Neurological Disorders Linked to Disrupted Phospholipid Regulation of Nerve Cell Signaling Pathways

Neurochemical studies carried out in rodent models have yielded information about the functioning of nerve cell signaling pathways that has implications for potential future treatment of epilepsy, stroke, and other neurological disorders.

Investigators at the University of Texas Health Science Center (San Antonio, USA) used isolated rat nerves to study the relationship between phosphoinositide kinase signaling enzymes and calcium ions. In particular, they were interested in the regulatory activity of the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2).

PIP2 is a minor phospholipid component of cell membranes where it is a substrate for a number of important signaling proteins. PIP2 functions as an intermediate in the IP3/DAG pathway, which ultimately opens calcium channels on the smooth endoplasmic reticulum, allowing mobilization of calcium ions through specific Ca2+ channels into the cytosol. Calcium participates in the cascade by activating other proteins.

Results of the study were published in the January 7, 2011, issue of the Journal of Biological Chemistry and were summarized by senior author Dr. Mark S. Shapiro, professor of physiology at the University of Texas Health Science Center, who said, "We now have novel targets for therapeutic intervention for a range of neurological and cardiovascular diseases, including stroke, epilepsy, dementia, hypertension, mental illness, and others. This study should guide clinicians and pharmaceutical companies in developing new therapies against mental, neurological, cardiovascular, or cerebrovascular diseases that afflict many millions of people.”

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University of Texas Health Science Center