Reduced phospholipid contents of brain synaptosomes in phosphate depletion

Author:

Smogorzewski M.1,Islam A.1,Koureta P.1,Fadda G. Z.1,Massry S. G.1

Affiliation:

1. Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Abstract

The effects of 6 wk phosphate depletion (PD) and pair-weight feeding (PW) without and with treatment with verapamil (PD-V and PW-V, respectively) on phospholipid (PL) and cholesterol content and on resting levels of cytosolic calcium concentration ([Ca2+]i) of brain synaptosomes of rats were examined. PD was associated with significantly (P less than 0.01) lower synaptosomal content of total PL, phosphatidylinositol (PI), phosphatidylserine (PS), and phosphatidylethanolamine (PE) and with significant (P less than 0.01) elevation in [Ca2+]i. Verapamil treatment of PD rats prevented the rise in [Ca2+]i of brain synaptosomes and the fall in PI and caused significant (P less than 0.01) improvement in the synaptosomal content of PS and PE; values of PS and PE in PD-V rats, however, were still significantly (P less than 0.01) lower than those of PD rats. Verapamil treatment of PW rats did not affect synaptosomal content of the various PL or resting levels of [Ca2+]i. Cholesterol content of brain synaptosomes of the various groups was not significantly different, but cholesterol-to-total PL ratios were significantly (P less than 0.01) higher in PD and PD-V rats than in PW or PW-V animals. Results indicate that PD affects metabolism of total phospholipids, PI, PS, and PE of brain synaptosomes, and these derangements are due to reduced availability of phosphorus and to the rise in [Ca2+]i. The data are consistent with the proposition that PD-induced changes in PL render the synaptosomal membrane more permeable to calcium, an event that may lead to a rise in [Ca2+]i.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

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