Physiological role of NO production in invertebrate nervous system

2006 ◽  
Vol 145 (3-4) ◽  
pp. 405-406
Author(s):  
Y. Kitamura ◽  
H. Aonuma ◽  
K. Oka ◽  
H. Ogawa
Keyword(s):  
Nervous System ◽  
Physiological Role ◽  
No Production ◽  
Invertebrate Nervous System

Immunomodulation by 17β-estradiol in bivalve hemocytes

2006 ◽  
Vol 291 (3) ◽  
pp. R664-R673 ◽  
Author(s):  
Laura Canesi ◽  
Caterina Ciacci ◽  
Lucia Cecilia Lorusso ◽  
Michele Betti ◽  
Tiziana Guarnieri ◽  
...  
Keyword(s):  
Kinase Inhibitors ◽  
Hydrolytic Enzymes ◽  
Physiological Role ◽  
Estrogen Receptor Α ◽  
Nitrite Accumulation ◽  
No Production ◽  
17Β Estradiol

In mammals, estrogens have dose- and cell-type-specific effects on immune cells and may act as pro- and anti-inflammatory stimuli, depending on the setting. In the bivalve mollusc Mytilus, the natural estrogen 17β-estradiol (E2) has been shown to affect neuroimmune functions. We have investigated the immunomodulatory role of E2 in Mytilus hemocytes, the cells responsible for the innate immune response. E2 at 5–25 nM rapidly stimulated phagocytosis and oxyradical production in vitro; higher concentrations of E2 inhibited phagocytosis. E2-induced oxidative burst was prevented by the nitric oxide (NO) synthase inhibitor NG-monomethyl-l-arginine and superoxide dismutase, indicating involvement of NO and O2−; NO production was confirmed by nitrite accumulation. The effects of E2 were prevented by the antiestrogen tamoxifen and by specific kinase inhibitors, indicating a receptor-mediated mechanism and involvement of p38 MAPK and PKC. E2 induced rapid and transient increases in the phosphorylation state of PKC, as well as of a aCREB-like (cAMP responsive element binding protein) transcription factor, as indicated by Western blot analysis with specific anti-phospho-antibodies. Localization of estrogen receptor-α- and -β-like proteins in hemocytes was investigated by immunofluorescence confocal microscopy. The effects of E2 on immune function were also investigated in vivo at 6 and 24 h in hemocytes of E2-injected mussels. E2 significantly affected hemocyte lysosomal membrane stability, phagocytosis, and extracellular release of hydrolytic enzymes: lower concentrations of E2 resulted in immunostimulation, and higher concentrations were inhibitory. Our data indicate that the physiological role of E2 in immunomodulation is conserved from invertebrates to mammals.

scholarly journals Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System

2020 ◽  
Vol 14 ◽  
Author(s):  
Isis Zhang ◽  
Huijuan Hu
Keyword(s):  
Nervous System ◽  
Calcium Channels ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Physiological Role ◽  
The Body ◽  
Store Operated Calcium Entry ◽  
Important Pathway ◽  
Molecular Components

Store-operated calcium channels (SOCs) are widely expressed in excitatory and non-excitatory cells where they mediate significant store-operated calcium entry (SOCE), an important pathway for calcium signaling throughout the body. While the activity of SOCs has been well studied in non-excitable cells, attention has turned to their role in neurons and glia in recent years. In particular, the role of SOCs in the nervous system has been extensively investigated, with links to their dysregulation found in a wide variety of neurological diseases from Alzheimer’s disease (AD) to pain. In this review, we provide an overview of their molecular components, expression, and physiological role in the nervous system and describe how the dysregulation of those roles could potentially lead to various neurological disorders. Although further studies are still needed to understand how SOCs are activated under physiological conditions and how they are linked to pathological states, growing evidence indicates that SOCs are important players in neurological disorders and could be potential new targets for therapies. While the role of SOCE in the nervous system continues to be multifaceted and controversial, the study of SOCs provides a potentially fruitful avenue into better understanding the nervous system and its pathologies.

scholarly journals Ganglioside Synthesis by Plasma Membrane-Associated Sialyltransferase in Macrophages

2020 ◽  
Vol 21 (3) ◽  
pp. 1063
Author(s):  
Aldo Vilcaes ◽  
Eduardo Garbarino-Pico ◽  
Vanina Torres Demichelis ◽  
Jose Daniotti
Keyword(s):  
Plasma Membrane ◽  
Cell Surface ◽  
Fluorescent Microscopy ◽  
Physiological Role ◽  
No Synthase ◽  
Raw264.7 Cells ◽  
No Production ◽  
Ganglioside Metabolism ◽  
Gd3 Ganglioside

Gangliosides are constituents of the mammalian cell membranes and participate in the inflammatory response. However, little is known about the presence and enzymatic activity of ganglioside sialyltransferases at the cell surface of macrophages, one of the most important immune cells involved in the innate inflammatory process. In the present study, using biochemical and fluorescent microscopy approaches, we found that endogenous ST8Sia-I is present at the plasma membrane (ecto-ST8Sia-I) of murine macrophage RAW264.7 cells. Moreover, ecto-ST8Sia-I can synthetize GD3 ganglioside at the cell surface in lipopolysaccharide (LPS)-stimulated macrophages even when LPS-stimulated macrophages reduced the total ST8Sia-I expression levels. Besides, cotreatment of LPS with an inhibitor of nitric oxide (NO) synthase recovered the ecto-ST8Sia-I expression, suggesting that NO production is involved in the reduction of ST8Sia-I expression. The diminution of ST8Sia-I expression in LPS-stimulated macrophages correlated with a reduction of GD3 and GM1 gangliosides and with an increment of GD1a. Taken together, the data supports the presence and activity of sialyltransferases at the plasma membrane of RAW264.7 cells. The variations of ecto-ST8Sia-I and ganglioside levels in stimulated macrophages constitutes a promissory pathway to further explore the physiological role of this and others ganglioside metabolism-related enzymes at the cell surface during the immune response.

scholarly journals NEUROMODULATOR LIGAND-RECEPTOR SYSTEM TIP39 - PTH2R

2020 ◽  
Vol 10 (2) ◽  
pp. 78-85
Author(s):  
A. N. Kurzanov ◽  
I. M. Bykov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Signal Transmission ◽  
Physiological Role ◽  
Receptor System ◽  
Axon Terminals ◽  
Nociceptive Information ◽  
The Central Nervous System ◽  
Anxiety Depression

Widely spread axon terminals of TIP39 neurons have a distribution similar to PTH2R containing neurons and their fibers which provides an anatomic base of neuromodulation action of TIP39. This functional and anatomic link- ing lets state that TIP39 and PTH2R form a neuromodulator ligand-receptor system. Basing on mechanisms of signal transmission used by TIP39 and PTH2R, they can form a neuromodulator system in many brain parts. TIP39-PTH2R system is a unique neuropeptide-receptor system, which localization and functions in the central nervous system differ from any other neuropeptides. Neuromodulator system TIP39-PTH2R predominantly participates in neuroendocrinal modulation by affecting the endocrinal system by means of its presence in several areas of hypothalamus. TIP39 influences neurons that contain somatostatin and corticotropin-releasing hormone. TIP39 can affect the release of adrenocorticotropin, luteinizing hormone, growth hormone and arginine-vasopressin from hypophysis. Experimental data prove that TIP39 modulates regulatory network of anxiety and depression, several aspects of stress reaction and also controls body temperature, participates in processing of auditory and nociceptive information. Physiological role of TIP39-PTH2R system is still to some extent unknown. However, distribution of PTH2R and TIP39 in tissues outside central nervous system assumes other potential physiological effects for this signal way. It is assumed that TIP39- PTH2R system should be probably considered as a potential therapeutic target for treatment of anxiety, depression and chronic pain, control and correction of neuroendocrine disruptions.

Evidence for a physiological role of nerve growth factor in the central nervous system of neonatal rats

Neuron ◽  
1989 ◽  
Vol 3 (3) ◽  
pp. 267-273 ◽  
Author(s):  
G. Vantini ◽  
N. Schiavo ◽  
A. Di Martino ◽  
P. Polato ◽  
C. Triban ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Physiological Role ◽  
Neonatal Rats ◽  
Nerve Growth ◽  
The Central Nervous System

scholarly journals Nitric Oxide: From Gastric Motility to Gastric Dysmotility

2021 ◽  
Vol 22 (18) ◽  
pp. 9990
Author(s):  
Eglantina Idrizaj ◽  
Chiara Traini ◽  
Maria Giuliana Vannucchi ◽  
Maria Caterina Baccari
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Gastric Motility ◽  
Muscle Relaxation ◽  
Physiological Role ◽  
Smooth Muscle Relaxation ◽  
No Production ◽  
Main Role ◽  
Motor Responses

It is known that nitric oxide (NO) plays a key physiological role in the control of gastrointestinal (GI) motor phenomena. In this respect, NO is considered as the main non-adrenergic, non-cholinergic (NANC) inhibitory neurotransmitter responsible for smooth muscle relaxation. Moreover, many substances (including hormones) have been reported to modulate NO production leading to changes in motor responses, further underlying the importance of this molecule in the control of GI motility. An impaired NO production/release has indeed been reported to be implicated in some GI dysmotility. In this article we wanted to focus on the influence of NO on gastric motility by summarizing knowledge regarding its role in both physiological and pathological conditions. The main role of NO on regulating gastric smooth muscle motor responses, with particular reference to NO synthases expression and signaling pathways, is discussed. A deeper knowledge of nitrergic mechanisms is important for a better understanding of their involvement in gastric pathophysiological conditions of hypo- or hyper-motility states and for future therapeutic approaches. A possible role of substances which, by interfering with NO production, could prove useful in managing such motor disorders has been advanced.

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