Role of Sigma Receptor in Cocaine-Mediated Induction of Glial Fibrillary Acidic Protein: Implications for HAND

The study aims to investigate the infuence of L-arginine on the content of nitrite anions (NO2¯) and nitrate anions (NO3¯) and the content of glial fibrillary acidic protein (GFAP) in the cerebellum and cerebral hemispheres of BALB/c mice with antiphospholipid syndrome. The studies were performed on 30 female BALB/c mice. The experimental animals were divided into 3 groups: 1 – control (intact) animals; 2 – animals with experimental antiphospholipid syndrome (APS), 3 – animals with APS, which were injected with L-arginine at a dose of 25 mg/kg, intraperitoneally once a day, for 10 consecutive days after the development of APS. The increase in glial fibrillary acidic protein and stable metabolites of nitric oxide NO2¯ and NO3¯ in the cerebellum and cerebral hemispheres, relative to the control, was observed in APS-developed BALB/c mice. In case of injection of the precursor of NO synthesis, L-arginine, animals with APS were found to have a further significant increase in the content of NO2¯ and NO3¯ in the cerebellum and the cerebral hemispheres. The introduction of L-arginine did not cause significant changes in GFAP (total) in cerebral hemispheres. However, GFAP content (49-37 kDa) was decreasing. The cerebellum showed an increase in GFAP (total) and GFAP (49-37 kDa) content, compared to the performance of animals with APS. Therefore, the increase in the content of GFAP in the cerebellum and the cerebral hemispheres of BALB/c mice under APS indicates the development of reactive astrogliosis. The introduction of the precursor of NO synthesis, L-arginine, is accompanied by an increase in the content of stable metabolites of nitric oxide (NO2¯, NO3¯) and GFAP in the cerebellum of BALB/c mice, which can indirectly confirm the role of NO in regulating of GFAP expression in astrocytes under APS.

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Role of anti-glial fibrillary acidic protein antibodies in the pathogenesis of neuropsychiatric systemic lupus erythematosus should be clarified: comment on the article by Trysberg et al

Arthritis & Rheumatism ◽

10.1002/art.20327 ◽

2004 ◽

Vol 50 (5) ◽

pp. 1698-1699 ◽

Cited By ~ 1

Author(s):

Cristiano Alessandri ◽

Fabrizio Conti ◽

Guido Valesini

Keyword(s):

Systemic Lupus Erythematosus ◽

Glial Fibrillary Acidic Protein ◽

Lupus Erythematosus ◽

Acidic Protein ◽

Systemic Lupus ◽

Neuropsychiatric Systemic Lupus Erythematosus

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Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration

Journal of Alzheimer s Disease ◽

10.3233/jad-200608 ◽

2020 ◽

Vol 77 (3) ◽

pp. 1129-1141 ◽

Cited By ~ 1

Author(s):

Alberto Benussi ◽

Nicholas J. Ashton ◽

Thomas K. Karikari ◽

Stefano Gazzina ◽

Enrico Premi ◽

...

Keyword(s):

Glial Fibrillary Acidic Protein ◽

Disease Severity ◽

Single Molecule ◽

Frontotemporal Lobar Degeneration ◽

Acidic Protein ◽

Cross Sectional ◽

Indirect Measures ◽

Neurophysiological Data ◽

Diagnostic And Prognostic Value

Background: It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD). Objective: To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD. Methods: In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer’s disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the correlation with clinical variables, neurophysiological data, and cross-sectional brain imaging. Moreover, we evaluated the role of serum GFAP as a prognostic marker of disease survival. Results: We observed significantly higher levels of serum GFAP in patients with FTLD syndromes, except progressive supranuclear palsy, compared with healthy controls, but not compared with AD patients. In FTLD, serum GFAP levels correlated with measures of cognitive dysfunction and disease severity, and were associated with indirect measures of GABAergic deficit. Serum GFAP concentration was not a significant predictor of survival. Conclusion: Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.

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Nerve Gas-Induced Seizures: Role of Acetylcholine in the Rapid Induction of Fos and Glial Fibrillary Acidic Protein in Piriform Cortex

Journal of Neuroscience ◽

10.1523/jneurosci.18-10-03897.1998 ◽

1998 ◽

Vol 18 (10) ◽

pp. 3897-3908 ◽

Cited By ~ 34

Author(s):

Lee A. Zimmer ◽

Matthew Ennis ◽

Ronald G. Wiley ◽

Michael T. Shipley

Keyword(s):

Glial Fibrillary Acidic Protein ◽

Piriform Cortex ◽

Acidic Protein ◽

Rapid Induction ◽

Nerve Gas

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Role of glial fibrillary acidic protein as a biomarker in differentiating intracerebral haemorrhage from ischaemic stroke and stroke mimics: a meta-analysis

Biomarkers ◽

10.1080/1354750x.2019.1691657 ◽

2019 ◽

Vol 25 (1) ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Amit Kumar ◽

Shubham Misra ◽

Arun Kumar Yadav ◽

Ram Sagar ◽

Bhawna Verma ◽

...

Keyword(s):

Glial Fibrillary Acidic Protein ◽

Ischaemic Stroke ◽

Intracerebral Haemorrhage ◽

Meta Analysis ◽

Acidic Protein ◽

Stroke Mimics

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Chronic vs. Acute Interactions between Supraoptic Oxytocin Neurons and Astrocytes during Lactation: Role of Glial Fibrillary Acidic Protein Plasticity

The Scientific World JOURNAL ◽

10.1100/tsw.2009.148 ◽

2009 ◽

Vol 9 ◽

pp. 1308-1320 ◽

Cited By ~ 12

Author(s):

Yu-Feng Wang ◽

Kathryn A. Hamilton

Keyword(s):

Glial Fibrillary Acidic Protein ◽

Supraoptic Nucleus ◽

Acidic Protein ◽

Dynamic Interactions ◽

Neuronal Interactions ◽

Initial Stage ◽

The Central Nervous System ◽

Acute Changes ◽

Related Proteins

In this article, we review studies of astrocytic-neuronal interactions and their effects on the activity of oxytocin (OXT) neurons within the magnocellular hypothalamo-neurohypophysial system. Previous work over several decades has shown that withdrawal of astrocyte processes increases OXT neuron excitability in the hypothalamic supraoptic nucleus (SON) during lactation. However, chronically disabling astrocyte withdrawal does not significantly affect the functioning of OXT neurons during suckling. Nevertheless, acute changes in a cytoskeletal element of astrocytes, glial fibrillary acidic protein (GFAP), occur in concert with changes in OXT neuronal activity during suckling. Here, we compare these changes in GFAP and related proteins with chronic changes that persist throughout lactation. During lactation, a decrease in GFAP levels accompanies retraction of astrocyte processes surrounding OXT neurons in the SON, resulting from high extracellular levels of OXT. During the initial stage of suckling, acute increases in OXT levels further strengthen this GFAP reduction and facilitate the retraction of astrocyte processes. This change, in turn, facilitates burst discharges of OXT neurons and leads to a transient increase in excitatory neurochemicals. This transient neurochemical surge acts to reverse GFAP expression and results in postburst inhibition of OXT neurons. The acute changes in astrocyte GFAP levels seen during suckling likely recur periodically, accompanied by rhythmic changes in glutamate metabolism, water transport, gliotransmitter release, and spatial relationships between astrocytes and OXT neurons. In the neurohypophysis, astrocyte retraction and reversal with accompanying GFAP plasticity also likely occur during lactation and suckling, which facilitates OXT release coordinated with its action in the SON. These studies of the dynamic interactions that occur between astrocytes and OXT neurons mediated by GFAP extend our understanding of astrocyte functions within the central nervous system.

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