Expression of type 1 inositol 1,4,5-trisphosphate receptor during axogenesis and synaptic contact in the central and peripheral nervous system of developing rat

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 1029-1039 ◽  
Author(s):  
M.A. Dent ◽  
G. Raisman ◽  
F.A. Lai
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Peripheral Neurons ◽  
Inositol 1,4,5 Trisphosphate ◽  
Adult Spinal Cord ◽  
Trisphosphate Receptor ◽  
First Time

Release of intracellular Ca2+ is triggered by the second messenger inositol 1,4,5-trisphosphate, which binds to the inositol 1,4,5-trisphosphate receptor and gates the opening of an intrinsic calcium channel in the endoplasmic reticulum. In order to understand the importance of this mechanism in development, we have examined the distribution of the type 1 inositol 1,4,5-trisphosphate receptor during development, in some areas of the rat brain and spinal cord and in peripheral neurons, using in situ hybridization and immunohistochemistry. In brain, we find that type 1 inositol 1,4,5-trisphosphate receptor is expressed in neurons from very early in development; low levels of expression are first detected after the neurons have migrated to their final positions, when they start to differentiate and begin axonal growth. Increasing levels of expression are observed later in development, during the time of synaptogenesis and dendritic contact. Glial cells do not express type 1 inositol 1,4,5-trisphosphate receptor, except for a transient period of expression, probably by oligodendrocytes, in developing fibre tracts during the onset of myelination. In contrast with the brain, both grey and white matter of the spinal cord express type 1 inositol 1,4,5-trisphosphate receptor throughout development, and it remains present in the adult spinal cord. We also show, for the first time, that type 1 inositol 1,4,5-trisphosphate receptor is expressed in the peripheral nervous system. Strong labelling was observed in the dorsal root ganglia and during development this expression seems to coincide with the onset of axogenesis. These results suggest that type 1 inositol 1,4,5-trisphosphate may be involved in the regulatory mechanism controlling Ca2+ levels in neurons during the periods of cell differentiation, axogenesis and synaptogenesis.

scholarly journals Intracellular calcium stores and inositol 1,4,5-trisphosphate receptor in rat liver cells

1996 ◽  
Vol 314 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Jean-Philippe LIÈVREMONT ◽  
Anne-Marie HILL ◽  
Dien TRAN ◽  
Jean-François COQUIL ◽  
Nicole STELLY ◽  
...  
Keyword(s):  
Protein A ◽  
The Other ◽  
Calcium Stores ◽  
Inositol 1,4,5 Trisphosphate ◽  
Rat Liver Cells ◽  
Intense Labelling ◽  
Discrete Domains ◽  
Trisphosphate Receptor

The D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] receptor was localized by immunofluorescence experiments in situ in liver cryosections. Two anti-Ins(1,4,5)P3 receptor antibodies (against the 14 C-terminal residues of the type 1 receptor or against the entire cerebellar receptor) weakly decorated the whole cytoplasm, and a more intense labelling was observed at the periphery of the hepatocytes, particularly beneath the canalicular and the sinusoidal domains of the plasma membrane (PM). Antibodies against calreticulin, the Ca2+ pump (SERCA2b) or endoplasmic reticulum (ER) membranes homogeneously labelled the cytoplasm and the subplasmalemmal area. These data indicate that the ER can be divided into at least two specialized subregions: one is located throughout most of the cytoplasm and contains markers of the rough ER (RER), calreticulin, SERCA2b and a low density of Ins(1,4,5)P3 receptor, and the other is confined to the periphery of the cells and contains calreticulin, Ca2+ pump, RER markers and a high density of Ins(1,4,5)P3 receptor. A membrane fraction enriched in Ins(1,4,5)P3 receptor and in markers of the PM was immuno-adsorbed with the antibody against the C-terminal end of the Ins(1,4,5)P3 receptor and pelleted with Sepharose protein A. The immuno-isolated material was enriched in Ins(1,4,5)P3 receptor, but none of the markers of the ER or of the PM could be detected. This suggests that the Ins(1,4,5)P3 receptor is localized on discrete domains of the ER membrane beneath the canalicular and the sinusoidal membranes, where it was found at higher densities than the other markers.

scholarly journals PATH-23. ADULT SPINAL CORD ASTROBLASTOMA WITH EWSR1-BEND2 FUSION

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii429-iii429
Author(s):  
Takeyoshi Tsutsui ◽  
Yoshiki Arakawa ◽  
Yasuhide Makino ◽  
Hiroharu Kataoka ◽  
Sachiko Minamiguti ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Residual Tumor ◽  
Intramedullary Tumor ◽  
Partial Removal ◽  
Weighted Image ◽  
Eosinophilic Cytoplasm ◽  
S 100 ◽  
High Cellularity ◽  
Adult Spinal Cord

Abstract The most recurrent fusion of CNS high-grade neuroepithelial tumor with MN1alteration(HGNET-MN1) is MN1- BEN Domain Containing 2(BEND2) fusion. Recently, there was a report of a 3-month-old boy with spinal astroblastoma, classified as CNS HGNET-MN1 by DKFZ methylation classification but positive for EWSR1-BEND2 fusion(Yamasaki, 2019). Here, we report a 36-year old man with a spinal cord astroblastoma with EWSR1 alternation. The patient presented with back pain, gait disorder and dysesthesia in lower extremities and trunk was referred to our hospital. MRI showed intramedullary tumor in Th3-5 level, displaying low-intensity on T1 weighted image, high-intensity on T2 weighted image, and homogeneous gadolinium enhancement. Partial removal was performed with the laminectomy. The tumor extended to extramedullary and its boundary was unclear. Histological examinations showed the epithelium-like tumor cells with eosinophilic cytoplasm with high cellularity palisade, intracellar fibrosis, and mitosis. Immunohistochemical staining showed positive for Olig2, GFAP, EMA, SSTR2, S-100, but negative for p53, PgRAE1/AE3. The tumor was diagnosed as astroblastoma, and was classified as HGNET-MN1 by the DKFZ methylation classifier. However, the MN1 alternation was not detected by fluorescence in situ hybridization, instead EWSR1 and BEND2 alternations which suggested EWSR1-BEND2 fusion were detected. After radiation therapy of 54Gy/30fr with bevacizumab and temozolomide, the residual tumor reduced the size and his symptoms improved. This case provides evidence that EWSR1-BEND2 fusion is recurrent in HGNET-MN1 and, as previously reported, suggests the importance of BEND2 in this entity. These two cases suggested that it may be the BEND2 alteration that biologically defines the HGNET-MN1 subclass rather than MN1.

Differential modulation of inositol 1,4,5-trisphosphate receptor type 1 and type 3 by ATP

Cell Calcium ◽  
2000 ◽  
Vol 27 (5) ◽  
pp. 257-267 ◽  
Author(s):  
K. Maes ◽  
L. Missiaen ◽  
P. De Smet ◽  
S. Vanlingen ◽  
G. Callewaert ◽  
...  
Keyword(s):  
Receptor Type ◽  
Differential Modulation ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor ◽  
Type 3

scholarly journals An Integrated View on Neuronal Subsets in the Peripheral Nervous System and Their Role in Immunoregulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Manuel O. Jakob ◽  
Michael Kofoed-Branzk ◽  
Divija Deshpande ◽  
Shaira Murugan ◽  
Christoph S. N. Klose
Keyword(s):  
Nervous System ◽  
Immune Responses ◽  
Peripheral Nervous System ◽  
Tissue Homeostasis ◽  
Therapeutic Approaches ◽  
Immune Reactions ◽  
Peripheral Neurons ◽  
Inflammatory Signals ◽  
Neuronal Regulation

The peripheral nervous system consists of sensory circuits that respond to external and internal stimuli and effector circuits that adapt physiologic functions to environmental challenges. Identifying neurotransmitters and neuropeptides and the corresponding receptors on immune cells implies an essential role for the nervous system in regulating immune reactions. Vice versa, neurons express functional cytokine receptors to respond to inflammatory signals directly. Recent advances in single-cell and single-nuclei sequencing have provided an unprecedented depth in neuronal analysis and allowed to refine the classification of distinct neuronal subsets of the peripheral nervous system. Delineating the sensory and immunoregulatory capacity of different neuronal subsets could inform a better understanding of the response happening in tissues that coordinate physiologic functions, tissue homeostasis and immunity. Here, we summarize current subsets of peripheral neurons and discuss neuronal regulation of immune responses, focusing on neuro-immune interactions in the gastrointestinal tract. The nervous system as a central coordinator of immune reactions and tissue homeostasis may predispose for novel promising therapeutic approaches for a large variety of diseases including but not limited to chronic inflammation.

Control of noradrenergic differentiation and Phox2a expression by MASH1 in the central and peripheral nervous system

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 599-608 ◽  
Author(s):  
M.R. Hirsch ◽  
M.C. Tiveron ◽  
F. Guillemot ◽  
J.F. Brunet ◽  
C. Goridis
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Peripheral Nervous System ◽  
Genetic Circuits ◽  
Autonomic Nervous ◽  
Peripheral Neurons ◽  
Dopamine Beta Hydroxylase ◽  
Targeted Mutation ◽  
The Brain ◽  
Noradrenergic Differentiation

Mash1, a mammalian homologue of the Drosophila proneural genes of the achaete-scute complex, is transiently expressed throughout the developing peripheral autonomic nervous system and in subsets of cells in the neural tube. In the mouse, targeted mutation of Mash1 has revealed a role in the development of parts of the autonomic nervous system and of olfactory neurons, but no discernible phenotype in the brain has been reported. Here, we show that the adrenergic and noradrenergic centres of the brain are missing in Mash1 mutant embryos, whereas most other brainstem nuclei are preserved. Indeed, the present data together with the previous results show that, except in cranial sensory ganglia, Mash1 function is essential for the development of all central and peripheral neurons that express noradrenergic traits transiently or permanently. In particular, we show that, in the absence of MASH1, these neurons fail to initiate expression of the noradrenaline biosynthetic enzyme dopamine beta-hydroxylase. We had previously shown that all these neurons normally express the homeodomain transcription factor Phox2a, a positive regulator of the dopamine beta-hydroxylase gene and that a subset of them depend on it for their survival. We now report that expression of Phox2a is abolished or massively altered in the Mash1−/− mutants, both in the noradrenergic centres of the brain and in peripheral autonomic ganglia. These results suggest that MASH1 controls noradrenergic differentiation at least in part by controlling expression of Phox2a and point to fundamental homologies in the genetic circuits that determine the noradrenergic phenotype in the central and peripheral nervous system.

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