Trophic actions of extracellular nucleotides and nucleosides on glial and neuronal cells

Neary, Joseph T.; Rathbone, Michel P.; Cattabeni, Flaminio; Abbracchio, Maria P.; Burnstock, Geoffrey

doi:10.1016/0166-2236(96)81861-3

Cited by 402 publications

(281 citation statements)

References 68 publications

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“…Uridine also affects PtdCho synthesis and, possibly, ACh release via UTP-mediated activation of the P2Y receptor (Neary et al, 1996). A subset of the metabotropic P2Y (P2Y 2 , P2Y 4 , and P2Y 6 ) receptors, once activated by UTP, increases intracellular levels of DAG and inositol triphosphate (IP 3 ), and subsequently, calcium influx.…”

Section: Discussionmentioning

confidence: 99%

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

2007

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The biosynthesis of brain membrane phosphatides, e.g., phosphatidylcholine (PtdCho), may utilize three circulating compounds: choline, uridine (a precursor for UTP, CTP, and CDP-choline), and a PUFA (e.g., docosahexaenoic acid); moreover oral administration of the uridine source uridine-5′-monophosphate (UMP) can significantly increase levels of the phosphatides throughout the rodent brain. Since PtdCho can provide choline for acetylcholine (ACh) synthesis, we determined whether UMP administration also affects ACh levels in striatum and striatal extracellular fluid, in aged and young rats. Among aged animals consuming a UMP-containing diet (2.5%, w/w) for 1 or 6 weeks, baseline ACh levels in striatal dialysates rose from 73 fmol/min to 148 or 197 fmol/min (P<0.05). Consuming a lower dose (0.5%) for 1 week produced a smaller but still significant increase (from 75 to 92 fmol/min, P<0.05), and elevated striatal Ach content (by 16%; P<0.05). Dietary UMP (0.5%, 1 week) also amplified the increase in ACh caused by giving atropine (10 μM in the aCSF); atropine alone increased ACh concentrations from 81 to 386 fmol/min in control rats and from 137 to 680 fmol/min in those consuming UMP (P<0.05). Young rats eating the UMP-containing diet exhibited similar increases in basal ECF ACh (from 105 to 118 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05). These data suggest that giving a uridine source may enhance some cholinergic functions, perhaps by increasing brain phosphatide levels. Scope: Section 3 (Neurophysiology, Neuropharmacology and other forms of Intercellular Communication)

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Section: Discussionmentioning

confidence: 99%

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

2007

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“…Other than released enzymes, cellular nucleotides will also be released, which are diffusible and may play a role in microglial chemotaxis [16,23,27,47]. One such example of microglial-activating material detected in dense-core but not diffuse plaques is a nuclear remnant [11,13,15] as ATP or ADP can induce chemotaxis for cultured microglia through G i/o -coupled P2Y receptors [27], which is completely blocked by either AR-C69931MX, a potent and selective antagonist against P2T AC receptors or pertussis toxin pretreatment [27].…”

Section: Unique Mechanisms Of Plaque Formationmentioning

confidence: 99%

The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

D’Andrea

Cole

Ard

2004

Neurobiology of Aging

198

131

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Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques. The role of the microglial cells in the AD brain is controversial, as it remains unclear if the microglia form the amyloid fibrils of plaques or react to them in a macrophage-phagocytic role. Also, it is not known why microglia are preferentially associated with some amyloid plaque types. This review will provide substantial evidence to support the phagocytic role of microglia in the brain as well as explain why microglia are generally associated with specific plaque types that may be explained through their unique mechanisms of formation. In summary, the data presented suggests that plaque associated microglial activation is typically subsequent to specific amyloid plaque formations in the AD brain.

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“…ATP can serve as a neurotransmitter in brain and activates responses in both neurons (Edwards et al, 1992;Gu and McDermott, 1997) and glial cells (Salter and Hicks, 1994) via either ligand-gated cation channels or metabotropic receptors that promote release of calcium from intracellular stores by the activation of the inositol triphosphate (IP 3 ) signaling cascade (Kastrikis et al, 1992;Salter and Hicks, 1994). In addition, ATP and its related metabolites have important trophic effects on several brain cell populations by regulating neurite outgrowth (Neary et al, 1996), astrocytic shape changes (Neary et al, 1994;Rathbone et al, 1998), or survival of motor neurons via intracellular elevation of cyclic adenosine monophosphate (cAMP; Hanson et al, 1998).…”

Section: Astrocytes As Active Participantsmentioning

confidence: 99%

Astrocytes in the aging brain

Cotrina¹,

Nedergaard²

2002

J. Neurosci. Res.

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Trophic actions of extracellular nucleotides and nucleosides on glial and neuronal cells

Cited by 402 publications

References 68 publications

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

Astrocytes in the aging brain

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