ArticleThe Biochemical journal1995
Glutamate stably enhances the activity of two cytosolic forms of phospholipase A2 in brain cortical cultures.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 94 citations in OpenAlex.
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- Inflammation and JNK's Role in Niacin-GPR109A Diminished Flushed Effect in Microglial and Neuronal Cells With Relevance to Schizophrenia.Frontiers in psychiatry · 2021Review
- Current knowledge on the neuroprotective and neuroregenerative properties of citicoline in acute ischemic stroke.Journal of experimental pharmacology · 2015Review
- The role of secretory phospholipase A₂ in the central nervous system and neurological diseases.Molecular neurobiology · 2014Review
- Inflammation & apoptosis in spinal cord injury.The Indian journal of medical research · 2012Review
- Characterizing phospholipase A2-induced spinal cord injury-a comparison with contusive spinal cord injury in adult rats.Translational stroke research · 2011Article
- Phospholipase A2 and its molecular mechanism after spinal cord injury.Molecular neurobiology · 2010Review
- Low molecular weight phospholipases A2 in mammalian brain and neural cells: roles in functions and dysfunctions.Molecular neurobiology · 2010Review
- Differential effects of lysophospholipids on exocytosis in rat PC12 cells.Journal of neural transmission (Vienna, Austria : 1996) · 2010Article
- Chronic administration of valproic acid reduces brain NMDA signaling via arachidonic acid in unanesthetized rats.Neurochemical research · 2008Article
- Cytosolic phospholipase A2 alpha inhibition prevents neuronal NMDA receptor-stimulated arachidonic acid mobilization and prostaglandin production but not subsequent cell death.Journal of neurochemistry · 2008Article
- Chronic carbamazepine administration reduces N-methyl-D-aspartate receptor-initiated signaling via arachidonic acid in rat brain.Biological psychiatry · 2007Article
- Receptor-specific inhibition of GABAB-activated K+ currents by muscarinic and metabotropic glutamate receptors in immature rat hippocampus.The Journal of physiology · 2007Article
- Differential effects of polyunsaturated fatty acids on membrane capacitance and exocytosis in rat pheochromocytoma-12 cells.Neurochemical research · 2006Article
- Phospholipases A2 in ischemic and toxic brain injury.Neurochemical research · 2000Review
- Lipid-dependent modulation of Ca2+ availability in isolated mossy fiber nerve endings.Neurochemical research · 1997Article
- Release of secretory phospholipase A2 from rat neuronal cells and its possible function in the regulation of catecholamine secretion.The Biochemical journal · 1996Article
- Role of Mitochondria in Neonatal Hypoxic-Ischemic Brain Injury.Journal of neuroscience and rehabilitationArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms by which glutamatergic neurotransmitters modulate neuronal lipid metabolism are not well established. We have directly measured phospholipase A2 (PLA2) enzymic activity in cell-free extracts from cortical neuronal cultures from rat brain and have found that the PLA2 activity is up-regulated after cells are exposed to glutamate. Brief exposure to a calcium ionophore or phorbol 12-myristate 13-acetate (PMA) stably enhanced PLA2 activity. Down-regulation of protein kinase C activity partially blocked glutamate's effects. Two Ca(2+)-and pH-dependent forms of PLA2 were identified in cytosolic extracts. Activation of both forms of PLA2 was enhanced by prior exposure of the cultures to glutamate. One of the two forms had chromatographic characteristics on heparin-Sepharose, Mono Q and Superose 12 columns similar to the 100 kDa cytosolic PLA2 (cPLA2), and was recognized by an antibody raised to pig spleen cPLA2. The second form was similar in size to Group-I and -II PLA2s but differed in chromatographic characteristics. It was not inhibited by dithiothreitol, and did not react with antibodies to pancreatic Group-I PLA2, features that distinguish it from Group-I and -II PLA2. In extracts from cells pretreated with glutamate, the activity-Ca2+ concentration dose-response relationship of the 13.5 kDa form of PLA2 was shifted to the left with activation at lower Ca2+ concentration as the result of stable modification of the enzyme induced by glutamate. Thus glutamate-induced stable enhancement of PLA2 activity, by processes involving calcium and protein kinase C activation, is a potential molecular switch probably mediating changes in synaptic function and contributing to excitotoxicity.
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