Pax7 is expressed in the capsules surrounding adult mouse neuromuscular spindles

1999 ◽  
Vol 77 (2) ◽  
pp. 153-156 ◽  
Author(s):  
J Rodger ◽  
M R Ziman ◽  
J M Papadimitriou ◽  
P H Kay
Keyword(s):  
Skeletal Muscle ◽  
Adult Mouse ◽  
In Situ Hybridisation ◽  
Adult Brain ◽  
Neural Cells ◽  
The Central Nervous System ◽  
Neuromuscular Spindles ◽  
Neural Crest Origin ◽  
Neuromuscular Spindle ◽  
Pax Family

The multigene Pax family of transcription factors plays an important role in the development of the central nervous system as well as in organ morphogenesis. Expression of one of the members of the family, Pax7, has been described in embryonic muscle and in both embryonic and adult brain. We recently detected Pax7 transcripts in RNA isolated from adult mouse skeletal muscle and brain and here use in situ hybridisation to localise the expression within these tissues. Pax7 expression was observed in neural cells of the brain and in cells of neural crest origin in the inner and outer capsules of neuromuscular spindles. The results suggest that Pax7 may be implicated in the formation and maintenance of neuromuscular contacts within the muscle spindle throughout life.Key words: Pax7 expression, skeletal muscle, neuromuscular spindle, basal lamina, Schwann cells.

Heterogeneity and Proliferative and Differential Regulators of NG2-glia in Physiological and Pathological States

2020 ◽  
Vol 27 (37) ◽  
pp. 6384-6406 ◽  
Author(s):  
Zuo Zhang ◽  
Hongli Zhou ◽  
Jiyin Zhou
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Physiological State ◽  
Critical Role ◽  
Adult Brain ◽  
Pathological State ◽  
Peripheral Neurons ◽  
Neuronal Synapses ◽  
The Central Nervous System ◽  
Rapid Modulation

NG2-glia, also called Oligodendrocyte Precursor Cells (OPCs), account for approximately 5%-10% of the cells in the developing and adult brain and constitute the fifth major cell population in the central nervous system. NG2-glia express receptors and ion channels involved in rapid modulation of neuronal activities and signaling with neuronal synapses, which have functional significance in both physiological and pathological states. NG2-glia participate in quick signaling with peripheral neurons via direct synaptic touches in the developing and mature central nervous system. These distinctive glia perform the unique function of proliferating and differentiating into oligodendrocytes in the early developing brain, which is critical for axon myelin formation. In response to injury, NG2-glia can proliferate, migrate to the lesions, and differentiate into oligodendrocytes to form new myelin sheaths, which wrap around damaged axons and result in functional recovery. The capacity of NG2-glia to regulate their behavior and dynamics in response to neuronal activity and disease indicate their critical role in myelin preservation and remodeling in the physiological state and in repair in the pathological state. In this review, we provide a detailed summary of the characteristics of NG2-glia, including their heterogeneity, the regulators of their proliferation, and the modulators of their differentiation into oligodendrocytes.

scholarly journals Cannabidiol induces autophagy via ERK1/2 activation in neural cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Talita A. M. Vrechi ◽  
Anderson H. F. F. Leão ◽  
Ingrid B. M. Morais ◽  
Vanessa C. Abílio ◽  
Antonio W. Zuardi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Cannabis Sativa ◽  
Autophagic Flux ◽  
Neural Cells ◽  
Human Neuroblastoma ◽  
Trpv1 Receptor ◽  
The Central Nervous System ◽  
Catabolic Process

AbstractAutophagy is a lysosomal catabolic process essential to cell homeostasis and is related to the neuroprotection of the central nervous system. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid present in Cannabis sativa. Many therapeutic actions have been linked to this compound, including autophagy activation. However, the precise underlying molecular mechanisms remain unclear, and the downstream functional significance of these actions has yet to be determined. Here, we investigated CBD-evoked effects on autophagy in human neuroblastoma SH-SY5Y and murine astrocyte cell lines. We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively. This result strongly indicates that the activation of these receptors mediates the autophagic flux. Additionally, we demonstrated that CBD activates autophagy through ERK1/2 activation and AKT suppression. Interestingly, CBD-mediated autophagy activation is dependent on the autophagy initiator ULK1, but mTORC1 independent. Thus, it is plausible that a non-canonical pathway is involved. Our findings collectively provide evidence that CBD stimulates autophagy signal transduction via crosstalk between the ERK1/2 and AKT kinases, which represent putative regulators of cell proliferation and survival. Furthermore, our study sheds light on potential therapeutic cannabinoid targets that could be developed for treating neurodegenerative disorders.

scholarly journals The Skeletal Muscle Emerges as a New Disease Target in Amyotrophic Lateral Sclerosis

2021 ◽  
Vol 11 (7) ◽  
pp. 671
Author(s):  
Oihane Pikatza-Menoio ◽  
Amaia Elicegui ◽  
Xabier Bengoetxea ◽  
Neia Naldaiz-Gastesi ◽  
Adolfo López de Munain ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amyotrophic Lateral Sclerosis ◽  
Muscle Tissue ◽  
Motor Neurons ◽  
Neurodegenerative Disorder ◽  
Disease Onset ◽  
Fine Tuning ◽  
Current State ◽  
The Central Nervous System ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder that leads to progressive degeneration of motor neurons (MNs) and severe muscle atrophy without effective treatment. Most research on ALS has been focused on the study of MNs and supporting cells of the central nervous system. Strikingly, the recent observations of pathological changes in muscle occurring before disease onset and independent from MN degeneration have bolstered the interest for the study of muscle tissue as a potential target for delivery of therapies for ALS. Skeletal muscle has just been described as a tissue with an important secretory function that is toxic to MNs in the context of ALS. Moreover, a fine-tuning balance between biosynthetic and atrophic pathways is necessary to induce myogenesis for muscle tissue repair. Compromising this response due to primary metabolic abnormalities in the muscle could trigger defective muscle regeneration and neuromuscular junction restoration, with deleterious consequences for MNs and thereby hastening the development of ALS. However, it remains puzzling how backward signaling from the muscle could impinge on MN death. This review provides a comprehensive analysis on the current state-of-the-art of the role of the skeletal muscle in ALS, highlighting its contribution to the neurodegeneration in ALS through backward-signaling processes as a newly uncovered mechanism for a peripheral etiopathogenesis of the disease.

Assignment of the human slow skeletal muscle troponin gene (TNNI1) to 1q32 by fluorescence in situ hybridisation

1993 ◽  
Vol 62 (2-3) ◽  
pp. 181-182 ◽  
Author(s):  
H.J. Eyre ◽  
P.A. Akkari ◽  
C. Meredith ◽  
S.D. Wilton ◽  
D.C. Callen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
In Situ Hybridisation ◽  
Fluorescence In Situ Hybridisation ◽  
Slow Skeletal Muscle

Hippocampal glutamine synthetase: insensitivity to glucocorticoids and stress

1990 ◽  
Vol 258 (5) ◽  
pp. E894-E897 ◽  
Author(s):  
G. C. Tombaugh ◽  
R. M. Sapolsky
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Glutamine Synthetase ◽  
Glutamate Metabolism ◽  
Glutamatergic Synapses ◽  
Adult Rats ◽  
Glucocorticoid Induction ◽  
The Central Nervous System ◽  
The Brain

Glucocorticoids enhance the neurotoxic potential of several insults to the rat hippocampus that involve overactivation of glutamatergic synapses. These hormones also stimulate the synthesis of glutamine synthetase (GS) in peripheral tissue. Because this enzyme helps regulate glutamate metabolism in the central nervous system, glucocorticoid induction of GS in the brain may underlie the observed synergy. We have measured GS activity in the hippocampus and skeletal muscle (plantaris) of adult rats after bilateral adrenalectomy (ADX), corticosterone (Cort) replacement, or stress. No significant changes in GS were observed in hippocampal tissue, whereas muscle GS was significantly elevated after Cort treatment or stress and was reduced after ADX. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy.

scholarly journals Differential Effects of RGK Proteins on L-Type Channel Function in Adult Mouse Skeletal Muscle

2014 ◽  
Vol 106 (9) ◽  
pp. 1950-1957 ◽  
Author(s):  
D. Beqollari ◽  
C.F. Romberg ◽  
U. Meza ◽  
S. Papadopoulos ◽  
R.A. Bannister
Keyword(s):  
Skeletal Muscle ◽  
Adult Mouse ◽  
Differential Effects ◽  
Mouse Skeletal Muscle ◽  
Channel Function ◽  
Rgk Proteins

Primitive Neuroectodermal Tumor of Cerebrum With Adipose Tissue

2001 ◽  
Vol 125 (2) ◽  
pp. 264-266
Author(s):  
Satish Krishnamurthy ◽  
Stephen Kent Powers ◽  
Javad Towfighi
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Primitive Neuroectodermal Tumor ◽  
Primitive Neuroectodermal Tumors ◽  
Mature Adipose Tissue ◽  
Neuroectodermal Tumors ◽  
The Central Nervous System

Abstract Primitive neuroectodermal tumors (PNETs) of the central nervous system are uncommon embryonal neoplasms, rarely occurring in adults. Differentiation into specific mesenchymal tissues, such as cartilage, bone, skeletal muscle, smooth muscle, or adipose tissue, is rare. We report a case of a 51-year-old woman with a PNET of cerebrum that showed extensive mature adipose tissue differentiation. This is the second case, to our knowledge, of PNET of cerebrum with adipose tissue elements that has been described.

Quantitative neurogenetics: applications in understanding disease

2021 ◽  
Author(s):  
Ali Afrasiabi ◽  
Jeremy T. Keane ◽  
Julian Ik-Tsen Heng ◽  
Elizabeth E. Palmer ◽  
Nigel H. Lovell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genetic Risk ◽  
Tissue Specificity ◽  
High Throughput Sequencing ◽  
Molecular Genetic ◽  
Brain Dysfunction ◽  
Neural Cells ◽  
Expression Index ◽  
The Central Nervous System ◽  
The Brain

Neurodevelopmental and neurodegenerative disorders (NNDs) are a group of conditions with a broad range of core and co-morbidities, associated with dysfunction of the central nervous system. Improvements in high throughput sequencing have led to the detection of putative risk genetic loci for NNDs, however, quantitative neurogenetic approaches need to be further developed in order to establish causality and underlying molecular genetic mechanisms of pathogenesis. Here, we discuss an approach for prioritizing the contribution of genetic risk loci to complex-NND pathogenesis by estimating the possible impacts of these loci on gene regulation. Furthermore, we highlight the use of a tissue-specificity gene expression index and the application of artificial intelligence (AI) to improve the interpretation of the role of genetic risk elements in NND pathogenesis. Given that NND symptoms are associated with brain dysfunction, risk loci with direct, causative actions would comprise genes with essential functions in neural cells that are highly expressed in the brain. Indeed, NND risk genes implicated in brain dysfunction are disproportionately enriched in the brain compared with other tissues, which we refer to as brain-specific expressed genes. In addition, the tissue-specificity gene expression index can be used as a handle to identify non-brain contexts that are involved in NND pathogenesis. Lastly, we discuss how using an AI approach provides the opportunity to integrate the biological impacts of risk loci to identify those putative combinations of causative relationships through which genetic factors contribute to NND pathogenesis.

Skin and Bones—and Muscle Too

Bioprinting ◽  
2021 ◽  
pp. 98-118
Author(s):  
Kenneth Douglas
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Cell Membrane ◽  
Motor Neuron ◽  
Neuromuscular Junctions ◽  
Skeletal Muscle Cell ◽  
The Body ◽  
The Central Nervous System ◽  
Judicious Choice

Abstract: This chapter recounts bioprinting studies of skin, bone, skeletal muscle, and neuromuscular junctions. The chapter begins with a study of bioprinted skin designed to enable the creation of skin with a uniform pigmentation. The chapter relates two very different approaches to bioprinted bone: a synthetic bone called hyperelastic bone and a strategy that prints cartilage precursors to bone and then induces the conversion of the cartilage to bone by judicious choice of bioinks. Muscles move bone, and the chapter discusses an investigation of bioprinted skeletal muscle. Finally, the chapter considers an attempt to bioprint a neuromuscular junction, a synapse—a minute gap—of about 20 billionths of a meter between a motor neuron and the cell membrane of a skeletal muscle cell. A motor neuron is a nerve in the central nervous system that sends signals to the muscles of the body.

Neurodevelopment

2020 ◽  
pp. 91-100
Author(s):  
Karl Zilles ◽  
Nicola Palomero-Gallagher
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Neural Tube ◽  
Neural Plate ◽  
Adult Brain ◽  
The Central Nervous System ◽  
Specialized Region ◽  
The Brain ◽  
Rostral Part ◽  
Human Nervous System

The pre- and post-natal development of the human nervous system is briefly described, with special emphasis on the brain, particularly the cerebral and cerebellar cortices. The central nervous system originates from a specialized region of the ectoderm—the neural plate—which develops into the neural tube. The rostral part of the neural tube forms the adult brain, whereas the caudal part (behind the fifth somite) differentiates into the spinal cord. The embryonic brain has three vesicular enlargements: the forebrain, the midbrain, and the hindbrain. The histogenesis of the spinal cord, hindbrain, cerebellum, and cerebral cortex, including myelination, is discussed. The chapter closes with a description of the development of the hemispheric shape and the formation of gyri.

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