scholarly journals Selectivity in regeneration of the oculomotor nerve in the cichlid fish, Astronotus ocellatus

Development ◽  
1965 ◽  
Vol 14 (3) ◽  
pp. 307-317
Author(s):  
R. W. Sperry ◽  
H. L. Arora

It has long been considered a general rule for nerve regeneration that the reinnervation of skeletal muscle is nonselective. Regenerating nerve fibers are supposed to reconnect with one skeletal muscle as readily as another according to studies covering a wide range of vertebrates (Weiss, 1937; Weiss & Taylor, 1944; Weiss & Hoag, 1946; Bernstein & Guth, 1961; Guth, 1961, 1962, 1963). Similarly, in embryogenesis proper functional connexions between nerve centers and particular muscles are supposedly attained, not by selective nerve outgrowth but rather through a process of ‘myotypic modulation’ (Weiss, 1955) that presupposes nonselective peripheral innervation. Doubt about the general validity of this rule and the concepts behind it has come from a series of studies on regeneration of the oculomotor nerve in teleosts, urodeles, and anurans and of spinal fin nerves in teleosts (Sperry, 1946, 1947, 1950, 1965; Sperry & Deupree, 1956; Arora & Sperry, 1957a, 1964).

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 481
Author(s):  
Gemma G. Martínez-García ◽  
Raúl F. Pérez ◽  
Álvaro F. Fernández ◽  
Sylvere Durand ◽  
Guido Kroemer ◽  
...  

Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals.


2004 ◽  
Vol 78 (13) ◽  
pp. 6792-6798 ◽  
Author(s):  
Ellyn R. Mulcahy ◽  
Jason C. Bartz ◽  
Anthony E. Kincaid ◽  
Richard A. Bessen

ABSTRACT The presence of the prion agent in skeletal muscle is thought to be due to the infection of nerve fibers located within the muscle. We report here that the pathological isoform of the prion protein, PrPSc, accumulates within skeletal muscle cells, in addition to axons, in the tongue of hamsters following intralingual and intracerebral inoculation of the HY strain of the transmissible mink encephalopathy agent. Localization of PrPSc to the neuromuscular junction suggests that this synapse is a site for prion agent spread between motor axon terminals and muscle cells. Following intracerebral inoculation, the majority of PrPSc in the tongue was found in the lamina propria, where it was associated with sensory nerve fibers in the core of the lingual papillae. PrPSc staining was also identified in the stratified squamous epithelium of the lingual mucosa. These findings indicate that prion infection of skeletal muscle cells and the epithelial layer in the tongue can be established following the spread of the prion agent from nerve terminals and/or axons that innervate the tongue. Our data suggest that ingestion of meat products containing prion-infected tongue could result in human exposure to the prion agent, while sloughing of prion-infected epithelial cells at the mucosal surface of the tongue could be a mechanism for prion agent shedding and subsequent prion transmission in animals.


2021 ◽  
Vol 22 (13) ◽  
pp. 6845
Author(s):  
Rebecca L. Pratt

The buzz about hyaluronan (HA) is real. Whether found in face cream to increase water volume loss and viscoelasticity or injected into the knee to restore the properties of synovial fluid, the impact of HA can be recognized in many disciplines from dermatology to orthopedics. HA is the most abundant polysaccharide of the extracellular matrix of connective tissues. HA can impact cell behavior in specific ways by binding cellular HA receptors, which can influence signals that facilitate cell survival, proliferation, adhesion, as well as migration. Characteristics of HA, such as its abundance in a variety of tissues and its responsiveness to chemical, mechanical and hormonal modifications, has made HA an attractive molecule for a wide range of applications. Despite being discovered over 80 years ago, its properties within the world of fascia have only recently received attention. Our fascial system penetrates and envelopes all organs, muscles, bones and nerve fibers, providing the body with a functional structure and an environment that enables all bodily systems to operate in an integrated manner. Recognized interactions between cells and their HA-rich extracellular microenvironment support the importance of studying the relationship between HA and the body’s fascial system. From fasciacytes to chronic pain, this review aims to highlight the connections between HA and fascial health.


1996 ◽  
Vol 271 (2) ◽  
pp. E253-E260 ◽  
Author(s):  
C. E. Torgan ◽  
W. E. Kraus

Skeletal muscle exhibits a wide range in functional phenotype in response to changes in physiological demands. We have observed that, in response to changes in work patterns, alterations in gene expression of some proteins coincide with changes in adenylyl cyclase (AC) activity [Kraus, W.E., J.P. Longabaugh, and S. B. Liggett. Am. J. Physiol 263 (Endocrinol. Metab. 26): E266-E230, 1992]. We now examine AC isoform transcript prevalence in various rabbit skeletal muscles and in response to changing work demands. Using reverse transcriptase-polymerase chain reaction, we detected type II AC isoform transcripts in rabbit skeletal muscle. Ribonuclease protection analyses revealed that expression of the type II isoform significantly correlated with the percentage of fast-twitch type IIb/IId fibers (r2 = 0.765, P < 0.01). When a fast-twitch muscle was converted to a slow-twitch muscle via chronic electrical pacing, expression of type II AC mRNA significantly decreased. This response occurred 3 days after the onset of stimulation (78% decrease) and was still present after 21 days of stimulation (76% decrease). As type II AC is relatively insensitive to calcium regulation while sensitive to protein kinase C (PKC) signaling, these data provide further impetus for investigations of protein kinase A and PKC cross-talk signaling mechanisms in the regulation of gene expression.


2003 ◽  
Vol 89 (6) ◽  
pp. 3070-3082 ◽  
Author(s):  
Jason S. Rothman ◽  
Paul B. Manis

In the ventral cochlear nucleus (VCN), neurons transform information from auditory nerve fibers into a set of parallel ascending pathways, each emphasizing different aspects of the acoustic environment. Previous studies have shown that VCN neurons differ in their intrinsic electrical properties, including the K+ currents they express. In this study, we examine these K+ currents in more detail using whole cell voltage-clamp techniques on isolated VCN cells from adult guinea pigs at 22°C. Our results show a differential expression of three distinct K+ currents. Whereas some VCN cells express only a high-threshold delayed-rectifier-like current ( IHT), others express IHT in combination with a fast inactivating current ( IA) and/or a slow-inactivating low-threshold current ( ILT). IHT, ILT, and IA, were partially blocked by 1 mM 4-aminopyridine. In contrast, only ILT was blocked by 10–100 nM dendrotoxin-I. A surprising finding was the wide range of levels of ILT, suggesting ILT is expressed as a continuum across cell types rather than modally in a particular cell type. IA, on the other hand, appears to be expressed only in cells that show little or no ILT, the Type I cells. Boltzmann analysis shows IHT activates with 164 ± 12 (SE) nS peak conductance, -14.3 ± 0.7 mV half-activation, and 7.0 ± 0.5 mV slope factor. Similar analysis shows ILT activates with 171 ± 22 nS peak conductance, -47.4 ± 1.0 mV half-activation, and 5.8 ± 0.3 mV slope factor.


2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.


2011 ◽  
Vol 437 (2) ◽  
pp. 215-222 ◽  
Author(s):  
Christopher G. R. Perry ◽  
Daniel A. Kane ◽  
Chien-Te Lin ◽  
Rachel Kozy ◽  
Brook L. Cathey ◽  
...  

Assessment of mitochondrial ADP-stimulated respiratory kinetics in PmFBs (permeabilized fibre bundles) is increasingly used in clinical diagnostic and basic research settings. However, estimates of the Km for ADP vary considerably (~20–300 μM) and tend to overestimate respiration at rest. Noting that PmFBs spontaneously contract during respiration experiments, we systematically determined the impact of contraction, temperature and oxygenation on ADP-stimulated respiratory kinetics. BLEB (blebbistatin), a myosin II ATPase inhibitor, blocked contraction under all conditions and yielded high Km values for ADP of >~250 and ~80 μM in red and white rat PmFBs respectively. In the absence of BLEB, PmFBs contracted and the Km for ADP decreased ~2–10-fold in a temperature-dependent manner. PmFBs were sensitive to hyperoxia (increased Km) in the absence of BLEB (contracted) at 30 °C but not 37 °C. In PmFBs from humans, contraction elicited high sensitivity to ADP (Km<100 μM), whereas blocking contraction (+BLEB) and including a phosphocreatine/creatine ratio of 2:1 to mimic the resting energetic state yielded a Km for ADP of ~1560 μM, consistent with estimates of in vivo resting respiratory rates of <1% maximum. These results demonstrate that the sensitivity of muscle to ADP varies over a wide range in relation to contractile state and cellular energy charge, providing evidence that enzymatic coupling of energy transfer within skeletal muscle becomes more efficient in the working state.


Author(s):  
Valentina Pegoraro ◽  
Antonio Merico ◽  
Corrado Angelini

Amyotrophic lateral sclerosis (ALS) is a rare, progressive, neurodegenerative disorder caused by degeneration of upper and lower motor neurons. The disease process leads from lower motor neuron involvement to progressive muscle atrophy, weakness, fasciculations for the upper motor neuron involvement to spasticity. Muscle atrophy in ALS is caused by a dysregulation in the molecular network controlling fast and slow muscle fibres. Denervation and reinnervation processes in skeletal muscle occur in the course of ALS and are modulated by rehabilitation. MicroRNAs (miRNAs) are small non-coding RNAs that modulate a wide range of biological functions under various pathophysiological conditions. MiRNAs can be secreted by various cell types and they are markedly stable in body fluids. MiR-1, miR-133 a, miR-133b, and miR-206 are called &ldquo;myomiRs&rdquo; and are considered markers of myogenesis during muscle regeneration and neuromuscular junction stabilization or sprouting. We observed a positive effect of a standard aerobic exercise rehabilitative protocol conducted for six weeks in 18 ALS patients during hospitalization in our center. We correlated clinical scales with molecular data on myomiRs. After six weeks of moderate aerobic exercise, myomiRNAs were down-regulated, suggesting an active proliferation of satellite cells in muscle and increased neuromuscular junctions. Our data suggest that circulating miRNAs modulate during skeletal muscle recovery in response to physical rehabilitation in ALS.


Author(s):  
Milutin Mrvaljević ◽  
Srbislav Pajić ◽  
Pavle Popović ◽  
Jovan Grujić ◽  
Marko Petrović ◽  
...  

Although the terminal branches of brachial plexus that originate from lateral and medial fasciculus are well protected by muscle mass and vascular-neuronal petal of axilla and upper arm, the number of traumatic damage and injuries increases, according to the published reports of neurosurgeons working on pathology of peripheral nerves, as well as traumatologists, orthopedics, microsurgeons and plastic surgeons. This is certainly contributed by urbanization, industrialization, migration and increased number of traffic accidents. Knowing the microstructure of the peripheral nerve truncus leads to the possibility of applying various techniques of nerve grafting, as well as possibility of re-implantation of detached spinal roots, seen in traction injuries of brachial plexus, in which the mechanism of injury needs to be considered. Considering frequent injuries of terminal branches of lateral and medial fasciculus and a substantial pathology of plexus brachialis, the aim of our research was to study surgical-anatomical relations between terminal branches of medial and lateral fasciculus and substantial morphology of terminal branches of both fasciculi, particularly regarding the place and way of formation, as well as the number of their anastomoses. The studies of the terminal branches of medial and lateral fasciculus on our preparation materials are based on the dissection of axilla and anterior part of the upper arm, on 50 cadavers, adults of both genders, at Institute of Anatomy and Institute of Forensic Medicine at School of Medicine in Belgrade. The way of formation of the terminal branches of lateral fasciculus on our preparation materials was always the same. These branches were usually formed after the bifurcation or diverging of lateral fasciculus to radix lateralis nervi mediani and musculocutaneous nerve. Exceptionally, after fusion of lateral fasciculus and medial root of nervus medianus, there is no bifurcation, and formed nervous truncus is a result of existence of the pre- or postfixational type of brachial plexus. Analyzing our preparation materials, we determined that high bifurcation of lateral fasciculus (LF) exists in 18% of cases and that it is projected in the line of anterior edge of clavicle. Medium high bifurcation of LF is projected in the line of the top of the acromion of scapula and is seen in 61% of all cases. Low bifurcation is usually placed in the line of inferior edge of pectoral minor muscle, in 8% of cases. Fasciculus without bifurcation is noticed in 13% of cases. Measuring the shortest distance between anterior edge of clavicle and the point of bifurcation of LF resulted in a wide range from 0.5 to 9.7 cm, with 4.2 cm average. In cases of transplantation, implantation and re-implantation of nervous trunci of plexus brachialis, it is very important to consider the shape and the thickness of nervous truncus, the number of fasciculi, the number of nerve fibers, as well as the quantity and schedule of peri- and intrafascicular connective tissue, providing the normal irrigation of the nerve. Finally, we can conclude that mentioned facts prompted us to undertake a systematic research of great terminal branches of plexus brachialis that originate from lateral and medial fasciculus, trying to ensure that our anatomical findings receive a comprehensive clinical confirmation.


Genetica ◽  
2008 ◽  
Vol 136 (3) ◽  
pp. 461-469 ◽  
Author(s):  
Juliana Mazzuchelli ◽  
Cesar Martins

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