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We evaluated the effects of two consecutive concussive injuries on brain energy metabolism and N-acetylaspartate (NAA) to investigate how the temporal interval between traumatic events influences overall injury severity. Rats were injured... more
We evaluated the effects of two consecutive concussive injuries on brain energy metabolism and N-acetylaspartate (NAA) to investigate how the temporal interval between traumatic events influences overall injury severity. Rats were injured to induce diffuse traumatic brain injury (TBI) (mild, 450 g/1 m; severe, 450 g/2 m). In two groups, two mild TBIs were delivered in 3- or 5-day intervals. Three additional animal groups were used: single mild TBI, single severe TBI, and sham. All animals were killed 48 hours postinjury. Adenosine 5'-triphosphate (ATP), adenosine diphosphate, and NAA concentrations were analyzed with high-performance liquid chromatography on deproteinized whole brain extracts. In control animals, the NAA concentration was 9.17 +/- 0.38 micromol/g wet weight, the ATP concentration was 2.25 +/- 0.21 micromol/g wet weight, and the ATP-to-adenosine diphosphate ratio was 9.38 +/- 1.23. These concentrations decreased to 6.68 +/- 1.12 micromol/g wet weight, 1.68 +/- 0.24 micromol/g wet weight, and 6.10 +/- 1.21 micromol/g wet weight, respectively, in rats that received two mild TBIs at a 5-day interval (P < 0.01; not different from results in rats with single mild TBI). When a second TBI was delivered after 3 days, the NAA concentration was 3.86 +/- 0.53 micromol/g wet weight, the ATP concentration was 1.11 +/- 0.18 micromol/g wet weight, and the ATP-to-adenosine diphosphate ratio was 2.64 +/- 0.43 (P < 0.001 versus both controls and 3-day interval; not different from rats receiving a single severe TBI). The biochemical modification severity in double TBI is dependent on the interval between traumatic events, which demonstrates the metabolic state of the vulnerable brain after mild TBI. These data support the hypothesis of the application of proton magnetic resonance spectroscopy to measure NAA as a possible tool to monitor the full recovery of brain metabolic functions in the clinical setting, particularly in sports medicine.
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Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same... more
Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same perfusion conditions, the effect of exogenous 5mM fructose-1,6-bisphosphate has been investigated. The xanthine dehydrogenase to xanthine oxidase ratio, concentrations of high-energy phosphates and of TBA-reactive material (TBARS) were determined at the end of each perfusion period in both control and fructose-1,6-bisphosphate-treated hearts. Results indicate that anoxia induces the irreversible transformation of xanthine dehydrogenase into oxidase as a consequence of the sharp decrease of the myocardial energy metabolism. This finding is supported by the protective effect exerted by exogenous fructose-1,6-bisphosphate which is able to maintain the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds during anoxia. Moreover, in control hearts, the release of lactate dehydrogenase during reperfusion, is paralleled by a 50% increase in the concentration of tissue TBARS. On the contrary, in fructose-1,6-bisphosphate-treated hearts this concentration does not significantly change after reoxygenation, while a slight but significant increase of lactate dehydrogenase activity in the perfusates is observed. On the whole these data indicate a direct contribution of oxygen-derived free radicals to the worsening of post-anoxic hearts. A hypothesis on the mechanism of action of fructose-1,6-bisphosphate in anoxic and reperfused rat heart and its possible application in the clinical therapy of myocardial infarction are presented.
Research Interests: Chemistry, Free Radicals, Medicine, Energy Metabolism, Free Radical, and 15 moreBiological Sciences, Internal Medicine, Anoxia, Animals, Male, Fructose, Lipid peroxidation, CHEMICAL SCIENCES, Rats, Oxygen, Reperfusion injury, Lactate dehydrogenase, High energy, Medical and Health Sciences, and In Vitro Techniques
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CONCUSSION AND TRAUMATIC ENCEPHALOPATHY: CAUSES, DIAGNOSIS, AND MANAGEMEN
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Research Interests: Endocrinology, Traumatic Brain Injury, Biology, Medicine, Energy Metabolism, and 11 moreBiological Sciences, Internal Medicine, Physical sciences, Glycolysis, Enzyme, Clinical Sciences, Mitochondrial dysfunction, Oxidative phosphorylation, Biochemistry and cell biology, Pentose Phosphate Pathway, and Medical biochemistry and metabolomics
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Research Interests: Oxidative Stress, Folic acid, Medicine, Prodrugs, Ischemia, and 15 moreNitric oxide, Animals, Vascular endothelium, Clinical Sciences, Rats, Myocardial Infarction, Nitric Oxide Synthase, Public health systems and services research, Circulation, Reperfusion injury, Superoxides, High energy, Adenosine Triphosphate, Adenosine Diphosphate, and Cardiovascular medicine and haematology
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Research Interests: Chemistry, Mitochondria, Medicine, Platelet, Humans, and 7 moreGlucose, Female, Pubmed, Male, Plasma, Blood Transfusion, and Blood platelets
The effect of reperfusion with L-propionyl-carnitine-taurinammide 1 mM was evaluated on the metabolic recovery of the isolated postischemic rat heart. Data referring to the tissue concentration of the high-energy phosphates, oxypurines,... more
The effect of reperfusion with L-propionyl-carnitine-taurinammide 1 mM was evaluated on the metabolic recovery of the isolated postischemic rat heart. Data referring to the tissue concentration of the high-energy phosphates, oxypurines, nucleosides, nicotinic coenzymes, lactate and pyruvate indicate that L-propionyl-carnitine-taurinammide significantly improves the metabolism of the reperfused myocardium. In particular, ATP, creatinphosphate, GTP, sum of adenine nucleotides and the energy charge resulted 1.80, 1.83, 3.47, 1.47 and 1.20 times higher respectively than the corresponding values recorded in control reperfused heart (p < 0.01 all). These data, out of supplying the necessary biochemical support to the beneficial effects of L-propionyl-carnitine-taurinammide on hemodynamics obtained in previous studies, suggest that L-propionyl-carnitine-taurinammide might represent a useful tool for the pharmacological treatment of myocardial infarction.
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Ischemia and reperfusion damage has been evaluated by determining the sum of adenine nucleotides, nucleosides, oxypurines and the concentration of malondialdehyde, ascorbic acid, lactate and pyruvate in the isolated rat heart subjected to... more
Ischemia and reperfusion damage has been evaluated by determining the sum of adenine nucleotides, nucleosides, oxypurines and the concentration of malondialdehyde, ascorbic acid, lactate and pyruvate in the isolated rat heart subjected to global normothermic ischemia and subsequent reperfusion. In addition, the sum of oxypurines and nucleosides, and the concentration of malondialdehyde has been determined in the perfusate collected during the reperfusion. Data indicate that ischemia and reperfusion induce an oxidative stress to myocardial tissue (increase of tissue malondialdehyde and decrease of ascorbic acid, and release of malondialdehyde during reperfusion) that, due to the output of relevant amount of oxypurines (congruent to 6.7 mumol/g dry weight) and of nucleosides (congruent to 7.0 mumol/30/min/g dry weight), it is not even able to restore its energy metabolism after reperfusion.
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AimsSeveral studies reported that astrocytes support neuronal communication by the release of gliotransmitters, including ATP and glutamate. Astrocytes also play a fundamental role in buffering extracellular glutamate in the synaptic... more
AimsSeveral studies reported that astrocytes support neuronal communication by the release of gliotransmitters, including ATP and glutamate. Astrocytes also play a fundamental role in buffering extracellular glutamate in the synaptic cleft, thus limiting the risk of excitotoxicity in neurons. We previously demonstrated that extracellular tau oligomers (ex‐oTau), by specifically targeting astrocytes, affect glutamate‐dependent synaptic transmission via a reduction in gliotransmitter release. The aim of this work was to determine if ex‐oTau also impair the ability of astrocytes to uptake extracellular glutamate, thus further contributing to ex‐oTau‐dependent neuronal dysfunction.MethodsPrimary cultures of astrocytes and organotypic brain slices were exposed to ex‐oTau (200 nM) for 1 h. Extracellular glutamate buffering by astrocytes was studied by: Na+ imaging; electrophysiological recordings; high‐performance liquid chromatography; Western blot and immunofluorescence. Experimental paradigms avoiding ex‐oTau internalisation (i.e. heparin pre‐treatment and amyloid precursor protein knockout astrocytes) were used to dissect intracellular vs extracellular effects of oTau.ResultsEx‐oTau uploading in astrocytes significantly affected glutamate‐transporter‐1 expression and function, thus impinging on glutamate buffering activity. Ex‐oTau also reduced Na‐K‐ATPase activity because of pump mislocalisation on the plasma membrane, with no significant changes in expression. This effect was independent of oTau internalisation and it caused Na+ overload and membrane depolarisation in ex‐oTau‐targeted astrocytes.ConclusionsEx‐oTau exerted a complex action on astrocytes, at both intracellular and extracellular levels. The net effect was dysregulated glutamate signalling in terms of both release and uptake that relied on reduced expression of glutamate‐transporter‐1, altered function and localisation of NKA1A1, and NKA1A2. Consequently, Na+ gradients and all Na+‐dependent transports were affected.
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Concussion, a peculiar type of mild traumatic brain injury (mTBI) frequently encountered in sports medicine, is characterized by complex molecular alterations of various important functions of neuronal cells, including... more
Concussion, a peculiar type of mild traumatic brain injury (mTBI) frequently encountered in sports medicine, is characterized by complex molecular alterations of various important functions of neuronal cells, including mitochondrial-related energy supply, ionic homeostasis, neurotransmitters, N-acetylaspartate (NAA) homeostasis, and even gene expression. Most of these molecular and metabolic derangements are of limited duration (spontaneous recovery of metabolism and cell functions), representing the bases of the metabolic brain vulnerability occurring after mTBI. In this chapter, we describe results of experimental studies evidencing the connections among mTBI, energy metabolism, mitochondrial dysfunctions, and NAA, as well as we summarize results of clinical studies demonstrating that the monitoring of brain metabolism (NAA and creatine) by proton magnetic resonance spectroscopy (1H-MRS) is a useful tool to increase the safety of return to play of athletes after a concussion. The application of 1H-MRS in concussed athletes shows that clinical symptoms clear much faster than normalization of brain metabolism. 1H-MRS allows to measure objective parameters of biochemical relevance and is suitable to determine the end of the period of brain vulnerability. This information cannot otherwise be obtained with clinical tests of current use and is important to minimize the risks related to an early return on the field of concussed athletes.
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Background: It is essential that the quality of platelet metabolism and function remains high during storage in order to ensure the clinical effectiveness of a platelet transfusion. New storage conditions and additives are constantly... more
Background: It is essential that the quality of platelet metabolism and function remains high during storage in order to ensure the clinical effectiveness of a platelet transfusion. New storage conditions and additives are constantly evaluated in order to achieve this. Using glucose as a substrate is controversial because of its potential connection with increased lactate production and decreased pH, both parameters triggering the platelet lesion during storage. Materials and methods: In this study, we analysed the morphological status and metabolic profile of platelets stored for various periods in autologous plasma enriched with increasing glucose concentrations (13.75, 27.5 and 55 mM). After 0, 2, 4, 6 and 8 days, high energy phosphates (ATP, GTP, ADP, AMP), oxypurines (hypoxanthine, xanthine, uric acid), lactate, pH, mitochondrial function, cell lysis and morphology, were evaluated. Results: The data showed a significant dose-dependent improvement of the different parameters in platelets stored with increasing glucose, compared to what detected in controls. Interestingly, this phenomenon was more marked at the highest level of glucose tested and in the period of time generally used for platelet transfusion (0-6 days). Conclusion: These results indicate that the addition of glucose during platelet storage ameliorates, in a dose-dependent manner, the biochemical parameters related to energy metabolism and mitochondrial function. Since there was no correspondence between glucose addition, lactate increase and pH decrease in our experiments, it is conceivable that platelet derangement during storage is not directly caused by glucose through an increase of anaerobic glycolysis, but rather to a loss of mitochondrial functions caused by reduced substrate availability.
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The efficacy of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) against the replication of human immunodeficiency virus (HIV) and herpes simplex virus type 1 (HSV-1) and its cellular metabolism were investigated in human primary macrophages... more
The efficacy of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) against the replication of human immunodeficiency virus (HIV) and herpes simplex virus type 1 (HSV-1) and its cellular metabolism were investigated in human primary macrophages from seronegative donors. PMEA potently inhibited the replication of both HIV and HSV-1 in macrophages, with similar EC50 values (0.025 and 0.032 microM, respectively), whereas the EC50 values of PMEA in lymphocytic C8166 cells and fibroblastoid Vero cells were 150-200-fold higher (3.5 and 7.9 microM, respectively). Granulocyte/macrophage colony-stimulating factor and macrophage colony-stimulating factor, two cytokine enhancers of the replication of HIV (and HSV-1), decreased the activity of PMEA against both viruses, yet EC50 values were still lower than in lymphocytes and fibroblasts. Thus, the selectivity index of PMEA in macrophages was > 2 orders of magnitude higher than that in lymphocytes and fibroblasts and still > 1 log higher under conditions of enhancement of virus replication in macrophages. The intracellular levels of 2'-deoxyadenosine-5'-triphosphate, the natural competitor of PMEA-diphosphate at the level of viral DNA polymerase (either RNA or DNA dependent), were 5-12-fold lower in macrophages than in other cells. Furthermore, intracellular concentrations of PMEA-diphosphate (the active metabolite of PMEA) were unusually much higher in macrophages (with or without cytokines) than in lymphocytes and fibroblasts. Consequently, the ratio of PMEA-diphosphate to 2'-deoxyadenosine-5'-triphosphate in monocytes/macrophages was approximately 2 orders of magnitude higher in macrophages than in the other cells and correlated closely with the pronounced antiviral potency of PMEA. The dual potent activity of PMEA against HIV and HSV-1 stresses the importance of clinical trials to assess the role of this drug in the therapy of HIV-related disease.
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Research Interests: Pharmacology, Chemistry, Life Sciences, Oxidative Stress, Medicine, and 15 moreEnergy Metabolism, Mice, DBA, Animals, Male, Morphine, Neutrophils, Energy Production, Opioid Receptor, Naloxone, Malondialdehyde, Catabolism, Biochemistry and cell biology, Oxidative Metabolism, and Pharmacology and pharmaceutical sciences
Isolated rat hearts were perfused by the recirculating Langendorff mode under normoxic conditions for 60 min. The Krebs-Ringer buffer was supplemented with 10 mM glucose + 12 IU/l insulin and either [U-14C]-fructose-1,6-bisphosphate... more
Isolated rat hearts were perfused by the recirculating Langendorff mode under normoxic conditions for 60 min. The Krebs-Ringer buffer was supplemented with 10 mM glucose + 12 IU/l insulin and either [U-14C]-fructose-1,6-bisphosphate (together with 5 mM cold fructose-1,6-bisphosphate) or [U-14C]-fructose (together with 5 mM cold fructose). At the end of perfusion, gaseous 14CO2, 14CO2 trapped in the perfusates, 14C-lactate output and tissue 14C-lactate were assayed in both groups of hearts. Analysis of high-energy compounds, glycogen, lactate, and pyruvate was also performed on the neutralized perchloric acid extracts of the freeze-clamped hearts. Data obtained from the 14C catabolites, originating from the metabolism of the radiolabeled substrates, indicated that the isolated normoxic rat heart metabolizes an 8.5 times higher amount of fructose-1,6-bisphosphate (7.07 mumoles/min/g d.w.) than of fructose (0.83 mumoles/min/g d.w.). CrP, CrP/Cr, glycogen, and total lactate in both tissue and perfusate were significantly higher in fructose-1,6-bisphosphate-perfused hearts. The overall indication is that fructose-1,6-bisphosphate can be taken up in its intact form by myocytes and successively metabolized to support their energy demand, and that its effects on myocardial performance and metabolism should be attributed to the molecule itself rather than to its eventual degradation products.
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Research Interests: Clinical Biochemistry, Medicine, Energy Metabolism, Brain Death, Cerebrospinal Fluid, and 15 moreCase Report, Humans, Clinical, Male, High Performance Liquid Chromatography, Middle Aged, Ascorbic Acid, Head injury, Nucleosides, Intracranial Pressure, Brain Damage, Malondialdehyde, Head Trauma, Brain injuries, and Medical biochemistry and metabolomics
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An ion-pairing high-performance liquid chromatographic method for the direct and simultaneous determination of nucleotides, deoxynucleotides, cAMP, nicotinic coenzymes, oxypurines, nucleosides, and bases in perchloric acid cell extracts... more
An ion-pairing high-performance liquid chromatographic method for the direct and simultaneous determination of nucleotides, deoxynucleotides, cAMP, nicotinic coenzymes, oxypurines, nucleosides, and bases in perchloric acid cell extracts is presented. By using an Alltima C-18, 250 x 4.6-mm, 5-microns particle size column, a high resolution of 38 acid-soluble compounds, including ATP, GTP, dTTP, CTP, UTP, ADP, GDP, dTDP, CDP, UDP, dATP, dGTP, dCTP, dUTP, dADP, dGDP, dCDP, dUDP, and cAMP, is obtained. Elution is performed with a step gradient from buffer A (consisting of 10 mM tetrabutylammonium hydroxide, 10 mM KH2PO4, 0.25% methanol, pH 7.00) to buffer B (consisting of 2.8 mM tetrabutylammonium hydroxide, 100 mM KH2PO4, 30% methanol, pH 5.50). Perchloric acid extracts of resting and phytohemagglutinin-stimulated human lymphocytes were analyzed. Data indicate that this chromatographic method offers, for the first time to the best of our knowledge, the possibility of simultaneously determining di- and triphosphate nucleosides and their corresponding deoxynucleosides without any chemical manipulation of samples except for perchloric acid deproteinization. Hence, the present HPLC assay minimizes the risks of modification or loss of metabolite concentration and allows one to obtain, with a single chromatographic run, the complete pattern of those metabolites which are known to be involved in energy metabolism and in DNA and RNA synthesis, resulting therefore of great advantage in cell biology studies.
Research Interests: Chemistry, Analytical Chemistry, Chromatography, Cell Biology, Medicine, and 15 moreEnergy Metabolism, Cell line, Humans, Analytical, High Resolution, Analytical Biochemistry, NAD, Lymphocytes, Nucleosides, Metabolite, Ions, Nucleotide, Nucleotides, Biochemistry and cell biology, and human lymphocyte
Research Interests: Medicine, Adenosine, Humans, Female, Male, and 15 moreLipid peroxidation, Clinical Sciences, Aged, Middle Aged, Myocardium, Circulation, Aorta, Malondialdehyde, Postoperative Period, Constriction, Intraoperative Period, Tissue distribution, purines, Cardiovascular medicine and haematology, and Coronary Artery Bypass
Research Interests: Neuroscience, Traumatic Brain Injury, Oxidative Stress, Medicine, Gene expression, and 14 moreEnergy Metabolism, Pathophysiology, Brain, Humans, Reactive Oxygen Species, Animals, D-Aspartic Acid, Clinical Sciences, Concussion, Biological markers, Intracranial Hypertension, Brain Edema, Adenosine Triphosphate, and Brain concussion
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Research Interests: Traumatic Brain Injury, Creatine, Mitochondria, Medicine, Animals, and 13 moreD-Aspartic Acid, Clinical Sciences, High Pressure Liquid Chromatography, Mitochondrial dysfunction, Rats, Neurotrauma, Somatic Cell Count, Diffuse Axonal Injury, Brain Chemistry, Choline, Neurosciences, Oxidation-Reduction, and Adenosine Triphosphate
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Research Interests: Chemistry, Analytical Chemistry, Chromatography, Medicine, Brain Tumor, and 15 moreAnimals, Male, Analytical, High Performance Liquid Chromatography, Rats, Phenylalanine, Particle Size, Derivatization, Clinical Study, Body Weight, Analytical Biochemistry, Flow Rate, Boron Compounds, Biochemistry and cell biology, and Reference standards
Macrophages are widely recognized as the second major target of HIV in the body. The cellular characteristics of such resting cells markedly affect the dynamics of virus lifecycle, that is slower but far more prolonged that in... more
Macrophages are widely recognized as the second major target of HIV in the body. The cellular characteristics of such resting cells markedly affect the dynamics of virus lifecycle, that is slower but far more prolonged that in lymphocytes. In addition, the limited concentrations of endogenous nucleotide pools in macrophages downregulate the enzymatic activity of reverse transcriptase. As a consequence, both the anti-HIV activity and the development of resistance to antiviral drugs in macrophages are substantially different than those found in activated lymphocytes. These peculiar characteristics of virus replication and efficacy of antiviral drugs in macrophages have a natural in vivo counterpart in extralymphoid tissues, where macrophages account for the majority of cells infected by HIV. Furthermore, the replication of HIV in macrophages of testis and central nervous system is far less affected by antiviral drugs than in lymph nodes, because of the presence of natural barriers that markedly diminish the concentration of such drugs. For all these reasons, HIV infection of macrophages should be taken into account in therapeutic strategies aimed to achieve an optimal therapeutic effect in all tissue compartments where the virus hides and replicates.
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Research Interests: Cardiology, Free Radicals, Medicine, Adenosine, Humans, and 15 moreInternal Medicine, Female, Male, Acute Myocardial Infarction, Creatine Kinase, Middle Aged, Uric Acid, Myocardial Infarction, Time Dependent, Time Factors, Thrombolytic Therapy, Malondialdehyde, Thrombolysis, Cardiovascular medicine and haematology, and Peripheral blood
Research Interests: Chemistry, Medicine, Brain, Humans, Ischemia, and 15 moreAnimals, Male, Acute Myocardial Infarction, Lipid peroxidation, Rats, Myocardial Infarction, Myocardium, Analysis of Variance, Cerebral Ischemia, Biological markers, Reference Values, Malondialdehyde, High energy, Myocardial Ischemia, and In Vitro Techniques
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Astrocytes provide metabolic support for neurons and modulate their functions by releasing a plethora of neuroactive molecules diffusing to neighboring cells. Here we report that astrocytes also play a role in cortical neurons'... more
Astrocytes provide metabolic support for neurons and modulate their functions by releasing a plethora of neuroactive molecules diffusing to neighboring cells. Here we report that astrocytes also play a role in cortical neurons' vulnerability to Herpes simplex virus type‐1 (HSV‐1) infection through the release of extracellular ATP. We found that the interaction of HSV‐1 with heparan sulfate proteoglycans expressed on the plasma membrane of astrocytes triggered phospholipase C‐mediated IP3‐dependent intracellular Ca2+ transients causing extracellular release of ATP. ATP binds membrane purinergic P2 receptors (P2Rs) of both neurons and astrocytes causing an increase in intracellular Ca2+ concentration that activates the Glycogen Synthase Kinase (GSK)‐3β, whose action is necessary for HSV‐1 entry/replication in these cells. Indeed, in co‐cultures of neurons and astrocytes HSV‐1‐infected neurons were only found in proximity of infected astrocytes releasing ATP, whereas in the presence of fluorocitrate, an inhibitor of astrocyte metabolism, switching‐off the HSV‐1‐induced ATP release, very few neurons were infected. The addition of exogenous ATP, mimicking that released by astrocytes after HSV‐1 challenge, restored the ability of HSV‐1 to infect neurons co‐cultured with metabolically‐inhibited astrocytes. The ATP‐activated, P2R‐mediated, and GSK‐3‐dependent molecular pathway underlying HSV‐1 infection is likely shared by neurons and astrocytes, given that the blockade of either P2Rs or GSK‐3 activation inhibited infection of both cell types. These results add a new layer of information to our understanding of the critical role played by astrocytes in regulating neuronal functions and their response to noxious stimuli including microbial agents via Ca2+‐dependent release of neuroactive molecules.
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... S 9 2&amp;amp;amp;amp;amp;amp;lt; ~ S B Page 3. SEQUENCE OF pol GENE OF HIV-1 BaL 631 Lys 65 Lys Asp Ser Thr Lys Trp Arg Lys Leu Val Asp Phe 5&amp;amp;amp;amp;amp;amp;#x27;- AAA - AAA - GAC - AGT - ACT - AAA - TGG - AGA -... more
... S 9 2&amp;amp;amp;amp;amp;amp;lt; ~ S B Page 3. SEQUENCE OF pol GENE OF HIV-1 BaL 631 Lys 65 Lys Asp Ser Thr Lys Trp Arg Lys Leu Val Asp Phe 5&amp;amp;amp;amp;amp;amp;#x27;- AAA - AAA - GAC - AGT - ACT - AAA - TGG - AGA - AAA - TTA - GTA - GAT - TTC Arg Glu 79 Leu Asn Lys Lys 83 Thr Gin Asp Phe Trp Glu Val ...