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The article presents abstracts of research papers related to cell death. The papers were presented at a poster session held at the joint meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, in Buenos Aires, Argentina from August 26-31, 2001. They include "Caspase-3 in brain: role in adaptive plasticity," "ICER-evoked cell death of different types of neurons," and "Incidence of different cell death types in the newborn rat retina."

The article presents an abstract of the medical research paper "Translocation of PKC Isoforms Towards PSD After Cerebral Ischemia." This paper is to be discussed in 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 at Berlin, Germany from August 8-14, 1999. This paper is to discuss the role of PKC in pathological nerve cell function.

The article presents an abstract of the medical research paper "Mediation of Neuronal Growth by Radicicol." The paper discusses a study which states that nanomolar concentrations of radicicol enhances the survival and neurite outgrowth of neurons from dorsal root ganglia (DRG) and sympathetic ganglia.

The article presents an abstract of the medical research paper "RAP-PCR Study on Differentially Expressed Transcripts in Primary Culture of Cerebral Cortical Neurons." The paper states that RAP-PCR is efficient in identifying differentially expressed transcripts and the newly identified genes will be useful in revealing the mechanism of neuronal development and differentiation.

The article presents an abstract of the research paper "Activity-Dependent Long-Term Depression and Synapse Silencing." It will be presented in the joint meeting of the International Society for Neurochemistry and the European Society for Neurochemistry that will be held in Berlin, Germany from August 8-14, 1999. The paper examines long-term depression (LTD) in dissociated hippocampal neurons grown in culture to identify the cellular and molecular mechanisms of LTD.

The article presents an abstract of the paper "L- and D- Threo-1-Phenyl-2-Decanoylamino-3-Morpholino-J-Ppropanol (PDMP) Inhibit Neurite Outgrowth From SH-SY5Y Cells," which will be presented at the 30th Annual Meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. The paper suggests that neurite outgrowth in SH-SY5Y cells were decreased by both an inhibitor and stimulator of ganglioside biosynthesis.

The article presents an abstract of a paper titled "Nicotine Protects Cultured Spinal Cord Neurons Against Arachidonic Acid-Mediated Injury." The paper will be presented at the 30th meeting of the American Society for Neurochemistry. The meeting is scheduled to be held in New Orleans, Louisiana, from March 14-17, 1999. The paper discusses that upregulation of neuronal nitric oxide synthase is one of the most significant mechanisms of arachidonic acid induced neuronal dysfunction.

The article presents the abstract of the paper "Mechanisms of Arachidonic Acid-Mediated Secondary Injury to Cultured Spinal Cord Neurons," which will be presented at the 30th meeting of the American Society for Neurochemistry. The meeting will be held in New Orleans, Louisiana, from March 14-17, 1999. According to the paper, secondary tissue injury and dysfunction of spinal cord neurons are greatly affected by the release of fatty acids during spinal cord trauma.

The article presents an abstract of the paper "Involvement of Par-4 and Oxidative Stress in Trophic Factor Withdrawal-induced Apoptosis of Hippocampal Neurons: Protection by Estrogen and Anti-oxidants," which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. The paper discusses the role of Par-4 and oxidative stress in neuronal apoptosis resulting from trophic factor withdrawal.

The article presents an abstract of the paper "Mechanisms of ADNF Peptide Protection Against Oxidative and Excitotoxic Neuronal Death," which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. The paper discusses how 9 amino acid fragment of activity-dependent neurotrophic factor peptide protects rat hippocampal neurons from oxidative injury and neuronal apoptosis.

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."

Nuclear factor of activated T-cells ( NFAT) is a family of transcription factors comprising four calcium-regulated members: NFATc1, NFATc2, NFATc3, and NFATc4. Upon activation by the calcium-dependent phosphatase calcineurin (CaN), NFATs translocate from cytosol to the nucleus and regulate their target genes, which in the nervous system are involved in axon growth, synaptic plasticity, and neuronal survival. We have shown previously that there are a number of different splice variants of NFAT genes expressed in the brain. Here, we studied the subcellular localizations and transactivation capacities of alternative human NFAT isoforms in rat primary cortical or hippocampal neurons in response to membrane depolarization and compared the induced transactivation levels in neurons to those obtained from HEK293 cells in response to calcium signaling. We confirm that in neurons the translocation to the nucleus of all NFAT isoforms is reliant on the activity of CaN. However, our results suggest that both the regulation of subcellular localization and transcriptional activity of NFAT proteins in neurons is isoform specific. We show that in primary hippocampal neurons NFATc2 isoforms have very fast translocation kinetics, whereas NFATc4 isoforms translocate relatively slowly to the nucleus. Moreover, we demonstrate that the strongest transcriptional activators in HEK293 cells are NFATc1 and NFATc3, but in neurons NFATc3 and NFATc4 lead to the highest induction, and NFATc2 and NFATc1 display isoform-specific transcription activation capacities. Altogether, our results indicate that the effects of calcium signaling on the action of NFAT proteins are isoform-specific and can differ between cell types. [ABSTRACT FROM AUTHOR]

The cholesterol, sphingolipid, and glycerophospholipid content of total brain, of detergent-resistant membranes prepared from the total brain, and of cerebellar granule cells differentiated in culture from wild type (WT) and acid sphingomyelinase knockout (ASMKO) were studied. Brains derived from 7-month-old ASMKO animals showed a fivefold higher level of sphingomyelin and a significant increase in ganglioside content, mainly because of monosialogangliosides GM3 and GM2 accumulation, while the cholesterol and glycerophospholipid content was unchanged with respect to WT animals. An increase in sphingomyelin, but not in gangliosides, was also detected in cultured cerebellar granule neurons from ASMKO mice, indicating that ganglioside accumulation is not a direct consequence of the enzyme defect. When a detergent-resistant membrane fraction was prepared from ASMKO brains, we observed that a higher detergent-to-protein ratio was needed than in WT animals. This likely reflects a reduced fluidity in restricted membrane areas because of a higher enrichment in sphingolipids in the case of ASMKO brain. [ABSTRACT FROM AUTHOR]

Repulsive guidance molecule A (RGM A) was recently described as a potent inhibitor of neuroregeneration in a rat spinal cord injury model. The receptor mediating RGM A’s repulsive activity was shown to be Neogenin, a member of the Deleted in Colorectal Cancer (DCC) family of netrin receptors. Binding of RGM A to Neogenin induces activation of the small GTPase RhoA and of its effector Rho-kinase by an unknown mechanism. Here we show, that the cytoplasmic tail of Neogenin interacts directly with the transcriptional coactivator LIM domain only 4 (LMO4) in human SH-SY5Y cells, human Ntera neurons, and in embryonic rat cortical neurons. RGM A binding to Neogenin but not binding of Netrin-1, induces release of LMO4 from Neogenin. Down-regulation of LMO4 neutralizes the repulsive activity of RGM A in neuronal cell lines and embryonic rat cortical neurons and prevents RhoA activation. These results show for the first time that an interaction of Neogenin with LMO4 is involved in the RGM A – Neogenin signal transduction pathway for RhoA activation. [ABSTRACT FROM AUTHOR]

Oligodendrocytes (OLs) are mature glial cells that myelinate axons in the brain and spinal cord. As such, they are integral to functional and efficient neuronal signaling. The embryonic lineage and postnatal development of OLs have been well-studied and many features of the process have been described, including the origin, migration, proliferation, and differentiation of precursor cells. Less clear is the extent to which OLs and damaged/dysfunctional myelin are replaced following injury to the adult CNS. OLs and their precursors are very vulnerable to conditions common to CNS injury and disease sites, such as inflammation, oxidative stress, and elevated glutamate levels leading to excitotoxicity. Thus, these cells become dysfunctional or die in multiple pathologies, including Alzheimer’s disease, spinal cord injury, Parkinson’s disease, ischemia, and hypoxia. However, studies of certain conditions to date have detected spontaneous OL replacement. This review will summarize current information on adult OL progenitors, mechanisms that contribute to OL death, the consequences of their loss and the pathological conditions in which spontaneous oligodendrogenesis from endogenous precursors has been observed in the adult CNS. [ABSTRACT FROM AUTHOR]

The NMDA receptor regulates spine morphological plasticity by modulating Rho GTPases. However, the molecular mechanisms for NMDA receptor-mediated regulation of Rho GTPases remain elusive. In this study, we show that p250GAP, an NMDA receptor-associated RhoGAP, regulates spine morphogenesis by modulating RhoA activity. Knock-down of p250GAP increased spine width and elevated the endogenous RhoA activity in primary hippocampal neurons. The increased spine width by p250GAP knock-down was suppressed by the expression of a dominant-negative form of RhoA. Furthermore, p250GAP is involved in NMDA receptor-mediated RhoA activation. In response to NMDA receptor activation, exogenously expressed green fluorescent protein (GFP)-tagged p250GAP was redistributed. Thus, these data suggest that p250GAP plays an important role in NMDA receptor-mediated regulation of RhoA activity leading to spine morphological plasticity. [ABSTRACT FROM AUTHOR]

The neuronal protein tyrosine phosphatases encoded by mouse gene Ptprr (PTPBR7, PTP-SL, PTPPBSγ-42 and PTPPBSγ-37) have been implicated in mitogen-activated protein (MAP) kinase deactivation on the basis of transfection experiments. To determine their physiological role in vivo, we generated mice that lack all PTPRR isoforms. Ptprr−/− mice were viable and fertile, and not different from wildtype littermates regarding general physiology or explorative behaviour. Highest PTPRR protein levels are in cerebellum Purkinje cells, but no overt effects of PTPRR deficiency on brain morphology, Purkinje cell number or dendritic branching were detected. However, MAP kinase phosphorylation levels were significantly altered in the PTPRR-deficient cerebellum and cerebrum homogenates. Most notably, increased phospho-ERK1/2 immunostaining density was observed in the basal portion and axon hillock of Ptprr−/− Purkinje cells. Concomitantly, Ptprr−/− mice displayed ataxia characterized by defects in fine motor coordination and balance skills. Collectively, these results establish the PTPRR proteins as physiological regulators of MAP kinase signalling cascades in neuronal tissue and demonstrate their involvement in cerebellum motor function. [ABSTRACT FROM AUTHOR]

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."

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]

Alzheimer's disease (AD) is neuropathologically characterized by depositions of extracellular amyloid and intracellular neurofibrillary tangles, associated with loss of neurons in the brain. Amyloidβ-peptide (Aβ) is the major component of senile plaques and is considered to have a causal role in the development and progress of AD. Several lines of evidence suggest that enhanced oxidative stress and inflammation play important roles in the pathogenesis or progression of AD. The present study aimed to investigate the protective effects of ethyl-4-hydroxy-3-methoxycinnamic acid (FAEE), a phenolic compound which shows antioxidant and anti-inflammatory activity, on Aβ(1–42)-induced oxidative stress and neurotoxicity. We hypothesized that the structure of FAEE would facilitate radical scavenging and may induce protective proteins. Aβ(1–42) decreases cell viability, which was correlated with increased free radical formation, protein oxidation (protein carbonyl, 3-nitrotyrosine), lipid peroxidation (4-hydroxy-2-trans-nonenal) and inducible nitric oxide synthase. Pre-treatment of primary hippocampal cultures with FAEE significantly attenuated Aβ(1–42)-induced cytotoxicity, intracellular reactive oxygen species accumulation, protein oxidation, lipid peroxidation and induction of inducible nitric oxide synthase. Treatment of neurons with Aβ(1–42) increases levels of heme oxygenase-1 and heat shock protein 72. Consistent with a cellular stress response to the Aβ(1–42)-induced oxidative stress, FAEE treatment increases the levels of heme oxygenase-1 and heat shock protein 72, which may be regulated by oxidative stresses in a coordinated manner and play a pivotal role in the cytoprotection of neuronal cells against Aβ(1–42)-induced toxicity. These results suggest that FAEE exerts protective effects against Aβ(1–42) toxicity by modulating oxidative stress directly and by inducing protective genes. These findings suggest that FAEE could potentially be of importance for the treatment of AD and other oxidative stress-related diseases. [ABSTRACT FROM AUTHOR]

An inflammatory process in association with reactive gliosis has been suggested to play an important role in the pathogenesis of amyotrophic lateral sclerosis (ALS). One of the key findings is a marked increase in the level of cyclooxygenase-2 (COX-2), a therapeutic target of ALS. We investigated the expression of CD40 in the spinal cord of a transgenic mouse model of ALS (G93A mice), and its relevance to COX-2 upregulation. CD40 was predominantly expressed in neurons in normal spinal cord and upregulated in reactive glial cells in spinal cord injury. In the spinal cord of G93A mice, the expression of CD40 was increased in both reactive microglia and astrocytes, where COX-2 was especially increased. The level of COX-2 was upregulated in microglia and astrocytes by CD40 stimulation in vitro. CD40 stimulation in primary spinal cord cultures caused motor neuron loss that was protected by selective COX-2 inhibitor. These results suggest that CD40, which is upregulated in reactive glial cells in ALS, participates in motor neuron loss via induction of COX-2. [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]

Based on our initial finding that the nitric oxide (NO) sensitive fluorochrome diaminofluorescein (DAF) was localized to mitochondria in cultured primary neurons, we investigated whether brain mitochondria produce NO through a mitochondrial NO synthase (mtNOS) enzyme. Isolated brain mitochondria were loaded with DAF and subjected to flow cytometry analysis. Neither the application of NOS inhibitors nor the genetic disruption of either NOS gene diminished the DAF-fluorescence. However, peroxynitrite scavengers reduced the mitochondrial DAF fluorescence, indicating that the DAF signal is not specific to NO. Chemiluminescence detection in the head space gas and a Clark-type NO-sensitive electrode in the solution failed to detect NO release in brain mitochondria. NOS activity in mitochondria was only 1% of the whole brain NOS activity level, which may be attributed to extramitochondrial contamination. Extensive immunoblotting and immunoprecipitation experiments failed to show the presence of endothelial, neuronal, or inducible NOS in mouse brain mitochondria using a variety of primary antibodies. Arginine, calmodulin or 2,5-ADP affinity purification protocols successfully concentrated eNOS and nNOS from full brain tissue but failed to show any signal in mitochondria. We conclude that mouse brain mitochondria do not contain NOS isoforms, nor do they produce NO through a NOS-dependent mechanism. [ABSTRACT FROM AUTHOR]

Agrin is a proteoglycan that can inhibit neurite outgrowth from multiple neuronal types when present as a substrate. Agrin's neurite inhibitory activity is confined to the N-terminal segment of the protein (agrin N150), which contains heparan sulfate (HS) and chondroitin sulfate (CS) side chains. We have examined the activities of various purified recombinant agrin fragments and their glycosaminoglycan (GAG) side chains in neurite outgrowth inhibition. Inhibitory activity was tested using dissociated chick ciliary ganglion neurons or dorsal root ganglion explants growing on laminin or N-cadherin. Initial experiments demonstrated that agrin N150 lacking GAG chains inhibited neurite outgrowth. Both halves of N150, each containing HS and/or CS side chains, could also inhibit neurite growth. Experiments using agrin fragments in which the GAG acceptor residues were mutated, or using agrin fragments purified from cells deficient in GAG synthesis, demonstrated that inhibition by the N-terminal portion of N150 requires GAGs, but that inhibition from the C-terminal part of N150 does not. Thus, the core protein or other types of glycosylation are important for inhibition from the more C-terminal region. Our results suggest that there are two distinct mechanisms for neurite outgrowth inhibition by agrin, one that is GAG-dependent and one that is GAG-independent. [ABSTRACT FROM AUTHOR]

Synaptophysin is one of the most abundant membrane proteins of small synaptic vesicles. In mature nerve terminals it forms a complex with the vesicular membrane protein synaptobrevin, which appears to modulate synaptobrevin's interaction with the plasma membrane-associated proteins syntaxin and SNAP25 to form the SNARE complex as a prerequisite for membrane fusion. Here we show that synaptobrevin is preferentially cleaved by tetanus toxin while bound to synaptophysin or when existing as a homodimer. The synaptophysin/synaptobrevin complex is, however, not affected when neuronal secretion is blocked by botulinum A toxin which cleaves SNAP25. Excessive stimulation with α-latrotoxin or Ca2+-ionophores dissociates the synaptophysin/synaptobrevin complex and increases the interaction of the other SNARE proteins. The stimulation-induced dissociation of the synaptophysin/synaptobrevin complex is not inhibited by pre-incubating neurones with botulinum A toxin, but depends on extracellular calcium. However, the synaptophysin/synaptobrevin complex cannot be directly dissociated by calcium alone or in combination with magnesium. The dissociation of synaptobrevin from synaptophysin appears to precede its interaction with the other SNARE proteins and does not depend on the final fusion event. This finding further supports the modulatory role the synaptophysin/synaptobrevin complex may play in mature neurones. [ABSTRACT FROM AUTHOR]

We have investigated the molecular mechanisms of neurotrophin-mediated cell survival in HT22 cells, a murine cell line of hippocampal origin, expressing the brain-derived neurotrophic factor (BDNF) receptor TrkB as well as the TrkB.T1 splice variant. Stimulation with BDNF protected HT22-TrkB cells, but not HT22-TrkB.T1 cells, against programmed cell death induced by serum deprivation. BDNF did not, however, provide protection against oxidative glutamate toxicity, indicating that serum deprivation-induced cell death differs substantially from glutamate-induced cell death. Using a pharmacological strategy to block either the extracellular signal-regulated protein kinase (ERK) or the phosphatidylinositol 3-kinase (PI3) pathway, we show that activation of PI3 kinase is required for the neuroprotective activity of BDNF in HT22 cells. To further analyse the role of ERK in neuroprotection we expressed an inducible ΔRaf-1:ER fusion protein in HT22 cells. Activation of this conditionally active form of Raf-1 induced a sustained phosphorylation of ERK, and protected the cells from serum withdrawal-induced cell death. Inhibition of ERK activation at different time points revealed that a prolonged activation of ERK is essential to protect HT22 cells from cell death triggered by the withdrawal of serum, indicating that the duration of ERK activation is of major importance for its neuroprotective biological function. [ABSTRACT FROM AUTHOR]

Abstract We investigated the neuroprotective effects of brain-derived neurotrophic factor (BDNF) and its influence on the functional recovery of the retina following light-induced retinal damage by electroretinogram (ERG). Rats were exposed to constant fluorescent light for 2, 5, 7, or 14 days, then returned to a cyclic light environment for 14 days. The result indicated that BDNF had few effects on the a-wave amplitude, but there was a statistically significant difference in the b-wave amplitudes between BDNF-treated and control eyes from day 0–14 of the recovery period following 2 days of light exposure (p < 0.05). Our findings suggest that BDNF not only protects the retinal neuronal function but also enhances the recovery from retinal light damage. [ABSTRACT FROM AUTHOR]

Abstract Activation of NMDA receptors has been shown to induce either neuronal cell death or neuroprotection against excitotoxicity in cultured cerebellar granule neurons in vitro. We have investigated the effects of pretreatment with NMDA on kainate-induced neuronal cell death in mouse hippocampus in vivo. The systemic administration of kainate (30 mg/kg), but not NMDA (100 mg/kg), induced severe damage in pyramidal neurons of the hippocampal CA1 and CA3 subfields 3–7 days later, without affecting granule neurons in the dentate gyrus. An immunohistochemical study using an anti-single-stranded DNA antibody and TdT-mediated dUTP nick end labeling analysis both revealed that kainate, but not NMDA, induced DNA fragmentation in the CA1 and CA3 pyramidal neurons 1–3 days after administration. Kainate-induced neuronal loss was completely prevented by the systemic administration of NMDA (100 mg/kg) 1 h to 1 day previously. No pyramidal neuron was seen with fragmented DNA in the hippocampus of animals injected with kainate 1 day after NMDA treatment. The neuroprotection mediated by NMDA was prevented by the non-competitive NMDA receptor antagonist MK-801. Taken together these results indicate that in vivo activation of NMDA receptors is capable of protecting against kainate-induced neuronal damage through blockade of DNA fragmentation in murine hippocampus. [ABSTRACT FROM AUTHOR]

High-mobility-group (HMG) proteins are a family of non-histone chromosomal proteins which bind to DNA. They have been implicated in multiple aspects of gene regulation and cellular differentiation. Sulfoglucuronyl carbohydrate binding protein, SBP-1, which is also localized in the neuronal nuclei, was shown to be required for neurite outgrowth and neuronal migration during development of the nervous system. In order to establish relationship between SBP-1 and HMG family proteins, two HMG proteins were isolated and purified from developing rat cerebellum by heparin–sepharose and sulfatide-octyl–sepharose affinity column chromatography and their biochemical and biological properties were compared with those of SBP-1. Characterization by high performance liquid chromatography–mass spectrometry (HPLC–MS), partial peptide sequencing and western blot analysis showed the isolated HMG proteins to be HMG-1 and HMG-2. Isoelectric focusing, HPLC–MS and peptide sequencing data also suggested that HMG-1 and SBP-1 were identical. Similar to SBP-1, both HMG proteins bound specifically to sulfated glycolipids, sulfoglucuronylglycolipids (SGGLs), sulfatide and seminolipid in HPTLC-immuno-overlay and solid-phase binding assays. The HMG proteins promoted neurite outgrowth in dissociated cerebellar cells, which was inhibited by SGGLs, anti-Leu7 hybridoma (HNK -1) and anti-SBP-1 peptide antibodies, similar to SBP-1. The proteins also promoted neurite outgrowth in explant cultures of cerebellum. The results showed that the cerebellar HMG-1 and -2 proteins have similar biochemical and biological properties and HMG-1 is most likely identical to SBP-1. [ABSTRACT FROM AUTHOR]

Previously we found that some cyclopentenone prostaglandin derivatives promoted neurite outgrowth from PC12 cells and dorsal root ganglia explants in the presence of nerve growth factor; and so we referred to them as neurite outgrowth-promoting prostaglandins (NEPPs). In this study, NEPPs protected HT22 cells against oxidative glutamate toxicity. NEPP6, one of the most effective promoters of neurite outgrowth in PC12 cells, protected the cells most potently among NEPPs 1–10. Several derivatives, NEPPs 11–19, were newly synthesized based on the chemical structure of NEPP6. NEPP11 had a more potent neuroprotective effect than NEPP6. NEPP11 also prevented the death of cortical neurons induced by various stimuli and reduced ischemic brain damage in mice. Biotinylated compounds of NEPPs were synthesized to investigate their cellular accumulation. NEPP6-biotin protected the cells and emitted potent signals from the cells. In contrast, biotinylated non-neuroprotective derivatives emitted much weaker signals. These results suggest that NEPPs are novel types of neurotrophic compounds characterized by their dual biological activities of promoting neurite outgrowth and preventing neuronal death and that their accumulation in the cells is closely associated with their neuroprotective actions. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the research paper "Is Serum [U-13C] Lactate a Substrate In Rat Brain." The research finds that lactate is a major substrate for neuronal metabolism. It determines that glucose is more effective in labeling neuronal metabolites and metabolized by both neurons and astrocytes.

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 research paper "Short-Term Effects of Glutamate Receptor Stimulation on Neuronal Energy Metabolism." The study determined the short-term effects of glutamate receptor stimulation on energy metabolism in rat neurons in primary culture. The results of the study concluded that activation of glutamate receptor might cause the mitochondrial inner membrane pore to poem which leads to membrane depolarization.

The article presents an abstract of the research paper "Cell Signaling Abnormalities in Alzheimer's Disease." Due to apoptotic or excitotoxic mechanisms, several neurons of Alzheimer's disease (AD) may die. And in this whole process amyloid-ß-peptide play a very significant role. Mutations in the presenilin-1 gene account for many cases of early-onset autosomal dominant inherited forms of AD.

The article presents an abstract of the research paper "Neurogenesis and Differentiation of Olfactory Epithelium Neurons in Anterior Chamber of Rat Eye." Researchers in the study determine the development of primary olfactory neurons in anterior chamber of the rat eye. The study shows the similarity between the grafts and intact olfactory mucosa.

The article presents an abstract of the research paper "Pre- and Postnatal Ontogeny of D2-Type Dopaminergic Receptors in Rat Brain." The study findings highlight the pre- and postnatal ontogeny of D2 type dopaminergic receptors in frontal cortex and striatum of rat brain. It shows that the developmental pattern for D2 and D3 receptors in frontal cortex and striatum is similar to D4.

The article presents an abstract of the research paper "Development of Rat Serotonergic Neurons from Various Raphe Subregions in Serum-Free Culture." The study determines a differential pattern in the development of the functional equipment in the various subgroups of serotonergic neurons. It determines that the serotonergic system is one of the earliest developing neurotransmitter systems in the mammalian brain.

The article presents an abstract of the research paper "A Role for Pax6 in Rhombic Lip Derived Neurons." The study shows that Pax6 is a key regulator in central nervous system, and eye development. The study determines that Pax6 plays a strong role during hindbrain migration processes. According to the study, neurons of the precerebellar nuclei are generated at the lower rhombic lip.

The article presents an abstract of the research paper "The Expression of Carbohydrate Antigens on Dorsal Root Ganglia Neurons, Regulatory Mechanisns and Biological Functions." Several sensation modalities are mediate by the neurons of Dorsal root ganglia. The frequent presence of antibodies against carbohydrate antigens in patient sera with autoimmune neuropathies suggests the biological significance of the carbohydrate antigens.

The article presents an abstract of the research paper "Expression of Mnb/Dyrk, a Dual-Specificity Protein Kinase, in Brain During Rat Development." MNB is a dual-specificity kinase that can catalyze phosphorylation on tyrosine and threonine residues. The MNB protein plays an important role during embryonic and postnatal stages of heart and brain. The level of MNB gradually decreased during the development in various regions of brain and organs.

The article presents an abstract of the research paper "Functional Expression of GFP-Kv Channels and PSD-95-YFP in Hippocampal Neurons." 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. Many researchers have created several GFP-Kv channel fusion proteins and PSD-95-YFP to monitor the expression pattern of a PSD-95 kv channel complex in living neurons.

The article presents an abstract of the research paper "Visualization of Acetylcholine Receptor-γ-Subunit at the Neuromuscular Junction by Green Fluorescent Protein." The findings of the research study suggest that acetylcholine receptors (AChR) γ-green fluorescent protein is assembled into structurally intact AChR complexes which are integrated selectively into the postsynaptic membrane.

The article presents an abstract of the research paper "Metabotropic Glutamate Receptors Modulate [3H]Acetylcholine Release From Cultured Amacrine-Like Neurons." The findings show that the effect of group III metabotropic glutamate receptors (mGluR) on [3H]acetylcholine release may be due to a direct inhibition of L-type Ca2+ channels, and is modulated by group I and group II mGluR.

The article presents an abstract of a research paper analyzing the levels of DNA polymerases in aging rat brain cells. Isolated neurons and astroglia from cerebral cortex of inbred Wistar rats of three ages: 4 days, 6 months and 2 years, were suspended in extraction buffer and sonicated. From the results at all ages studied and in both types of brain cells, β polymerase appears to be the predominant one although other DNA-polymerases seem to be present in reasonable amounts.

The article presents an abstract of a research paper concerning the effect of insulin and insulin like growth factor (IGF-1) on protein synthesis rate and eukaryotic initiation factor 2B (eIF-2B) activity. Neuronal cells from rat embryos were cultured in conditioned medium for 6 days and were maintained for 16 hours in medium. After 30 minutes of treatment, both insulin and IGF-1 induced an increase in eIF-2B activity, in parallel with the observed rise in protein synthesis.

The article presents an abstract of the research paper "Serum Enhancement of Microglial Production of Superoxide, Nitric Oxide, and Tumor Necrosis Factor-alpha in Culture." 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. By the release of neurotoxic mediators, activated microglia can have an impact on neurons.

The article presents an abstract of the research paper "Immunocytochemical Localization of ß-Methylcrotonyl-Coa Carboxylase in Astroglial Cells and Neurons in Culture." 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. Branched-chain amino acids particularly leucine were metabolized as energy substrates.

The article presents an abstract of the research paper "Effect of Aspartate on Acid Secretion in the Rat Stomach." Using immunohistochemical method with specific antibodies, L-Aspartate neurons and their processes were localized in the rat stomach, against either Asp or its synthesizing enzyme, aspartate aminotransferase.