Heterogeneous patterns of pH regulation in glial cells in the dorsal and ventral medulla

2004 ◽  
Vol 286 (2) ◽  
pp. R289-R302 ◽  
Author(s):  
Joseph S. Erlichman ◽  
Aaron Cook ◽  
Mary C. Schwab ◽  
Thomas W. Budd ◽  
J. C. Leiter
Keyword(s):  
Glial Cells ◽  
Nucleus Tractus Solitarius ◽  
Ph Regulation ◽  
Brain Slices ◽  
Regulatory Function ◽  
Glial Fibrillary Acid Protein ◽  
Retrotrapezoid Nucleus ◽  
Alkaline Shift ◽  
Immunohistochemical Studies ◽  
The Brain

We examined pH regulation in two chemosensitive areas of the brain, the retrotrapezoid nucleus (RTN) and the nucleus tractus solitarius (NTS), to identify the proton transporters involved in regulation of intracellular pH (pHi) in medullary glia. Transverse brain slices from young rats [postnatal day 8 (P8) to P20] were loaded with the pH-sensitive probe 2′,7′-bis (2-carboxyethyl)-5,6-carboxyfluorescein after kainic acid treatment removed neurons. Cells were alkalinized when they were depolarized (extracellular K+ increased from 6.24 to 21.24 mM) in the RTN but not in the NTS. This alkaline shift was inhibited by 0.5 mM DIDS. Removal of [Formula: see text] or Na+ from the perfusate acidified the glial cells, but the acidification after Na+ removal was greater in the RTN than in the NTS. Treatment of the slice with 5-( N-ethyl- N-isopropyl)amiloride (100 μM) in saline containing [Formula: see text] acidified the cells in both nuclei, but the acidification was greater in the NTS. Restoration of extracellular Cl- after Cl- depletion during the control condition acidified the cells. Immunohistochemical studies of glial fibrillary acid protein demonstrated much denser staining in the RTN compared with the NTS. We conclude that there is evidence of [Formula: see text] cotransport and Na+/H+ exchange in glia in the RTN and NTS, but the distribution of glia and the distribution of these pH-regulatory functions are not identical in the NTS and RTN. The differential strength of glial pH regulatory function in the RTN and NTS may also alter CO2 chemosensory neuronal function at these two chemosensitive sites in the brain stem.

scholarly journals Current ideas on central chemoreception by neurons and glial cells in the retrotrapezoid nucleus

2010 ◽  
Vol 108 (5) ◽  
pp. 1433-1439 ◽  
Author(s):  
Daniel K. Mulkey ◽  
Ian C. Wenker ◽  
Orsolya Kréneisz
Keyword(s):  
Blood Flow ◽  
Glial Cells ◽  
Ventilatory Response ◽  
Purinergic Signaling ◽  
Ph Sensitive ◽  
Tissue Ph ◽  
Retrotrapezoid Nucleus ◽  
Central Chemoreception ◽  
The Brain

Central chemoreception is the mechanism by which CO2/pH-sensitive neurons (i.e., chemoreceptors) regulate breathing in response to changes in tissue pH. A region of the brain stem called the retrotrapezoid nucleus (RTN) is thought to be an important site of chemoreception ( 23 ), and recent evidence suggests that RTN chemoreception involves two interrelated mechanisms: H+-mediated activation of pH-sensitive neurons ( 38 ) and purinergic signaling ( 19 ), possibly from pH-sensitive glial cells. A third, potentially important, aspect of RTN chemoreception is the regulation of blood flow, which is an important determinate of tissue pH and consequently chemoreceptor activity. It is well established in vivo that changes in cerebral blood flow can profoundly affect the chemoreflex ( 2 ); e.g., limiting blood flow by vasoconstriction acidifies tissue pH and increases the ventilatory response to CO2, whereas vasodilation can wash out metabolically produced CO2 from tissue to increase tissue pH and decrease the stimulus at chemoreceptors. In this review, we will summarize the defining characteristics of pH-sensitive neurons and discuss potential contributions of pH-sensitive glial cells as both a source of purinergic drive to pH-sensitive neurons and a modulator of vasculature tone.

Abstract 441: Sex Differences in Microglia Activation During Subpressor Dose of Angiotensin (Ang) II Sensitization of Subsequent Pressor Dose of Ang II

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Meredith Hay ◽  
Farmin Samareh- Jahani ◽  
Baojian Xue ◽  
Alan K Johnson
Keyword(s):  
Sex Differences ◽  
Experimental Design ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Brain Slices ◽  
Microglia Activation ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Activated Microglia ◽  
The Brain

In previous studies using the Induction-Delay-Expression (I-D-E) experimental design we have shown that there are sex differences in the effects of one-week Ang II pre-treatment to sensitize the brain to produce an enhanced hypertensive response to subsequent Ang II. In other studies, we have shown that females are protected from hypertension and brain infiltration of T lymphocytes during Ang II infusion. The purpose of the present study was to test whether there is a sex difference in brain microglia activation on the sensitizing effects of Ang II. The present studies followed an I-D-E experimental design. Three male and three female Sprague-Dawley rats were assigned to each of the following experimental groups: 1) Control ( I saline + D) ; 2) I-Ang II+D ( I with subpressor dose of Ang II, 10 ng/kg/min); 3) I-saline+D+E-Ang II (I with saline plus E with a pressor dose of Ang II, 120 ng/kg/min); 4) I-Ang II+D+E-Ang II (I with subpressor dose of Ang II plus E with pressor dose of Ang II). At the end of the experiment, animals were anesthetized and perfused with formalin. Thirty-micron frozen slices of the area postrema (AP), nucleus tractus solitarius (NTS), and subfornical organ (SFO) were processed for IHC staining with IBa-1 microglia antibody (WAKO, 1:200). The number of IBa-1+ activated microglia (MG) in each region were counted in an approx 3 consecutive brain slices from 3 separate animals. The subpressor dose of Ang II resulted in a significant increase in NTS activated microglia in males (MG 19.2 vs. 5.1) but not in females (MG 1.5 vs 2.3) when compared to control. In females, the pressor dose of Ang II did not increase the activated microglia in the NTS. The numbers of activated microglia in the AP was similar in males and females in the I-Ang II+D+E-Ang II group, but in the I-Sal+D+E-Ang II, males had greater number of MG in the AP as compared to females (21.5 vs 11.8, P=0.05). The number of MG in the SFO were low across all groups compared to the number of MG in other regions examined (males I-Ang II+D+E-Ang II group averaged 3.9 MG vs females averaged 2.3 MG). These results suggest that sex differences observed in the brain sensitization to Ang II may involve differential induction of microglia activation in selective brain regions important for Ang II generation of hypertension.

scholarly journals The Microbiota–Gut–Brain Axis and Alzheimer Disease. From Dysbiosis to Neurodegeneration: Focus on the Central Nervous System Glial Cells

2021 ◽  
Vol 10 (11) ◽  
pp. 2358
Author(s):  
Maria Grazia Giovannini ◽  
Daniele Lana ◽  
Chiara Traini ◽  
Maria Giuliana Vannucchi
Keyword(s):  
Alzheimer Disease ◽  
Glial Cells ◽  
Cell Types ◽  
The Past ◽  
The Central Nervous System ◽  
Diseased State ◽  
The Brain ◽  
Alzheimer Disease Pathogenesis ◽  
Brain Homeostasis

The microbiota–gut system can be thought of as a single unit that interacts with the brain via the “two-way” microbiota–gut–brain axis. Through this axis, a constant interplay mediated by the several products originating from the microbiota guarantees the physiological development and shaping of the gut and the brain. In the present review will be described the modalities through which the microbiota and gut control each other, and the main microbiota products conditioning both local and brain homeostasis. Much evidence has accumulated over the past decade in favor of a significant association between dysbiosis, neuroinflammation and neurodegeneration. Presently, the pathogenetic mechanisms triggered by molecules produced by the altered microbiota, also responsible for the onset and evolution of Alzheimer disease, will be described. Our attention will be focused on the role of astrocytes and microglia. Numerous studies have progressively demonstrated how these glial cells are important to ensure an adequate environment for neuronal activity in healthy conditions. Furthermore, it is becoming evident how both cell types can mediate the onset of neuroinflammation and lead to neurodegeneration when subjected to pathological stimuli. Based on this information, the role of the major microbiota products in shifting the activation profiles of astrocytes and microglia from a healthy to a diseased state will be discussed, focusing on Alzheimer disease pathogenesis.

scholarly journals Neuron–Glia Interactions in Tuberous Sclerosis Complex Affect the Synaptic Balance in 2D and Organoid Cultures

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 134
Author(s):  
Stephanie Dooves ◽  
Arianne J. H. van Velthoven ◽  
Linda G. Suciati ◽  
Vivi M. Heine
Keyword(s):  
Tuberous Sclerosis ◽  
Glial Cells ◽  
Tuberous Sclerosis Complex ◽  
Neuronal Development ◽  
Transmembrane Proteins ◽  
Significant Burden ◽  
Epidermal Growth ◽  
And Control ◽  
Egf Signaling ◽  
The Brain

Tuberous sclerosis complex (TSC) is a genetic disease affecting the brain. Neurological symptoms like epilepsy and neurodevelopmental issues cause a significant burden on patients. Both neurons and glial cells are affected by TSC mutations. Previous studies have shown changes in the excitation/inhibition balance (E/I balance) in TSC. Astrocytes are known to be important for neuronal development, and astrocytic dysfunction can cause changes in the E/I balance. We hypothesized that astrocytes affect the synaptic balance in TSC. TSC patient-derived stem cells were differentiated into astrocytes, which showed increased proliferation compared to control astrocytes. RNA sequencing revealed changes in gene expression, which were related to epidermal growth factor (EGF) signaling and enriched for genes that coded for secreted or transmembrane proteins. Control neurons were cultured in astrocyte-conditioned medium (ACM) of TSC and control astrocytes. After culture in TSC ACM, neurons showed an altered synaptic balance, with an increase in the percentage of VGAT+ synapses. These findings were confirmed in organoids, presenting a spontaneous 3D organization of neurons and glial cells. To conclude, this study shows that TSC astrocytes are affected and secrete factors that alter the synaptic balance. As an altered E/I balance may underlie many of the neurological TSC symptoms, astrocytes may provide new therapeutic targets.

THE METABOLISM OF NORMAL BRAIN AND HUMAN GLIOMAS IN RELATION TO CELL TYPE AND DENSITY

1955 ◽  
Vol 33 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Irving H. Heller ◽  
K. A. C. Elliott
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Tumors ◽  
Corpus Callosum ◽  
Oxygen Uptake ◽  
Glial Cells ◽  
Cerebellar Cortex ◽  
Unit Weight ◽  
Uptake Rates ◽  
The Brain

Per unit weight, cerebral and cerebellar cortex respire much more actively than corpus callosum. The rate per cell nucleus is highest in cerebral cortex, lower in corpus callosum, and still lower in cerebellar cortex. The oxygen uptake rates of the brain tumors studied, with the exception of an oligodendroglioma, were about the same as that of white matter on the weight basis but lower than that of cerebral cortex or white matter on the cell basis. In agreement with previous work, an oligodendroglioma respired much more actively than the other tumors. The rates of glycolysis of the brain tumors per unit weight were low but, relative to their respiration rate, glycolysis was higher than in normal gray or white matter. Consideration of the figures obtained leads to the following tentative conclusions: Glial cells of corpus callosum respire more actively than the neurons of the cerebellar cortex. Neurons of the cerebral cortex respire on the average much more actively than neurons of the cerebellar cortex or glial cells. Considerably more than 70% of the oxygen uptake by cerebral cortex is due to neurons. The oxygen uptake rates of normal oligodendroglia and astrocytes are probably about the same as the rates found per nucleus in an oligodendroglioma and in astrocytomas; oligodendroglia respire much more actively than astrocytes.

scholarly journals Temporal gliosarcoma: case report and review of literature

2015 ◽  
Vol 22 (1) ◽  
pp. 112-116
Author(s):  
Amit Agrawal ◽  
Vissa Shanthi ◽  
Baddukonda Appala Ramakrishna ◽  
Kuppili Venkata Murali Mohan
Keyword(s):  
Case Report ◽  
Median Survival ◽  
Glial Cells ◽  
Primary Tumor ◽  
Clinical Presentation ◽  
Spindle Cell ◽  
Review Of Literature ◽  
Future Studies ◽  
Aggressive Tumor ◽  
The Brain

Abstract First characterized by Stroebe, the gliosarcomas are highly malignant and rare primary tumor of the brain composed of neoplastic glial cells in association with spindle cell sarcomatous elements (biphasic tissue patterns). In spite of being recognized as two different pathologies studies have not shown any significant differences between gliosarcoma and glioblastoma with regard to age, sex, size, clinical presentation, and median survival. In summary, gliosarcoma is an aggressive tumor with a propensity to recur and re-grow with poor outcome. Future studies are needed to understand the true pathology of these biphasic tumors.

The brain-specific protein MLC1 implicated in megalencephalic leukoencephalopathy with subcortical cysts is expressed in glial cells in the murine brain

Glia ◽  
2003 ◽  
Vol 44 (3) ◽  
pp. 283-295 ◽  
Author(s):  
Angelika Schmitt ◽  
Viktor Gofferje ◽  
Melanie Weber ◽  
Jobst Meyer ◽  
Rainald Mössner ◽  
...  
Keyword(s):  
Glial Cells ◽  
Specific Protein ◽  
Murine Brain ◽  
The Brain ◽  
Subcortical Cysts

scholarly journals Effects of cadmium on the glial architecture in lizard brain

2017 ◽  
Author(s):  
Rossana Favorito ◽  
Antonio Monaco ◽  
Maria C. Grimaldi ◽  
Ida Ferrandino
Keyword(s):  
Blood Brain Barrier ◽  
Glial Cells ◽  
Toxic Metal ◽  
Chemical Exposure ◽  
Brain Barrier ◽  
Cresyl Violet ◽  
Cytotoxic Action ◽  
Morphological Alterations ◽  
Blood Brain ◽  
The Brain

The glial cells are positioned to be the first cells of the brain parenchyma to face molecules crossing the blood-brain barrier with a relevant neuroprotective role from cytotoxic action of heavy metals on the nervous system. Cadmium is a highly toxic metal and its levels in the environment are increasing due to industrial activities. This element can pass the blood-brain barrier and have neurotoxic activity. For this reason we have studied the effects of cadmium on the glial architecture in the lizard Podarcis siculus, a significant bioindicator of chemical exposure due to its persistence in a variety of habitats. The study was performed on two groups of lizards. The first group of P. siculus was exposed to an acute treatment by a single i.p. injection (2 mg/kg-BW) of CdCl2 and sacrificed after 2, 7 and 16 days. The second one was used as control. The histology of the brain was studied by Hematoxylin/Eosin and Cresyl/Violet stains while the glial structures were analyzed by immunodetection of the glial fibrillary acidic protein (GFAP), the most widely accepted marker for astroglial cells. Evident morphological alterations of the brain were observed at 7 and 16 days from the injection, when we revealed also a decrease of the GFAP-immunopositive structures in particular in the rhombencephalic ventricle, telencephalon and optic tectum. These results show that in the lizards an acute exposure to cadmium provokes morphological cellular alterations in the brain but also a decrement of the expression of GFAP marker with possible consequent damage of glial cells functions.

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