Aging modulates calcium-dependent phosphatidylinositol degradation by cerebral cortex synaptic plasma membrane phospholipases

Strosznajder, Joanna B.; Samochocki, Marek; Wikiel, Hanna; Małecki, Andrzej

doi:10.1007/bf03160088

Cited by 10 publications

(3 citation statements)

References 34 publications

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“…Enhanced PLA 2 activity, and/or up-regulation of specific PLA 2 isoforms, is observed in the aging brain and well correlates with neuronal degeneration and accelerated senescence [37,38]. The same is observed in hypoxic myocardial cells [24] as well as in models of hypoxia in the lung [25], brain [26] and kidney [27].…”

Section: The Cross-talk Between No and Arachidonic Acid In The Contexmentioning

confidence: 83%

Cross-Talk Between NO and Arachidonic Acid in Inflammation

Mariotto¹,

Suzuki²,

Persichini³

et al. 2007

CMC

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Inducible nitric oxide synthase (iNOS) is expressed in a variety of cell types, in particular in inflammatory cells, in response to diverse pro-inflammatory stimuli. This process requires critical levels of arachidonic acid (AA), generated by constitutive phospholipase A(2) (PLA(2)), promoting tyrosine kinase-dependent phosphorylation, and inhibition, of constitutive NOS. Lowering basal NO levels is indeed critical for the activation of nuclear factor-kappaB (NF-kappaB), and thus for the expression of genes (e.g. iNOS) regulated by this transcription factor. It is interesting to note that NO and AA, two small lipid soluble molecules, rapidly cross the plasma membrane thereby allowing the triggering of the above responses in distal cells. That is, constitutive NO might inhibit NF-kappaB activity in the same cells (e.g. astrocytes) in which it is generated, as well as in other cells that do not express constitutive NOS (e.g. microglia). NO from cells unable to respond to pro-inflammatory stimuli (e.g. neurons) will also contribute to these effects. Along the same line, AA released by pro-inflammatory molecules in specific cell types (e.g. astrocytes) might suppress constitutive NOS activity in the same cells as well as in other cells (e.g. neurons). Thus, AA produced at the very early stages of the inflammatory response is a likely critical signal switching the regulation of the "NO tone" from physiological (i.e. mediated by constitutive NOS) to pathological (i.e. mediated by iNOS). This second phase of the inflammatory response is often accompanied by the onset of deleterious effects in the tissue in which a critical role is played by iNOS-derived NO (directly or indirectly, i.e. via formation of peroxynitrite) as well as by products of the AA cascade. In summary, we suggest that the relative amounts of NO and AA, released by their constitutive enzymes, produce autocrine and paracrine effects regulating the onset of an inflammatory response in which, in addition to other factors, NO and AA are extensively released by their inducible enzymes.

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Section: The Cross-talk Between No and Arachidonic Acid In The Contexmentioning

confidence: 83%

Cross-Talk Between NO and Arachidonic Acid in Inflammation

Mariotto¹,

Suzuki²,

Persichini³

et al. 2007

CMC

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“…We demonstrated that enzyme activities involved in alternative pathways for phospholipid synthesis, such as PLD, are modi®ed by the effect of aging in different brain areas (Ilincheta de Boschero et al, 2000). PLC and PLA 2 enzymes bound to aged synap-tosomal membranes show higher activity than in adult membranes (Strosznajder et al, 1994). The formation and accumulation of very potent lipid messengers such as DAG, lysophospholipids and arachidonic acid in neurotransmission processes may play a role in the deterioration of neuronal function during aging.…”

Section: Introductionmentioning

confidence: 90%

Differential modulation of phospholipase D and phosphatidate phosphohydrolase during aging in rat cerebral cortex synaptosomes

Salvador

Pasquaré

Boschero

et al. 2002

Experimental Gerontology

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“…On the other hand, the number of glutamate binding sites increases with age . Several alterations of biochemical events that take place during aging may inhibit GABAergic function in brain, such as a decreased cytoplasmic level of free Ca", activation of phospholipase AZ, enhancement of arachidonic acid (AA) and diacylglycerol (DAG) release, and gen-eration of oxygen radicals (Schwartz and Mindlin, 1988;Samochocki and Strosznajder, 1993;Strosznajder et al, 1994).…”

Section: Marek Samochocki and Joanna Strosznajdermentioning

confidence: 99%

Age‐Related Changes of GABA‐Activated Chloride Channel Properties in Brain Cortex Synaptic Plasma Membrane: Evidence for Phospholipase Involvement

Samochocki

Strosznajder

1994

Journal of Neurochemistry

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Brain aging decreases binding of tert‐butylbicyclophosphorothionate (TBPS), a specific ligand for Cl− channels, but has no effect on Cl− influx. Detailed studies on the kinetics of TBPS dissociation allowed the characterization of Cl− channel properties. Aging lowers, exclusively in the presence of GABA agonist, muscimol, the half‐life of the fast phase of TBPS dissociation, indicating an opening time of receptor‐dependent Cl− channels shorter than that in adult brain. The half‐life of the slow phase of TBPS dissociation is significantly lower in aged brain in the presence and absence of muscimol. These results suggest a sustained Cl− current, including also the other channel(s) not connected with GABAA receptor activation. The analysis of biphasic TBPS dissociation demonstrates a lowered number of binding sites resulted in the reduction of the number of Cl− channels in the “open” state. This may explain an observed decrease of TBPS binding in aged brain. One of the possible factors involved in modification of GABAA receptor behavior during aging may be arachidonic acid or diacylglycerol, known to be accumulated in aged brain. The action of these compounds on the Cl− channel, observed in this study, correlates well with the effect of aging.

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Aging modulates calcium-dependent phosphatidylinositol degradation by cerebral cortex synaptic plasma membrane phospholipases

Cited by 10 publications

References 34 publications

Cross-Talk Between NO and Arachidonic Acid in Inflammation

Cross-Talk Between NO and Arachidonic Acid in Inflammation

Differential modulation of phospholipase D and phosphatidate phosphohydrolase during aging in rat cerebral cortex synaptosomes

Age‐Related Changes of GABA‐Activated Chloride Channel Properties in Brain Cortex Synaptic Plasma Membrane: Evidence for Phospholipase Involvement

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