Pharmacological Properties of Phosphatidylserine in the Aging Brain: Biochemical Aspects and Therapeutic Potential

Calderini, G.; Bellini, F.; Bonetti, A; Galbiati, Enrico; Rubini, R.; Zanotti, A.; Toffano, G.

doi:10.1007/978-1-4899-0490-4_23

Cited by 7 publications

(3 citation statements)

References 24 publications

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“…PtdSer is the most effective phospholipid for full protein kinase C activation (Hirisawa and Nishizuka, 1985). In aging rats PtdSer administration counteracts the age-induced change in protein kinase C activity and distribution (Calderini et al, 1986). It may be assumed therefore that in aging rats, restoration of protein kinase C activity by PtdSer may increase extracellular Ch available for ACh synthesis.…”

Section: Discussionmentioning

confidence: 99%

Decrease of Acetylcholine Release from Cortical Slices in Aged Rats: Investigations into Its Reversal by Phosphatidylserine

Vannucchi

Casamenti

Pepeu

1990

Journal of Neurochemistry

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The release of total acetylcholine (ACh) and [3H]ACh was investigated in electrically stimulated cortical slices prepared from 4- and 18-month-old male Wistar rats. The slices were prelabeled with [3H]choline ([3H]Ch) and perfused with Krebs solution containing physostigmine. Total ACh was measured and the nature of the tritium efflux identified by HPLC. The total tritium content in the slices at the end of the incubation period was half as great in the old as in young rats. A linear relationship was found between stimulation frequencies (2, 5, and 10 Hz) and fractional [3H]ACh release in both young and old rats. In the latter the release was significantly smaller. At 10 Hz stimulation frequency the ratio between the two 2-min stimulation periods, S2/S1, was higher in the 18-month-old rats than in the young rats. Specific activity of the evoked ACh release was significantly smaller in S2 than in S1 in 4-month-old rats only. These findings indicate that the young synthetize ACh from endogenous unlabeled Ch more than older rats. In 18-month-old rats both the evoked total ACh and [3H]ACh release, expressed as picograms per minute, showed an approximately 50% decrease in both S1 and S2 stimulation periods, with no significant difference in specific activity. Phosphatidylserine (PtdSer) administration (15 mg/kg, i.p. daily) for 1 week to 18-month-old rats prevented the reduction in total evoked ACh release but not the reduction in evoked [3H]ACh release. The specific activity of ACh release was therefore significantly smaller than that of the young and untreated old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Decrease of Acetylcholine Release from Cortical Slices in Aged Rats: Investigations into Its Reversal by Phosphatidylserine

Vannucchi

Casamenti

Pepeu

1990

Journal of Neurochemistry

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“…Moreover, it has been recently demonstrated that cholinergic neurons utilize PC as a reservoir of choline to be used for acetylcholine synthesis . Both PC and PS administrations have been shown to improve several cognitive functions, including memory and behavior in the aged brain, and in Alzheimer's disease patients (Calderini et al, 1986;Delwaide et al, 1986;Farooqui et al, 1988). Because PC can be synthesized from PS by a base-exchange enzymatic reaction (Gaiti et al, 1989;Porcellatti et al, 1971), and since the uptake of exogenous phosphatidylserine stimulates the incorporation of choline into PC (Slack et al, 1989), the increase in the density of high affinity binding sites for 3H-OXO, observed after BC-PC or BC-PS administrations, could reflect the expression of a common mechanism of action.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of phosphatidylserine on the binding of muscarinic cholinergic receptor ligands

Raskovsky

Rivas

Bernik

et al. 1990

Molecular and Chemical Neuropathology

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The modulation of the binding of muscarinic cholinergic receptor ligands by phosphatidylserine purified from bovine cerebral cortex (BC-PS) was examined in vitro and in vivo. The enrichment of bovine cerebral cortical synaptosomal membranes with BC-PS, using a fusion technique, produced a concentration-dependent decrease in the affinity (increase in Kd) of [3H]quinuclidinyl benzylate (3H-QNB) specific binding to muscarinic acetylcholine receptors (mAChR), without changes in their maximal number (Bmax). Similar results were observed when [3H]oxotremorine (3H-OXO) was used to label a high affinity subpopulation of mAChR. On the other hand, preincubation of BC-PS liposomes with synaptosomal membranes in a nonoptimum fusion condition (at pH 7.4) did not alter the binding properties of both radioligands. Fusion experiments using a pure phosphatidylserine preparation from spinal cord revealed a similar decrement in the affinity of 3H-QNB specific binding. Five day's intraperitoneal (i.p.) administration of 15 mg/kg of BC-PS liposomes in rats increased the maximal number of cerebral cortical binding sites for 3H-OXO. Scatchard analysis revealed no changes in the apparent dissociation constant. This modification is selective in relation to the neural structure studied. Thus, BC-PS treatment did not modify 3H-OXO binding in the hippocampal formation and cerebellum. In contrast, parallel experiments using the muscarinic antagonist 3H-QNB showed no alteration in the binding properties of mAChR. Five day's i.p. administration of 15 mg/kg/d of phosphatidylcholine from bovine cerebral cortex (BC-PC) liposomes produced quite similar results to those obtained with BC-PS. These results indicate that mAChR are under the modulatory action of phosphatidylserine (PS) and phosphatidylcholine (PC), and suggest that this endogenous phospholipids may play a regulatory role on the mAChR. The possible implications of these findings on the effects of PC or PS treatment in neurological disorders involving a decrease in central cholinergic functions are discussed.

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“…In aging rats, it has been shown that there is a reduction in acetylcholine release [5] and protein kinase C activity [6]. PS restores acetylcholine release [5] and protein kinase C activity [7]. Protein kinase C facilitates the release of acetylcholine as well [8].…”

Section: Introductionmentioning

confidence: 98%

Determination of phosphatidylserine in milk-based nutritional products using online derivatization high-performance liquid chromatography

Lin

Jie

Pei

et al. 2015

Journal of Chromatography A

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Pharmacological Properties of Phosphatidylserine in the Aging Brain: Biochemical Aspects and Therapeutic Potential

Cited by 7 publications

References 24 publications

Decrease of Acetylcholine Release from Cortical Slices in Aged Rats: Investigations into Its Reversal by Phosphatidylserine

Decrease of Acetylcholine Release from Cortical Slices in Aged Rats: Investigations into Its Reversal by Phosphatidylserine

Modulatory effects of phosphatidylserine on the binding of muscarinic cholinergic receptor ligands

Determination of phosphatidylserine in milk-based nutritional products using online derivatization high-performance liquid chromatography

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