The fine structure of the nervous tissue of the metacestode of Hymenolepis microstoma

1976 ◽  
Vol 54 (7) ◽  
pp. 1206-1222 ◽  
Author(s):  
Rodney A. Webb ◽  
Kenneth G. Davey
Keyword(s):  
Nerve Cell ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Nervous Tissue ◽  
Cell Types ◽  
Multivesicular Bodies ◽  
Neuronal Perikaryon ◽  
Single Nucleus ◽  
Neuronal Type ◽  
Hymenolepis Microstoma

The cytology of the nervous tissue of the metacestode of Hymenolepis microstoma was studied by electron microscopy. The small (3–5 μm) nerve cell bodies are smooth to irregular in outline, possessing one to several neurites that form synapses in the neuropile. Each neuronal perikaryon contains a single nucleus with a single nucleolus, numerous free ribosomes, occasional polyribosomes, small numbers of β-glycogen granules, multivesicular bodies, mitochondria, complex (coated or alveolate) vesicles, one or more Golgi complexes, and variable numbers of vesicles. Microtubules and microfilaments, however, are absent from the perikaryon. Subsurface cisternae are well developed; the inner faces of them are studded with ribosomes. Five types of vesicles, believed to contain neurotransmitter and (or) neurosecretion were identified on the basis of vesicle osmophilia and size distribution. On the basis of vesicle content, four nerve cell types were identified: sensory neurons, two putative interneurons, and one neuronal type possessing characteristics of both interneurons and motor neurons.

scholarly journals Illuminating neural circuits and behaviour in Caenorhabditis elegans with optogenetics

2015 ◽  
Vol 370 (1677) ◽  
pp. 20140212 ◽  
Author(s):  
Christopher Fang-Yen ◽  
Mark J. Alkema ◽  
Aravinthan D. T. Samuel
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Neural Activity ◽  
Neural Circuits ◽  
Cell Types ◽  
Excitable Cell

The development of optogenetics, a family of methods for using light to control neural activity via light-sensitive proteins, has provided a powerful new set of tools for neurobiology. These techniques have been particularly fruitful for dissecting neural circuits and behaviour in the compact and transparent roundworm Caenorhabditis elegans . Researchers have used optogenetic reagents to manipulate numerous excitable cell types in the worm, from sensory neurons, to interneurons, to motor neurons and muscles. Here, we show how optogenetics applied to this transparent roundworm has contributed to our understanding of neural circuits.

Hymenolepis nana: the fine structure of the adult nervous system

Parasitology ◽  
1983 ◽  
Vol 86 (1) ◽  
pp. 89-103 ◽  
Author(s):  
I. Fairweather ◽  
L. T. Threadgold
Keyword(s):  
Nervous System ◽  
Fine Structure ◽  
Nerve Cell ◽  
Neck Region ◽  
Nerve Cell Body ◽  
Hymenolepis Nana ◽  
Neuronal Perikaryon ◽  
Transmission Electron ◽  
Single Nucleus ◽  
Outer Plasma Membrane

SUMMARYThe fine structure of the nervous system in the scolex and neck region of Hymenolepis nana has been investigated by transmission electron microscopy. A description of the gross neuroanatomy in these regions of the worm is presented. The ganglia, commissures and nerve cords consist of an incomplete cortex of nerve cell bodies, and a core of nerve fibres. A delimiting sheath or capsule is absent. The nerve cell bodies contain a single nucleus with a single nucleolus, mitochondria, many ribosomes, Golgi complexes and vesicles formed within the Golgi cisternae. Numerous sub-surface cisternae are present beneath the outer plasma membrane of the nerve cell body, and the inner surfaces of these cisternae are studded with ribosomes. Some of the cisternae run tangentially into the cytoplasm of the perikaryon, particularly in the vicinity of the Golgi complexes; both sides of these cisternae are studded with ribosomes. From each neuronal perikaryon arise one or more neurites that contain neurotubules, mitochondria, ribosomes and electron-lucent or dense-cored vesicles. Five types of vesicle have been distinguished on the basis of their size and content. The neurites are unmyelinated and form synapses in the neuropile; the synapses possess features typical of those where mechanical strength is of importance. Three types of sensory receptors have been observed in H. nana, two ciliated and one non-ciliated; the latter typically form double or triple nerve endings which terminate within the tegument.

scholarly journals An ex vivo murine model to study poliovirus-induced apoptosis in nerve cells

2002 ◽  
Vol 83 (8) ◽  
pp. 1925-1930 ◽  
Author(s):  
Thérèse Couderc ◽  
Florence Guivel-Benhassine ◽  
Viviane Calaora ◽  
Anne-Sophie Gosselin ◽  
Bruno Blondel
Keyword(s):  
Nerve Cell ◽  
Cell Cultures ◽  
Motor Neurons ◽  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Cell Types ◽  
Nerve Cells ◽  
Paralytic Poliomyelitis ◽  
Induced Apoptosis

Paralytic poliomyelitis results from destruction of motor neurons owing to poliovirus (PV) replication. Using a mouse model, we have previously shown that PV kills neurons of the central nervous system (CNS) as a result of apoptosis (Girard et al., Journal of Virology 73, 6066–6072, 1999). We report the development of mixed mouse primary nerve cell cultures from the cerebral cortex of neonatal mice transgenic for the human PV receptor. These cultures contained all three main cell types of the CNS, i.e. neurons, astrocytes and oligodendrocytes. All three cell types were susceptible to PV infection and virus replication in the cultures led to DNA fragmentation characteristic of apoptosis. PV-induced apoptosis was inhibited by the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD.FMK), indicating that this process involved caspases. Thus, these mixed mouse primary nerve cell cultures are a new in vitro model for studying the molecular mechanisms of PV-induced apoptosis in nerve cells.

scholarly journals Outputs of Radula Mechanoafferent Neurons inAplysia are Modulated by Motor Neurons, Interneurons, and Sensory Neurons

2000 ◽  
Vol 83 (3) ◽  
pp. 1621-1636 ◽  
Author(s):  
Steven C. Rosen ◽  
Mark W. Miller ◽  
Elizabeth C. Cropper ◽  
Irving Kupfermann
Keyword(s):  
Membrane Potential ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Activity Patterns ◽  
Motor Program ◽  
Cell Types ◽  
Afferent Input ◽  
Sensory Cells ◽  
Motor Programs ◽  
Sensory Inputs

The gain of sensory inputs into the nervous system can be modulated so that the nature and intensity of afferent input is variable. Sometimes the variability is a function of other sensory inputs or of the state of motor systems that generate behavior. A form of sensory modulation was investigated in the Aplysiafeeding system at the level of a radula mechanoafferent neuron (B21) that provides chemical synaptic input to a group of motor neurons (B8a/b, B15) that control closure and retraction movements of the radula, a food grasping structure. B21 has been shown to receive both excitatory and inhibitory synaptic inputs from a variety of neuron types. The current study investigated the morphological basis of these heterosynaptic inputs, whether the inputs could serve to modulate the chemical synaptic outputs of B21, and whether the neurons producing the heterosynaptic inputs were periodically active during feeding motor programs that might modulate B21 outputs in a phase-specific manner. Four cell types making monosynaptic connections to B21 were found capable of heterosynaptically modulating the chemical synaptic output of B21 to motor neurons B8a and B15. These included the following: 1) other sensory neurons, e.g., B22; 2) interneurons, e.g., B19; 3) motor neurons, e.g., B82; and 4) multifunction neurons that have sensory, motor, and interneuronal functions, e.g., B4/5. Each cell type was phasically active in one or more feeding motor programs driven by command-like interneurons, including an egestive motor program driven by CBI-1 and an ingestive motor program driven by CBI-2. Moreover, the phase of activity differed for each of the modulator cells. During the motor programs, shifts in B21 membrane potential were related to the activity patterns of some of the modulator cells. Inhibitory chemical synapses mediated the modulation produced by B4/5, whereas excitatory and/or electrical synapses were involved in the other instances. The data indicate that modulation is due to block of action potential invasion into synaptic release regions or to alterations of transmitter release as a function of the presynaptic membrane potential. The results indicate that just as the motor system of Aplysia can be modulated by intrinsic mechanisms that can enhance its efficiency, the properties of primary sensory cells can be modified by diverse inputs from mediating circuitry. Such modulation could serve to optimize sensory cells for the different roles they might play.

scholarly journals Interleukin-17 and Th17 Lymphocytes Directly Impair Motoneuron Survival of Wildtype and FUS-ALS Mutant Human iPSCs

2021 ◽  
Vol 22 (15) ◽  
pp. 8042
Author(s):  
Mengmeng Jin ◽  
Katja Akgün ◽  
Tjalf Ziemssen ◽  
Markus Kipp ◽  
Rene Günther ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Th17 Cells ◽  
Immune Cell ◽  
Cell Types ◽  
Positive Control ◽  
Interleukin 17 ◽  
Fused In Sarcoma ◽  
Th17 Lymphocytes ◽  
Human Ipscs ◽  
Als Patients

Amyotrophic lateral sclerosis (ALS) is a progressive disease leading to the degeneration of motor neurons (MNs). Neuroinflammation is involved in the pathogenesis of ALS; however, interactions of specific immune cell types and MNs are not well studied. We recently found a shift toward T helper (Th)1/Th17 cell-mediated, pro-inflammatory immune responses in the peripheral immune system of ALS patients, which positively correlated with disease severity and progression. Whether Th17 cells or their central mediator, Interleukin-17 (IL-17), directly affects human motor neuron survival is currently unknown. Here, we evaluated the contribution of Th17 cells and IL-17 on MN degeneration using the co-culture of iPSC-derived MNs of fused in sarcoma (FUS)-ALS patients and isogenic controls with Th17 lymphocytes derived from ALS patients, healthy controls, and multiple sclerosis (MS) patients (positive control). Only Th17 cells from MS patients induced severe MN degeneration in FUS-ALS as well as in wildtype MNs. Their main effector, IL-17A, yielded in a dose-dependent decline of the viability and neurite length of MNs. Surprisingly, IL-17F did not influence MNs. Importantly, neutralizing IL-17A and anti-IL-17 receptor A treatment reverted all effects of IL-17A. Our results offer compelling evidence that Th17 cells and IL-17A do directly contribute to MN degeneration.

scholarly journals Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types

2021 ◽  
Vol 7 (3) ◽  
pp. eabd9036
Author(s):  
Sara Saez-Atienzar ◽  
Sara Bandres-Ciga ◽  
Rebekah G. Langston ◽  
Jonggeol J. Kim ◽  
Shing Wan Choi ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Membrane Trafficking ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Polygenic Risk Score ◽  
Genome Wide ◽  
Genome Wide Data ◽  
Data Driven Approach ◽  
Single Nucleus ◽  
Lateral Sclerosis

Despite the considerable progress in unraveling the genetic causes of amyotrophic lateral sclerosis (ALS), we do not fully understand the molecular mechanisms underlying the disease. We analyzed genome-wide data involving 78,500 individuals using a polygenic risk score approach to identify the biological pathways and cell types involved in ALS. This data-driven approach identified multiple aspects of the biology underlying the disease that resolved into broader themes, namely, neuron projection morphogenesis, membrane trafficking, and signal transduction mediated by ribonucleotides. We also found that genomic risk in ALS maps consistently to GABAergic interneurons and oligodendrocytes, as confirmed in human single-nucleus RNA-seq data. Using two-sample Mendelian randomization, we nominated six differentially expressed genes (ATG16L2, ACSL5, MAP1LC3A, MAPKAPK3, PLXNB2, and SCFD1) within the significant pathways as relevant to ALS. We conclude that the disparate genetic etiologies of this fatal neurological disease converge on a smaller number of final common pathways and cell types.

scholarly journals The atlas of RNase H antisense oligonucleotide distribution and activity in the CNS of rodents and non-human primates following central administration

2020 ◽  
Author(s):  
Paymaan Jafar-nejad ◽  
Berit Powers ◽  
Armand Soriano ◽  
Hien Zhao ◽  
Daniel A Norris ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Muscular Atrophy ◽  
Neurological Diseases ◽  
Cell Types ◽  
Rnase H ◽  
Central Administration ◽  
Spinal Motor Neurons ◽  
New Class ◽  
Wide Range ◽  
Therapeutic Development

Abstract Antisense oligonucleotides (ASOs) have emerged as a new class of drugs to treat a wide range of diseases, including neurological indications. Spinraza, an ASO that modulates splicing of SMN2 RNA, has shown profound disease modifying effects in Spinal Muscular Atrophy (SMA) patients, energizing efforts to develop ASOs for other neurological diseases. While SMA specifically affects spinal motor neurons, other neurological diseases affect different central nervous system (CNS) regions, neuronal and non-neuronal cells. Therefore, it is important to characterize ASO distribution and activity in all major CNS structures and cell types to have a better understanding of which neurological diseases are amenable to ASO therapy. Here we present for the first time the atlas of ASO distribution and activity in the CNS of mice, rats, and non-human primates (NHP), species commonly used in preclinical therapeutic development. Following central administration of an ASO to rodents, we observe widespread distribution and target RNA reduction throughout the CNS in neurons, oligodendrocytes, astrocytes and microglia. This is also the case in NHP, despite a larger CNS volume and more complex neuroarchitecture. Our results demonstrate that ASO drugs are well suited for treating a wide range of neurological diseases for which no effective treatments are available.

scholarly journals Molecular Alterations in Sporadic and SOD1-ALS Immortalized Lymphocytes: Towards a Personalized Therapy

2021 ◽  
Vol 22 (6) ◽  
pp. 3007
Author(s):  
Isabel Lastres-Becker ◽  
Gracia Porras ◽  
Marina Arribas-Blázquez ◽  
Inés Maestro ◽  
Daniel Borrego-Hernández ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Therapeutic Interventions ◽  
Autophagic Flux ◽  
Metabolic Disturbances ◽  
Molecular Alterations ◽  
Healthy Donors ◽  
Inflammatory Profile ◽  
Als Patients

Amyotrophic lateral sclerosis (ALS) is a fatal neurological condition where motor neurons (MNs) degenerate. Most of the ALS cases are sporadic (sALS), whereas 10% are hereditarily transmitted (fALS), among which mutations are found in the gene that codes for the enzyme superoxide dismutase 1 (SOD1). A central question in ALS field is whether causative mutations display selective alterations not found in sALS patients, or they converge on shared molecular pathways. To identify specific and common mechanisms for designing appropriate therapeutic interventions, we focused on the SOD1-mutated (SOD1-ALS) versus sALS patients. Since ALS pathology involves different cell types other than MNs, we generated lymphoblastoid cell lines (LCLs) from sALS and SOD1-ALS patients and healthy donors and investigated whether they show changes in oxidative stress, mitochondrial dysfunction, metabolic disturbances, the antioxidant NRF2 pathway, inflammatory profile, and autophagic flux. Both oxidative phosphorylation and glycolysis appear to be upregulated in lymphoblasts from sALS and SOD1-ALS. Our results indicate significant differences in NRF2/ARE pathway between sALS and SOD1-ALS lymphoblasts. Furthermore, levels of inflammatory cytokines and autophagic flux discriminate between sALS and SOD1-ALS lymphoblasts. Overall, different molecular mechanisms are involved in sALS and SOD1-ALS patients and thus, personalized medicine should be developed for each case.

Sign in / Sign up

Export Citation Format

Share Document