Features of ion currents induced by acetylcholine in the muscle fibers of the lamprey

Spontaneous miniature end-plate currents (MEPC) and acetylcholine-induced noise were recorded in muscle fibres of m. longitudinalis linguae of lamprey. The MEPC decay time constant was 5.3 ms and amplitude 2.2 nA. The mean channel life time was 3.6 ms and conductance 13.6 pS. Ionic channels in synaptic and extrasynaptic zones had identical kinetics. Inhibition of acetylcholinesterase induced a 2.2-fold prolongation of MEPC, but did not affect the channel life time.     

Excitatory amino acid-evoked membrane currents and excitatory synaptic transmission in lamprey reticulospinal neurons

The characteristics of excitatory amino acid-evoked currents and of excitatory synaptic events have been examined in lamprey Müller neurons using voltage clamp and current clamp recording techniques. Application of glutamate evoked depolarizations associated with a decrease in input resistance. The reversal potential of the responses was -35 mV. Under voltage clamp conditions, a series of excitatory amino acid agonists evoked inward currents associated with little or no increase in baseline current noise. The order of potency of the excitatory amino acid agonists was quisqualate greater than kainate greater than glutamate greater than aspartate, while N-methyl-D-aspartic acid (NMDA) was inactive. Inward currents evoked by glutamate, as well as by kainate and quisqualate were attenuated reversibly by 1 mM kynurenic acid (KYN). In contrast, glutamate-evoked currents were not affected by 100 microM D(-)-2-amino-5-phosphonovaleric acid (APV), a selective NMDA antagonist. Spontaneously occurring and stimulus-evoked excitatory postsynaptic events were antagonized reversibly by 1 mM KYN. At this concentration, KYN had no effect on membrane potential, input resistance, or excitability of the cells. In contrast, excitatory postsynaptic currents were unaffected by APV. It is concluded that both glutamate responses and excitatory synaptic transmission in lamprey Müller neurons are mediated by non-NMDA-type receptors and that these receptors are associated with ionic channels with a low elementary conductance. The combined pharmacological and biophysical characteristics of these responses are therefore different from those previously reported in other preparations. Spontaneous (but not stimulus-evoked) inhibitory synaptic events in Müller neurons were blocked reversibly by 1 mM KYN but not by 100 microM APV, suggesting that excitation of interneurons inhibitory to Müller cells was also mediated by non-NMDA receptors.     

Plakins in striated muscle

Striated muscle cells contain numerous architectural proteins that contribute to the function of muscle as generators of mechanical force. Among these proteins are crosslinkers belonging to the plakin family, namely plectin, microtubule‐actin crosslinking factor (ACF7/MACF1), bullous pemphigoid antigen 1 (Bpag1/dystonin), and desmoplakin. These plakin family members, in particular plectin and Bpag1/dystonin, exist as several isoforms. The domain organization of these plakin variants dictates their subcellular location and the proteins with which they interact. Several studies suggest that plakins exert unique functions within various compartments of the muscle cell including the sarcolemma, the sarcomere, both neuromuscular and myotendinous junctions in skeletal muscle, and the intercalated discs in cardiac muscle. Plakins may also regulate the cellular placement and function of specific organelles, notably the nucleus, mitochondria, Golgi apparatus, and sarcoplasmic reticulum. Here we review and summarize our current knowledge of the function of plakins in striated muscle cells. Muscle Nerve, 2009     

On finding striated muscle in the brain

Well-developed striated muscle was found in the leptomeninges of a 2 day old infant with a 13-15 trisomy defect and multiple congenital anomalies. Except for arhinencephaly, minor sulcal abnormalities, and scattered microscopic cerebellar dysplasias the brain was well formed. The extreme rarity of this finding is noted and an attempt is made to explain it on an embryological basis. The implications of this observation in relation to some central nervous system tumours containing striated muscle are briefly discussed.     

Voltage clamp analysis of membrane currents in larval muscle fibers of Drosophila: alteration of potassium currents in Shaker mutants

The body wall muscles in Drosophila larvae are suitable for voltage clamp analysis of changes in membrane excitability caused by mutations. Both inward and outward ionic currents are present in these muscle fibers. The inward current is mediated by voltage-dependent Ca2+ channels. In Ca2+-free saline, the inward current is eliminated. The remaining outward K+ currents consist of two distinct components, an early transient IA and a delayed steady IK, which are separable by differences in the rate and voltage dependence of activation and inactivation. The steady-state and kinetic properties of the activation and inactivation processes of these two currents are analyzed. The results provide a basis for quantitative analysis of altered membrane currents in behavioral mutants of Drosophila. Previous studies indicate that mutations in the Shaker (Sh) locus alter excitability in both nerve and muscle in Drosophila. Our results support the idea that the channels mediating IA are molecularly distinct from those mediating IK. All Sh mutations studied specifically affect IA without changing the properties of the calcium current and IK. In certain alleles (ShKS133, Sh102, and ShM) IA is eliminated, permitting detailed studies of IK in isolation of IA. Studies of the alleles that do not eliminate IA provide additional information of the channels. In one such allele, Sh5, voltage dependence of IA activation is shifted to more positive potentials. This is accompanied by a less pronounced shift in the voltage dependence of inactivation. These results suggest that Sh5 mutation affects the voltage-sensitive mechanism of both activation and inactivation processes and that these two processes are not controlled by independent parts of the channel. Furthermore, the differential effects of these alleles on different excitable membranes imply that other genes take part in the control of IA. The effects of Sh5 on muscle depend on developmental stage. In larval muscle, Sh5 reduces the amplitude of IA because of the shift in the current-voltage (I-V) relation. In contrast, in adult Sh5 muscles, IA is reported to be normal in amplitude but shows abnormally rapid inactivation (Salkoff, L., and R. Wyman (1981) Nature 293: 228-230). A different allele, ShrK0120, causes a clear defect in nerve excitability, but analysis of IA in ShrK0120 larval muscle reveals I-V relations, inactivation, and recovery from inactivation similar to those seen in normal fibers. We suggest a possible mechanism of combinations of multiple interacting genes participating in the control of potassium channels to account for the presence of a variety of potassium channels in different excitable membranes.     

Effect of the alkaloid lappaconitine on ion currents through the somatic membrane of Helix pomatia neurons

The effect of alkoloid lappaconitine on ionic currents through the somatic membrane of identified neurons of the mollusc Helix pomatia was studied under voltage-clamp conditions. It is shown that 4 mM lappaconitine causes a reversible blocking action on the calcium channels. Concentration exceeding 4 mM causes irreversible changes. Lappaconitine had either an insignificant or no effect on sodium currents.     

Features of the postsynaptic potentials and ion currents in synapses of fast and slow rat muscle fibers

The time course of spontaneous miniature end-plate potentials (MEPP) and currents (MEPC) was compared in fast and slow muscle fibres using extracellular focal recording or voltage-clamp technique. The mean values of the rise and decline half-time of MEPP and MEPC in slow fibres was 1.3-1.4 times as much as those in fast ones. A smaller difference was observed after AChE inhibition. Decay of the end-plate currents remained generally exponential and its rate depended on the membrane potential level. Distribution of different muscle fibres according to the time course of MEPP and MEPC in fast and slow muscles correlates with the content of the different fibre types identified on other properties. The possible factors controlling the time course of postsynaptic responses (AChE activity, the length of diffusional pathways, differences in the membrane passive electrical properties) and their significance in synapses of different types are discussed.     

Light microscopic study of striated muscle in uremia

Summary Gastrocnemius muscle biopsies from 28 patients with chronic renal failure were analyzed with a light microscope after staining with Gomori trichrome stain and after histochemical reactions for ATPase and NADH diaphorase. Nineteen (68%) of the biopsies were pathological. Uremic myopathy was seen in eleven (39%) of the biopsies, eight of which were obtained from subjects on regular hemodialysis. Pure myopathic muscle damage was observed in three (11%), both myopathic and neuropathic muscle damage in eight (29%) and pure neuropathic muscle damage in eight (29%) of the biopsies. Fiber type atrophy and hypertrophy of both types were seen. The most common quantitative findings were Type II atrophy, small mean size and type grouping of Type II fibers, and Type I hypertrophy.     

Heterogeneity of adult human striated muscle tropomyosin

The amino acid sequences of the human skeletal muscle tropomyosins were elucidated. Of the three α-types identified, the major fraction (identical to the single myocardial species) differed by 23 and 25 amino acid residues from the two minor α-forms and by 42 residues from β-tropomyosin. The two β-components differed only by deletion of the C-terminal residue in the minor fraction. These sequences will facilitate analysis of tropomyosin from developmental and diseased states.     

Probing striated muscle mitochondrial phenotype in neuromuscular disorders

Multisystemic disorders with predominantly neurologic manifestations often present with mitochondrial abnormalities in striated muscle biopsies. Decreased respiratory complex activities and abnormalities in mitochondrial structure and DNA constitute the spectrum of mitochondrial changes used as diagnostic and prognostic indicators in patients with neuromuscular disorders. This study assessed mitochondrial defects present in a cohort of 154 young patients to determine diagnostic efficiency and probe the relationship of mitochondrial to clinical phenotype. Striated muscle biopsies were analyzed for mitochondrial structure and number, levels of enzyme activities of complex I-V and citrate synthase, mitochondrial DNA and specific mitochondrial DNA deletions, and presence of 15 pathogenic mitochondrial DNA point mutations. Reduced complex I, III, IV, and V activities were the most ubiquitous finding, with complex III most commonly affected. Mitochondrial structural defects (39%) included changes in mitochondria sizes/shapes and number and aberrant cristae formation. Mitochondrial DNA deletions were evident in 15 patients, three displayed mitochondrial DNA depletion, and only two harbored pathogenic point mutations. Reductions in specific enzyme activities may be the most sensitive diagnostic indicator, whereas defects in ultrastructure and mitochondrial DNA integrity were frequently accompanied by the full spectrum of mitochondrial abnormalities. Some phenotypes displayed specific mitochondrial abnormalities; however, most clinical phenotypes displayed little specificity with regard to mitochondrial phenotype.     

On the occurrence of striated muscle within the spinal leptomeninges

A clinically normal adult male rabbit was found to possess fascicles of muscle fibers within the leptomeninges over the spinal cord at L6, L7, and S1. The finding is believed to be purely incidental and unrelated to any experimental procedure. Morphologically, the fascicles had the characteristics of striated muscle; and, while most were of normal dimensions, several were made up of small fibers 4–10 μm in diameter. Motor endplates, capillaries, and endomysial and perimysial connective tissue were also present. Axons myelinated by Schwann cells were associated with the normal bundles but were absent from the bundles of small fibers. In such bundles, large, unmyelinated axons predominated, some of which lacked ensheathment while others were invested by perineurial-type cells. The observation of incidental intraleptomeningeal skeletal muscle probably reflects a rare developmental anomaly. Its occurrence in humans is also discussed.     

Neurotrophic control of RNA synthesis in amphibian striated muscle

When frog sartorius muscles are incubated in culture for 3 days, a 98% increase in RNA synthesis by the muscles is seen. A portion of this increase (60--100% in different experiments) is prevented by the presence of a 2 cm distal nerve stump left attached to the muscle, or by the addition to the culture medium of nerve and spinal cord extracts from frog, rat or cow. The effect of the nerve stump and the extract is seen under conditions of neuro-muscular blockade by 50 mg/l gentamicin sulfate present in the culture medium. Autoradiography of 1 micrometer sections of muscles previously labeled with [3H]uridine shows that isotope incorporation is largely confined to muscle fibers rather than connective tissue. Muscles cultured for 3 days display normal action and resting potentials either in the presence or absence of extract. The results are discussed in terms of control of muscle RNA synthesis by substances present in motor neurons.     

Enteric co-innervation of striated muscle fibres in human oesophagus

Abstract  Oesophageal striated muscle of several mammalian species receives dual innervation from both vagal motor fibres originating in the brain stem and enteric nerve fibres originating in myenteric ganglia. The aim of this study was to investigate this so-called enteric co-innervation in the human oesophagus. Histochemical and immunohistochemical methods combined with confocal laser scanning microscopy were utilized to study innervation of 14 oesophagi obtained from body donors (age range 47–95 years). In addition, the distribution of striated and smooth muscle in longitudinal and circular layers of the tunica muscularis was studied semiquantitatively. The upper half of the oesophagus was built up of both muscle types with a predominance (>50–60%) of striated muscle, whereas the lower half consisted of smooth muscle only. The majority of motor endplates was compact and ovoid. Enteric nerve fibres on ∼17% of motor endplates stained for neuronal nitric oxide synthase, vasoactive intestinal polypeptide, galanin and neuropeptide Y and were completely separated from vagal cholinergic nerve terminals. There was remarkable variability of co-innervation rates between striated muscle bundles with some reaching almost 50%. Myenteric neurons representing the putative source of enteric co-innervating nerve fibres, stained for all these markers, which were almost completely colocalized with NADPH-diaphorase. Our study provides evidence for enteric co-innervation of striated muscle in human oesophagus. From these and recent functional results in various rodent species, we suggest that this innervation component represents an integral part of an intramural reflex mechanism for local most likely inhibitory modulation of oesophageal motility.     

Histochemical studies of striated muscle after temporary ischemia in the rat

Summary Temporary ischaemia of the hind limb of the rat was produced using a tourniquet with controlled pressure. Changes in the muscle seen after Gomori trichrome staining and after histochemical reactions for NADHdiaphorase, ATPases and phosphorylase were correlated with the duration of the ischaemia and the time of recovery.Histopathological changes were seen first after 2 h of ischaemia and increased thereafter; necrosis of most of the muscles occurred between 4 and 6 h of ischaemia.Necrosis and phagocytosis of muscle fibres and later the amount of regenerating fibres with characteristic histochemical staining properties increased linearly with increasing duration of ischaemia. Even after the most severe lesions of seemingly total necrosis of the muscle after 6 h of ischaemia most of the muscle regenerated within 18 days. Morphological alterations such as variation in fibre size, split fibres and central nuclei were still observed 226 days after ischaemia at which time the follow-up was terminated. Fibre type grouping was seen first after 45–90 days subsequent to 4 and 6 h ischaemia after incubation for ATPase, indicating concomitant neurogenic lesion in addition to the direct ischaemia of the muscle fibres.     

Ultrastructure of developing human muscle: the problem of multinucleation of striated muscle cells

The authors studied by electron microscopy the muscle of 27 human foetuses ranging from 9 weeks to 9 months development. It was possible to observe that disintegration of the plasma membranes of adjacent myoblasts and myotubes which share a common basement membrane tube appears to occur in longitudinally disposed cells of those categories. This may help to explain how further nuclei may be incorporated into well developed myotubes and how the striated muscle cells become multinucleated during embryonic myogenesis and regeneration in vivo.