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Phospholipases A2 (PLA2s) are essential enzymes in cells. They are not only responsible for maintaining the structural organization of cell membranes, but also play a pivotal role in the regulation of cell functions. Activation of PLA2s results in the release of fatty acids and lysophospholipids, products that are lipid mediators and compounds capable of altering membrane microdomains and physical properties. Although not fully understood, recent studies have linked aberrant PLA2 activity to oxidative signaling pathways involving NADPH oxidase that underlie the pathophysiology of a number of neurodegenerative diseases. In this paper, we review studies describing the involvement of cytosolic PLA2 in oxidative signaling pathways leading to neuronal impairment and activation of glial cell inflammatory responses. In addition, this review also includes information on the role of cytosolic PLA2 and exogenous secretory PLA2 on membrane physical properties, dynamics, and membrane proteins. Unraveling the mechanisms that regulate specific types of PLA2s and their effects on membrane dynamics are important prerequisites towards understanding their roles in the pathophysiology of Alzheimer’s disease, and in the development of novel therapeutics to retard progression of the disease. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers about astrocyte biology and neuronal-glial interactions. They include "Connexin 43 regulates contact-directed distribution of exocytotic fusion sites on astrocytes," "Monitoring of exocytosis in astrocytes using synapto-pHluorins and total internal reflection fluorescence microscopy," "Effect of monocarboxylate transporter inhibition on NADH biphasic response and oxygen utilization after neuronal stimulation," and "Involvement of PI3-K/Akt signal pathway in acquired resistance against 6-OHDA in SH-SY5Ycell following interaction with astrocytes."

The article presents abstracts of research papers related to molecular and cellular mechanisms. The papers were presented at a meeting of the International Society for Neurochemistry and the American Society for Neurochemistry. The abstracts include "Roles of glutamate transporters in the brain," "Neuron glia cross-talk by glutamate transporter in the retina," and "Neuronal regulation of glutamate transporters: molecular and cellular mechanisms."

The article presents an abstract of the medical research paper "An Integrated Neuron-Glia Dialogue in the Processing of Brain Formation." The paper will be discussed at the Seventeenth Biennial Meeting of the International Society for Neurochemistry (ISN) and the Thirteenth General Meeting of the European Society for Neurochemistry (ESN) to be held in Berlin, Germany from August 8-14, 1999. The paper will discuss the role of astrocytes in the processing of brain formation.

Sonic hedgehog ( SHH) is a glycoprotein associated with development that is also expressed in the adult CNS and released after brain injury. Since the SHH receptors patched homolog-1 and Smoothened are highly expressed on astrocytes, we hypothesized that SHH regulates astrocyte function. Primary mouse cortical astrocytes derived from embryonic Swiss mouse cortices, were treated with two chemically distinct agonists of the SHH pathway, which caused astrocytes to elongate and proliferate. These changes are accompanied by decreases in the major astrocyte glutamate transporter-1 and the astrocyte intermediate filament protein glial fibrillary acidic protein. Multisite electrophysiological recordings revealed that the SHH agonist, smoothened agonist suppressed neuronal firing in astrocyte-neuron co-cultures and this was abolished by the astrocyte metabolic inhibitor ethylfluoroacetate, revealing that SHH stimulation of metabolically active astrocytes influences neuronal firing. Using three-dimensional co-culture, MAP2 western blotting and immunohistochemistry, we show that SHH-stimulated astrocytes protect neurons from kainate-induced cell death. Altogether the results show that SHH regulation of astrocyte function represents an endogenous neuroprotective mechanism. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers about axon growth in a reactive glial environment after spinal cord injury. They include "Variations in the cellular response and recovery after spinal cord injury in the mouse," "Chondroitin sulfate proteoglycans in a contusion spinal cord injury," "Astrocyte-secreted chondroitinase mitigates axon inhibition by chondroitin sulfate proteoglycans," and "Neuronal adaptation to inhibitory and collapsing factors."

The article presents abstracts of research papers about mitochondrial neuochemistry. They include "Mitochondrial heterogeneity in brain," "Brain mitochondrial dysfunction—the critical event in neurodegeneration?," "Differential responses of astrocyte and neuronal mitochondria to calcium and oxidative stress," and "Proapoptotic mitochondrial signaling: the hows and whens."

The article presents abstracts of research papers about the effects of neuroinflammation on gap junction communication. They include "Connexins and neuroprotection: minding the gap," "Connexins regulate gene expression: how, why, and implications for neuroinflammation," "Astrocyte gap junctions are a target for pro-inflammatory cytokines released from microglial cells," and "The gram-positive bacterium S. aureus differentially modulates gap junction communication in astrocytes and microglia."

The article presents abstracts of research papers about the role of astrocytes in disease and regeneration. They include "Intermediate filaments—the key to reactive gliosis?," "Astroglial S100B modulates neuronal activity in vivo," "The Nrf2-are pathway in astrocytes: potential role in neuroprotection," and "GFAP mutations in alexander disease."

J. Neurochem. (2012) 120, 269-278. Abstract The divalent metal transporter 1 (DMT1) is the best characterized Fe2+ transporter involved in cellular iron uptake in mammals. Four possible isoforms have been identified as a result of alternative promoter (DMT1-1A and DMT1-1B) and alternative splicing involving the C-terminus and producing transcripts with or without an iron responsive element [DMT1-IRE(+) and DMT1-IRE(−), respectively]. Despite the general importance of DMT1 in controlling iron homeostasis, the distribution and the role of the transporter in the CNS is still controversial. In this study, we characterize the expression of DMT1 in hippocampal neurons and astrocytes. We found that the main isoform endogenously expressed is DMT1-1B/IRE(+), which shows cytoplasmic distribution, colocalization with late endosome/lysosome markers and iron regulation, as expected from the presence of an iron responsive element. Our results also show that DMT1-1B/IRE(+) isoform does not sustain iron entry, even after its neuronal over-expression. Overall, our results argue against a physiological role of the endogenous DMT1 in neuronal iron uptake but do not exclude that, under pathological conditions, the expression of other DMT1 isoforms might contribute to iron overload. [ABSTRACT FROM AUTHOR]

J. Neurochem. (2010) 114, 1405–1413. Reactive aldehydes have been implicated in the etiology of several neurological and psychiatric disorders, and there is considerable interest in drugs to counteract the actions of these aldehydes. Increased formaldehyde (FA) and up-regulation of semicarbazide-sensitive amine oxidase, which forms FA from methylamine, have been implicated in disorders such as cerebrovascular disorders, alcohol abuse, diabetes and Alzheimer’s disease. Phenelzine (PLZ), a monoamine oxidase inhibitor, is an antidepressant that has recently received attention for its neuroprotective/neurorescue properties. We investigated FA-induced toxicity and the effects of PLZ using rat primary cortical neurons and astrocytes and found that FA induced toxicity in neurons and astrocytes by multiple means. In astrocytes, FA decreased glutamate transporter expression, inhibiting glutamate uptake. PLZ reversed the decrease of glutamate uptake and the alteration of the second messengers, AKT and p38, induced by FA. PLZ alone affected the GLT-1 glutamate transporter in opposite directions in astrocytes and neurons. Thus, PLZ has multiple actions in neurons and astrocytes that may contribute to its neuroprotection. [ABSTRACT FROM AUTHOR]

Recombinant baculoviral vectors efficiently transduce several types of cells in the brain. To characterize host responses to virus challenge, thus verifying the suitability of using baculovirus for the development of gene therapy strategies in the central nervous system, we used cDNA microarray technology to examine in vitro and in vivo global cellular gene expression profiles in the rat brain, cultured human astrocytes and human neuronal cells after viral transduction. We demonstrated that the transduction induced host antiviral responses as a major reaction in all three types of samples profiled. The related genes were mainly those associated with innate immunity, including several of the genes involved in Toll-like receptor signaling pathway and cytokine-cytokine receptor interaction. These findings should be useful in understanding the molecular basis for neural cell response to baculoviral transduction and in guiding rational therapeutic applications of baculoviral vectors in the central nervous systems. [ABSTRACT FROM AUTHOR]

Glial cells are currently viewed as active partners of neurons in synapse formation. The close proximity of astrocytes to the synaptic cleft suggests that these cells might be potential targets for neuronal-released molecules although this issue has been less addressed. Here, we evaluated the role of the excitatory neurotransmitter, glutamate, in astrocyte differentiation. We recently demonstrated that cortical neurons activate the gene promoter of the astrocyte maturation marker, GFAP (glial fibrillary acidic protein) of cerebral cortex astrocytes by inducing TGF-β1 (transforming growth factor beta 1) secretion in vitro. To access the effect of glutamate on GFAP gene, we used transgenic mice bearing the β-Galactosidase (β-Gal) reporter gene under the regulation of the GFAP gene promoter. We report that 100 μM glutamate activates the GFAP gene promoter of astrocytes from cerebral cortex revealed by a significant increase in the number of β-Gal positive astrocytes. Neutralizing antibodies against TGF-β completely prevented glutamate and neuronal-induction of GFAP gene, thus indicating that this event is mediated by TGF-β1. Further, induction of GFAP gene in response to glutamate was followed by nuclear translocation of the Smad transcription factor, a hallmark of TGF-β1 pathway activation. The antagonist of the metabotropic glutamate receptor, MCPG, inhibited neuronal effect suggesting that neuronal activation of GFAP gene promoter involves glutamate metabotropic receptors. MAPK (PD98059) and PI3K (LY294002) inhibitors fully prevented activation of GFAP gene promoter by all treatments. Surprisingly, these inhibitors also abrogated TGF-β1 direct action on GFAP gene although they did not inhibit Smad-2 phosphorylation, suggesting that TGF-β1-induced GFAP gene activation might involve cooperation between the canonical and non-canonical TGF-β pathways. Together, our results suggest that glial metabotropic glutamate 2/3 receptor activation by neurons induces TGF-β1 secretion, leading to GFAP gene activation and astrocyte differentiation and involves Smad and MAPK/PI3K pathways. Our work provides evidence that astrocytes surrounding synapses are target of neuronal activity and might shed light into the role of glial cells into neurological disorders associated with glutamate neurotoxicity. [ABSTRACT FROM AUTHOR]

Neurons are metabolically handicapped in the sense that they are not able to perform de novo synthesis of neurotransmitter glutamate and γ-aminobutyric acid (GABA) from glucose. A metabolite shuttle known as the glutamate/GABA-glutamine cycle describes the release of neurotransmitter glutamate or GABA from neurons and subsequent uptake into astrocytes. In return, astrocytes release glutamine to be taken up into neurons for use as neurotransmitter precursor. In this review, the basic properties of the glutamate/GABA-glutamine cycle will be discussed, including aspects of transport and metabolism. Discussions of stoichiometry, the relative role of glutamate vs. GABA and pathological conditions affecting the glutamate/GABA-glutamine cycling are presented. Furthermore, a section is devoted to the accompanying ammonia homeostasis of the glutamate/GABA-glutamine cycle, examining the possible means of intercellular transfer of ammonia produced in neurons (when glutamine is deamidated to glutamate) and utilized in astrocytes (for amidation of glutamate) when the glutamate/GABA-glutamine cycle is operating. A main objective of this review is to endorse the view that the glutamate/GABA-glutamine cycle must be seen as a bi-directional transfer of not only carbon units but also nitrogen units. [ABSTRACT FROM AUTHOR]

After our initial report of a mammalian gene for arginine decarboxylase, an enzyme for the synthesis of agmatine from arginine, we have determined the regional expression of ADC in rat. We have analyzed the expression of ADC in rat brain regions by activity, protein and mRNA levels, and the regulation of expression in neuronal cells by RNA interference. In rat brain, ADC was widely expressed in major brain regions, with a substantial amount in hypothalamus, followed by cortex, and with least amounts in locus coeruleus and medulla. ADC mRNA was detected in primary astrocytes and C6 glioma cells. While no ADC message was detected in fresh neurons (3 days old), significant message appeared in differentiated neurons (3 weeks old). PC12 cells, treated with nerve growth factor, had higher ADC mRNA compared with naive cells. The siRNA mixture directed towards the N-terminal regions of ADC cDNA down-regulated the levels of mRNA and protein in cultured neurons/C6 glioma cells and these cells produced lower agmatine. Thus, this study demonstrates that ADC message is expressed in rat brain regions, that it is regulated in neuronal cells and that the down-regulation of ADC activity by specific siRNA leads to lower agmatine production. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers related to the functioning of the brain. They include "Microarray analysis of developing oligodendrogia, neurons, and astrocytes reveal differential gene expression," "Genome-wide analysis of clock-controlled genes in Drosophila," and "Functional genomics of long-term memory."

The article presents abstracts of research papers related to neurons and glia. They include "Metabolic impairment elicits brain cell-type selective changes in oxidative stress and cell death in culture," "L-serine as an astrocyte-derived essential factor for CNS neurons: a previously unrecognized role of astrocytes in brain L-serine metabolism," and "Role of the microglial cystine-glutathione system in neuroprotective antioxidant strategies: relevance to excitotoxicity and Alzheimer's disease."

The article presents abstracts of papers related to neurons and glia, which were presented at the meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, in August 2001. They include "Neuronal glucose metabolism: real time monitoring of metabolic trafficking," "Supply of ketone bodies from astrocytes to neurons: potential pathophysiological implications," and "Energy on demand."

Erythropoietin (Epo) is a glycoprotein secreted by the kidney in response to hypoxia that stimulates erythropoiesis through interaction with cell surface Epo receptors. Pre-treatment with Epo has been shown to protect neurons in models of ischemic injury. The mechanism responsible for this neuroprotection and the effects of Epo on astroglial and other non-neuronal cell populations remain unknown. In the present study, we determined whether Epo pre-treatment protects neonatal rat astrocytes from apoptotic cell death resulting from treatment with nitric oxide, staurosporine (STS) and arsenic trioxide and possible mechanisms mediating Epo-related cytoprotection. Epo (5–20 U/mL) significantly attenuated multiple hallmarks of apoptotic cell death in astroglia exposed to nitric oxide and STS but not arsenic trioxide. Epo (20 U/mL) induced mild oxidative stress as shown by increases in heme oxygenase (HO)-1 mRNA and protein expression that could be suppressed by antioxidant coadministration. Moreover, coincubation with tin-mesoporphyrin, a competitive inhibitor of HO activity, abrogated the cytoprotective effects of Epo (20 U/mL) in the face of STS treatment. Thus, induction of theho-1 gene may contribute to the glioprotection accruing from high-dose Epo exposure. Epo may augment astroglial resistance to certain chemical stressors by oxidative stress-dependent and -independent mechanisms. [ABSTRACT FROM AUTHOR]

To evaluate the response of astrocytes in the auditory pathway to increased neuronal signaling elicited by acoustic stimulation, conscious rats were presented with a unilateral broadband click stimulus and functional activation was assessed by quantitative autoradiography using three tracers to pulse label different metabolic pools in brain:[2-14C]acetate labels the‘small’ (astrocytic) glutamate pool,[1-14C]hydroxybutyrate labels the‘large’ glutamate pool, and[14C]deoxyglucose, reflects overall glucose utilization (CMRglc) in all brain cells. CMRglc rose during brain activation, and increased activity of the oxidative pathway in working astrocytes during acoustic stimulation was registered with[2-14C]acetate. In contrast, the stimulation-induced increase in metabolic activity was not reflected by greater trapping of products of[1-14C]hydroxybutyrate. The[2-14C]acetate uptake coefficient in the inferior colliculus and lateral lemniscus during acoustic stimulation was 15% and 18% (p < 0.01) higher in the activated compared to contralateral hemisphere, whereas CMRglc in these structures rose by 66% (p < 0.01) and 42% (p < 0.05), respectively. Calculated rates of brain utilization of blood-borne acetate (CMRacetate) are about 15–25% of total CMRglc in non-stimulated tissue and 10–20% of CMRglc in acoustically activated structures; they range from 28 to 115% of estimated rates of glucose oxidation in astrocytes. The rise in acetate utilization during acoustic stimulation is modest compared to total CMRglc, but astrocytic oxidative metabolism of‘minor’ substrates present in blood can make a significant contribution to the overall energetics of astrocytes and astrocyte–neuron interactions in working brain. [ABSTRACT FROM AUTHOR]

The peptide transmitter N-acetylaspartylglutamate (NAAG) is present in millimolar concentrations in mammalian spinal cord. Data from the rat peripheral nervous system suggest that this peptide is synthesized enzymatically, a process that would be unique for mammalian neuropeptides. To test this hypothesis in the mammalian CNS, rat spinal cords were acutely isolated and used to study the incorporation of radiolabeled amino acids into NAAG. Consistent with the action of a NAAG synthetase, inhibition of protein synthesis did not affect radiolabel incorporation into NAAG. Depolarization of spinal cords stimulated incorporation of radiolabel. Biosynthesis of NAAG by cortical astrocytes in cell culture was demonstrated by tracing incorporation of [3H]-glutamate by astrocytes. In the first test of the hypothesis that NAA is an immediate precursor in NAAG biosynthesis, [3H]-NAA was incorporated into NAAG by isolated spinal cords and by cell cultures of cortical astrocytes. Data from cerebellar neurons and glia in primary culture confirmed the predominance of neuronal synthesis and glial uptake of NAA, leading to the hypothesis that while neurons synthesize NAA for NAAG biosynthesis, glia may take it up from the extracellular space. However, cortical astrocytes in serum-free low-density cell culture incorporated [3H]-aspartate into NAAG, a result indicating that under some conditions these cells may also synthesize NAA. Pre-incubation of isolated spinal cords and cultures of rat cortical astrocytes with unlabeled NAA increased [3H]-glutamate incorporation into NAAG. In contrast, [3H]-glutamine incorporation in spinal cord was not stimulated by unlabeled NAA. These results are consistent with the glutamate–glutamine cycle greatly favoring uptake of glutamine into neurons and glutamate by glia and suggest that NAA availability may be rate-limiting in the synthesis of NAAG by glia under some conditions. [ABSTRACT FROM AUTHOR]

A co-ordinated regulation between neurons and astrocytes is essential for the control of extracellular glutamate concentration. Here, we have investigated the influence of astrocytes and glia-derived cholesterol on the regulation of glutamate transport in primary neuronal cultures from rat embryonic cortices. Glutamate uptake rate and expression of the neuronal glutamate transporter EAAC1 were low when neurons were grown without astrocytes and neurons were unable to clear extracellular glutamate. Treatment of the neuronal cultures with glial conditioned medium (GCM) increased glutamate uptake Vmax , EAAC1 expression and restored the capacity of neurons to eliminate extracellular glutamate. Thus, astrocytes up-regulate the activity and expression of EAAC1 in neurons . We further showed that cholesterol, present in GCM, increased glutamate uptake activity when added directly to neurons and had no effect on glutamate transporter expression. Furthermore, part of the GCM-induced effect on glutamate transport activity was lost when cholesterol was removed from GCM (low cholesterol-GCM) and was restored when cholesterol was added to low cholesterol-GCM. This demonstrates that glia-derived cholesterol regulates glutamate transport activity. With these experiments, we provide new evidences for neuronal glutamate transport regulation by astrocytes and identified cholesterol as one of the factors implicated in this regulation. [ABSTRACT FROM AUTHOR]

Abstract Cerebral inflammatory events play an important part in the pathogenesis of Alzheimer's disease (AD). Agonists of the peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear hormone receptor that mediates anti-inflammatory actions of non-steroidal anti-inflammatory drugs (NSAIDs) and thiazolidinediones, have been therefore proposed as a potential treatment of AD. Experimental evidence suggests that cortical noradrenaline (NA) depletion due to degeneration of the locus ceruleus (LC) – a pathological hallmark of AD – plays a permissive role in the development of inflammation in AD. To study a possible relationship between NA depletion and PPARγ-mediated suppression of inflammation we investigated the influence of NA on PPARγ expression in murine primary cortical astrocytes and neurons. Incubation of astrocytes and neurons with 100 µm NA resulted in an increase of PPARγ mRNA as well as PPARγ protein levels in both cell types. These effects were blocked by the β-adrenergic antagonist propranolol but not by the α-adrenergic antagonist phentolamine, suggesting that they might be mediated by β-adrenergic receptors. Our results indicate for the first time that PPARγ expression can be modulated by the cAMP signalling pathway, and suggest that the anti-inflammatory effects of NA on brain cells may be partly mediated by increasing PPARγ levels. Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPARγ expression and therefore potentiate neuroinflammatory processes. [ABSTRACT FROM AUTHOR]

The activity of high-affinity glutamate transporters is essential for the normal function of the mammalian central nervous system. Using a combined pharmacological, confocal immunocytochemical, enzyme-based microsensor and fluorescence imaging approach, we examined glutamate uptake and transporter protein localization in single astrocytes of neuron-containing and neuron-free microislands prior to presynaptic transmitter secretion and during functional neuronal activity. Here, we report that the presence or absence of neurons strikingly affects the uptake capacity of the astroglial glutamate transporters GLT1 and GLAST1. Induction of transporter function is activated by neurons and this effect is mimicked by pre-incubation of astrocytes with micromolar concentrations of glutamate. Moreover, increased glutamate transporter activation is reproduced by endogenous release of glutamate via activation of neuronal nicotinic receptors. The increase in transport activity is dependent on neuronal release of glutamate, is associated with the local redistribution (clustering) of GLT1 and GLAST1 but is independent of transporter synthesis and of glutamate receptor activation. Together, these results suggest an activity-dependent neuronal feedback system for rapid astroglial glutamate transporter regulation where neuron-derived glutamate is the physiological signal that triggers transporter function. [ABSTRACT FROM AUTHOR]

Unlike in the adult brain, the newborn brain specifically takes up serum albumin during the postnatal period, coinciding with the stage of maximal brain development. Here we report that albumin stimulates oleic acid synthesis by astrocytes from the main metabolic substrates available during brain development. Oleic acid released by astrocytes is used by neurons for the synthesis of phospholipids and is specifically incorporated into growth cones. Oleic acid promotes axonal growth, neuronal clustering, and expression of the axonal growth-associated protein-43, GAP-43; all these observations indicating neuronal differentiation. The effect of oleic acid on GAP-43 synthesis is brought about by the activation of protein kinase C, since it was prevented by inhibitors of this kinase, such as H-7, polymyxin or sphingosine. The expression of GAP-43 was significantly increased in neurons co-cultured with astrocytes by the presence of albumin indicating that neuronal differentiation takes place in the presence of oleic acid synthesized and released by astrocytes in situ. In conclusion, during brain development the presence of albumin could play an important role by triggering the synthesis and release of oleic acid by astrocytes, which induces neuronal differentiation. [ABSTRACT FROM AUTHOR]

Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) occurs in astrocytes as well as in neurons in brain. We have reported that CaM kinase II is involved in the regulation of cytoskeletal proteins and gene expression in astrocytes. In this study, we identified all isoforms of CaM kinase II in astrocytes and examined their subcellular localization. When we amplified the isoforms of four subunits by RT-PCR followed by the “nested” PCR, totally 10 isoforms were obtained. Immunoblot analyses with five types of antibodies against CaM kinase II indicated that the most abundant isoform was δ2. Immunostaining suggested that the δ2 isoform was localized predominantly at the Golgi apparatus. The localization of the δ2 isoform at the Golgi apparatus was also observed in NG108-15 cells. We overexpressed all isoforms that contained the nuclear localization signal to examine their nuclear targeting in NG108-15 cells. In contrast to the αB and δ3 isoforms that entered the nucleus, as reported, the γA isoform was excluded from the nucleus in the transfected NG108-15 cells. These results suggest that the 15-amino acid insertion following the nuclear localization signal inhibits the nuclear targeting of the γA isoform. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the research paper "Alterations in Monocarboxylate & Glucose Transporters in Ischemic Rodent Brain." It will be presented in the joint meeting of the International Society for Neurochemistry and the European Society of Neurochemistry that will be held in Berlin, Germany from August 8-14, 1999. The increasing evidence of presence of monocarboxylic acids in glucose especially lactate and their involvement in metabolic trafficking between astrocytes and neurons.

The article presents an abstract of the research paper " How Maternal Insulin-Induced Hypoglycemia Affects Fetal Brain Neuronal-Glia Function in Comparison to the Maternal Brain: A Metabolic Study Using SING 13C MRS Isotopmer Analysis." The research results determine the lower glucose flux PC/PDH in the fetal brain.

The article presents an abstract of the study "Glutamate Transporters." The study reports that, Glutamatergic neurotransmission is terminated by glutamate high affinity transporters located in the plasma membrane of neurons and astrocytes. The research paper for the study would be presented in the 30th Annual Meeting of the American Society for Neurochemistry, on March 14-17, 1999, in New Orleans, Louisiana.

The article presents an abstract of the research paper "Early embryonic chick cortical neurons are susceptible to apoptosis induced by tyrosine phosphorylation and free radicals," which will be presented at the 30th American Society for Neurochemistry meeting to be held from March 14 to 17, 1999 in New Orleans, Louisiana. The study indicated the possibility of developing drugs to protect embryonic and mature neurons and glia from apoptotic cell death.

The author reflects on the study conducted by E. S. Lippmann and colleagues on the blood-brain barrier (BBB) modeling. The author states that the study is important, considering the difficulties in getting human neurons and astrocytes for the in vitro modeling of BBB. Meanwhile, author mentions that in vitro BBB models have become increasingly hard to analyze the interactions of neurovascular unit's various cell types.