Effect of Glutamate and Ionomycin on the Release of Arachidonic Acid, Prostaglandins and HETEs from Cultured Neurons and Astrocytes.

The release of arachidonic acid (ArA) metabolites from mouse neurons and astrocytes in primary culture has been studied in response to ionomycin or glutamate stimulation. Cells were preincubated with [3H]ArA for 24 h and the radioactivity released was examined by HPLC. In striatal, cortical and hippocampal neurons, glutamate and ionomycin strongly stimulated the release of ArA, but neither prostaglandins (PGs) nor hydroxyeicosatetraenoic acids (HETEs) could be detected.

Arachidonic acid released from striatal neurons by joint stimulation of ionotropic and metabotropic quisqualate receptors.

Associative stimulation of N-methyl-D-aspartate (NMDA) receptors and quisqualate ionotropic receptors (Qi) induces long-term potentiation at particular glutamatergic synapses. Release of arachidonic acid as a result of stimulation of NMDA receptors has been proposed to play a part in the establishment of long-term potentiation. But long-term plasticity events at some other glutamatergic synapses do not involve activation of NMDA receptors.

[A case of sepsis caused by Edwardsiella tarda complicated panophthalmitis and pyogenic spondylitis].

Edwardsiella tarda (E. tarda) is gram negative enterobacteriaceae which has been found generally in animal hosts and occasionally in human feces. We have reported a case of sepsis caused by E.

[Effects of morphine and diazepam pretreatment on immobilization stress-induced increase of serotonin metabolism in discrete brain areas of the rat].

Regional concentrations of serotonin (5HT) and 5-hydroxyindoleacetic acid (5HIAA) were measured by high performance liquid chromatography in 16 discrete brain areas of non-stressed control Wistar rats and of stressed Wistar rats. Stress was induced by immobilization for one hour. Also studied were the effects of morphine (10 mg/kg, i.