Biomedical subjects

L Pellerin

Publications and source records attributed to L Pellerin.

46 records · Page 3Linked to original sources

PubMed1991

Release of arachidonic acid by NMDA-receptor activation in the rat hippocampus.

In hippocampal slices arachidonic acid released after NMDA post-synaptic receptor activation is thought to act as a retrograde trans-synaptic messenger which facilitates the pre-synaptic release of L-glutamate to be involved in the expression of long-term synaptic potentiation (LTP). We measured the mass amount of arachidonic acid released from hippocampal slices incubated under conditions which maintain the electrophysiological responsiveness of the slice. Melittin released arachidonic, oleic and docosahexaenoic acids by phospholipase A2 activation but not palmitic or stearic acids. Of greater interest L-glutamate, N-methyl-D-aspartate and incubation conditions known to induce LTP selectively and rapidly increased the release of arachidonic acid in amounts over basal levels of 200-300 ng/mg protein. This is the first direct determination of the mass amount of arachidonic acid released following NMDA receptor activation in the hippocampus.

Animals↗

PubMed1990

Long-term changes of synaptic transmission induced by arachidonic acid in the CA1 subfield of the rat hippocampus.

The effects induced by arachidonic acid upon excitatory synaptic transmission were investigated in the CA1 subfield of rat hippocampal slices. Perfusion with medium containing 50 microM of arachidonic acid induced in 12 of 19 experiments a long-lasting potentiation of the stratum radiatum-induced responses recorded in the cell body and in the apical dendritic layers. In 5 of 19 experiments, arachidonic acid evoked a depression of the same responses. Both effects were antagonized by nordihydroguaiaretic acid which is an inhibitor of lipoxygenase enzymes. These results demonstrate that one or more than one of the arachidonic acid metabolites of the lipoxygenase pathways might be involved in the long-term modulation of synaptic transmission in the hippocampus.

Action Potentials↗

PubMed1990

Formation of 12-lipoxygenase metabolites in rat cerebral cortical slices: stimulation by calcium ionophore, glutamate and N-methyl-D-aspartate.

The 12-lipoxygenase pathway of arachidonic acid metabolism in rat cerebral cortex slices is stimulated by exogenous arachidonic acid, Ca2+ ionophore A23187, phorbol ester, glutamate, N-methyl-D-aspartate (NMDA) but not by kainate and other neurotransmitters except norepinephrine. The 12-hydroxyeicosatetraenoic acid formed is the (S)-enantiomer. A specific role for 12-lipoxygenase metabolites in NMDA receptor activation and long term potentiation is proposed.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1990

A protein assay program for Lotus 1-2-3.

Protein assays have become a widespread procedure not only in biochemistry but in many disciplines. This paper describes a program that takes advantage of the capacity of a spreadsheet program such as Lotus 1-2-3 to produce a graph and perform the calculations necessary for such assays. Its simplicity allows users with little or no experience with Lotus 1-2-3 to run it once installed.

Mathematical Computing↗

PubMed1989

Metabolism of prostaglandin D2 by human cerebral cortex into 9 alpha, 11 beta-prostaglandin F2 by an active NADPH-dependent 11-ketoreductase.

In homogenates of rat cerebral neocortex prostaglandin D2 (PGD2) was found to be quantitatively the main PG biosynthesized by a cytosolic PGD synthetase from endogenously released arachidonic acid. Amounts of 628 ng/g wet weight were found after 30-min incubation periods compared with basal levels of 2.3 ng/g wet weight. In human cerebral cortex, whether obtained at biopsy or postmortem, only small amounts of PGD2 (4.5-11.7 ng/g wet weight/30 min) were formed. Furthermore, PGD2, added to homogenates of human biopsy temporal cortex, was converted efficiently into 9 alpha,11 beta-PGF2 by a NADPH-dependent 11-ketoreductase as has been reported in other human tissues (liver and lung). PGF2 alpha was determined directly as the n-butylboronate derivative. It became clear that 9 alpha,11 beta-PGF2 was formed in considerably greater amounts than PGF2 alpha and that other metabolites are also formed. These results can account for the low amounts of PGD2 found in incubations of human brain tissue. The rat brain does not contain 11-ketoreductase activity. The present results indicate that the 9 alpha,11 beta-PGF2 must be considered along with other eicosanoids in pathophysiological situations in brain.

Adolescent↗

PubMed1989