific type that makes up the heart, allowing it to pump blood throughout the body.
The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.
Motor neurons are specialized nerve cells in the brain and spinal cord that play a crucial role in controlling voluntary muscle movements. They transmit electrical signals from the brain to the muscles, enabling us to perform actions such as walking, talking, and swallowing. There are two types of motor neurons: upper motor neurons, which originate in the brain's motor cortex and travel down to the brainstem and spinal cord; and lower motor neurons, which extend from the brainstem and spinal cord to the muscles. Damage or degeneration of these motor neurons can lead to various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).
Autonomic denervation is a medical term that refers to the interruption or loss of nerve supply to the autonomic nervous system. The autonomic nervous system is the part of the nervous system that controls involuntary actions, such as heart rate, blood pressure, digestion, and pupil dilation.
Autonomic denervation can occur due to various reasons, including surgical procedures, trauma, degenerative diseases, or medical conditions such as diabetes. The interruption of nerve supply can lead to a range of symptoms depending on the specific autonomic functions that are affected.
For example, autonomic denervation in the heart can lead to abnormal heart rhythms or low blood pressure. In the digestive system, it can cause problems with motility and secretion, leading to symptoms such as bloating, constipation, or diarrhea. Autonomic denervation in the eyes can result in pupil abnormalities, dry eyes, or light sensitivity.
Treatment for autonomic denervation depends on the underlying cause and the specific symptoms that are present. In some cases, medication may be used to manage symptoms, while in others, surgical intervention may be necessary to repair or restore nerve function.
Muscle proteins are a type of protein that are found in muscle tissue and are responsible for providing structure, strength, and functionality to muscles. The two major types of muscle proteins are:
1. Contractile proteins: These include actin and myosin, which are responsible for the contraction and relaxation of muscles. They work together to cause muscle movement by sliding along each other and shortening the muscle fibers.
2. Structural proteins: These include titin, nebulin, and desmin, which provide structural support and stability to muscle fibers. Titin is the largest protein in the human body and acts as a molecular spring that helps maintain the integrity of the sarcomere (the basic unit of muscle contraction). Nebulin helps regulate the length of the sarcomere, while desmin forms a network of filaments that connects adjacent muscle fibers together.
Overall, muscle proteins play a critical role in maintaining muscle health and function, and their dysregulation can lead to various muscle-related disorders such as muscular dystrophy, myopathies, and sarcopenia.
Smooth muscle, also known as involuntary muscle, is a type of muscle that is controlled by the autonomic nervous system and functions without conscious effort. These muscles are found in the walls of hollow organs such as the stomach, intestines, bladder, and blood vessels, as well as in the eyes, skin, and other areas of the body.
Smooth muscle fibers are shorter and narrower than skeletal muscle fibers and do not have striations or sarcomeres, which give skeletal muscle its striped appearance. Smooth muscle is controlled by the autonomic nervous system through the release of neurotransmitters such as acetylcholine and norepinephrine, which bind to receptors on the smooth muscle cells and cause them to contract or relax.
Smooth muscle plays an important role in many physiological processes, including digestion, circulation, respiration, and elimination. It can also contribute to various medical conditions, such as hypertension, gastrointestinal disorders, and genitourinary dysfunction, when it becomes overactive or underactive.
Sympathectomy is a surgical procedure that involves interrupting the sympathetic nerve pathways. These nerves are part of the autonomic nervous system, which controls involuntary bodily functions such as heart rate, blood pressure, sweating, and digestion. The goal of sympathectomy is to manage conditions like hyperhidrosis (excessive sweating), Raynaud's phenomenon, and certain types of chronic pain.
There are different types of sympathectomy, including thoracic sympathectomy (which targets the sympathetic nerves in the chest), lumbar sympathectomy (which targets the sympathetic nerves in the lower back), and cervical sympathectomy (which targets the sympathetic nerves in the neck). The specific type of procedure depends on the location of the affected nerves and the condition being treated.
Sympathectomy is usually performed using minimally invasive techniques, such as endoscopic surgery, which involves making small incisions and using specialized instruments to access the nerves. While sympathectomy can be effective in managing certain conditions, it carries risks such as nerve damage, bleeding, infection, and chronic pain.
Skeletal muscle fibers, also known as striated muscle fibers, are the type of muscle cells that make up skeletal muscles, which are responsible for voluntary movements of the body. These muscle fibers are long, cylindrical, and multinucleated, meaning they contain multiple nuclei. They are surrounded by a connective tissue layer called the endomysium, and many fibers are bundled together into fascicles, which are then surrounded by another layer of connective tissue called the perimysium.
Skeletal muscle fibers are composed of myofibrils, which are long, thread-like structures that run the length of the fiber. Myofibrils contain repeating units called sarcomeres, which are responsible for the striated appearance of skeletal muscle fibers. Sarcomeres are composed of thick and thin filaments, which slide past each other during muscle contraction to shorten the sarcomere and generate force.
Skeletal muscle fibers can be further classified into two main types based on their contractile properties: slow-twitch (type I) and fast-twitch (type II). Slow-twitch fibers have a high endurance capacity and are used for sustained, low-intensity activities such as maintaining posture. Fast-twitch fibers, on the other hand, have a higher contractile speed and force generation capacity but fatigue more quickly and are used for powerful, explosive movements.
A smooth muscle within the vascular system refers to the involuntary, innervated muscle that is found in the walls of blood vessels. These muscles are responsible for controlling the diameter of the blood vessels, which in turn regulates blood flow and blood pressure. They are called "smooth" muscles because their individual muscle cells do not have the striations, or cross-striped patterns, that are observed in skeletal and cardiac muscle cells. Smooth muscle in the vascular system is controlled by the autonomic nervous system and by hormones, and can contract or relax slowly over a period of time.
Muscle contraction is the physiological process in which muscle fibers shorten and generate force, leading to movement or stability of a body part. This process involves the sliding filament theory where thick and thin filaments within the sarcomeres (the functional units of muscles) slide past each other, facilitated by the interaction between myosin heads and actin filaments. The energy required for this action is provided by the hydrolysis of adenosine triphosphate (ATP). Muscle contractions can be voluntary or involuntary, and they play a crucial role in various bodily functions such as locomotion, circulation, respiration, and posture maintenance.
Muscle development, also known as muscle hypertrophy, refers to the increase in size and mass of the muscles through a process called myofiber growth. This is primarily achieved through resistance or strength training exercises that cause micro-tears in the muscle fibers, leading to an inflammatory response and the release of hormones that promote muscle growth. As the muscles repair themselves, they become larger and stronger than before. Proper nutrition, including adequate protein intake, and rest are also essential components of muscle development.
It is important to note that while muscle development can lead to an increase in strength and muscular endurance, it does not necessarily result in improved athletic performance or overall fitness. A well-rounded exercise program that includes cardiovascular activity, flexibility training, and resistance exercises is recommended for optimal health and fitness outcomes.
Fast-twitch muscle fibers, also known as type II fibers, are a type of skeletal muscle fiber that are characterized by their rapid contraction and relaxation rates. These fibers have a larger diameter and contain a higher concentration of glycogen, which serves as a quick source of energy for muscle contractions. Fast-twitch fibers are further divided into two subcategories: type IIa and type IIb (or type IIx). Type IIa fibers have a moderate amount of mitochondria and can utilize both aerobic and anaerobic metabolic pathways, making them fatigue-resistant. Type IIb fibers, on the other hand, have fewer mitochondria and primarily use anaerobic metabolism, leading to faster fatigue. Fast-twitch fibers are typically used in activities that require quick, powerful movements such as sprinting or weightlifting.