Phospholipids Of Slices Research Articles

Differences in the adenosine receptors modulating inositol phosphates and cyclic AMP accumulation in mammalian cerebral cortex

1. 2-Chloroadenosine stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation and potentiated (guinea-pig) or inhibited (mouse) the histamine H1-receptor-stimulated hydrolysis of inositol phospholipids in slices of guinea-pig and mouse cerebral cortex. 2. Two xanthine-based adenosine receptor antagonists were identified which were one order of magnitude more potent at the adenosine receptor mediating augmentation of the histamine-stimulated inositol phospholipid hydrolysis than at the receptor linked to cyclic AMP formation in guinea-pig cerebral cortical slices. 3. These compounds, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and 7-benzyl-3-(2-methylpropyl)xanthine (BMPX) retained their selectivity under near-identical incubation conditions in both assays. 4. These compounds also showed similar affinities and selectivity for the adenosine receptor mediating inhibition of histamine-stimulated inositol phospholipid hydrolysis in mouse cerebral cortical slices. 5. Inclusion of agents which give rise to, or mimic, high levels of cyclic AMP (forskolin (1 microM), 8-bromo-cyclic AMP (1 mM) and vasoactive intestinal polypeptide (1 microM] in the incubation medium failed to mimic the action of 2-chloroadenosine on inositol phospholipid turnover in cerebral cortical slices from either species. 6. These data suggest that the adenosine receptor modulating the hydrolysis of inositol phospholipid in mouse and guinea-pig cerebral cortical slices is different from the adenosine receptor linked to cyclic AMP formation, and, furthermore, that the modulation of inositol phospholipid metabolism in either species is not mediated via alterations in cyclic AMP levels.

Evidence for a carbachol stimulated phosphatidylinositol effect in heart

Incubation of canine heart slices with 32P-inorganic phosphate in physiological medium resulted in the incorporation of 32P into a number of cardiac phospholipids. Carbachol, a non-hydrolyzable acetylcholine analogue, selectively increased 32P-incorporation into phosphatidic acid and phosphatidylinositol in slices of right auricle 80 and 70% respectively. This effect of carbachol was half-maximal at 5-10 microM and was inhibited completely by atropine. Carbachol did not affect labeling of other phospholipids in right auricle and did not affect the labeling of any phospholipid in slices of left auricle or right or left ventricle. These results provide evidence for a muscarinic receptor mediated phospholipid effect which appears to be localized in the right atrial region of canine heart.

Acetylcholine and the incorporation of (P32) phosphate into phospholipids and phosphoproteins of nerve endings of developing rat brain.

IT has been shown that acetylcholine stimulates the incorporation of [32P] phosphate into the phospholipids of slices, homogenates, and microsomal fractions of guinea-pig cerebral hemispheres under conditions of oxidative phosphorylation1,2. Maximal stimulation of phosphorus-32 incorporation was found to occur in phosphatidic acid and phosphoinositide2.