EKF-diagnostic GmbH

A metalloporphyrin film modified platinum (Pt) electrode was prepared by electrochemical polymerizing of iron(III)‐tetra(3‐methoxy‐4‐hydroxy‐phenyl) porphyrin on a platinum electrode. Cyclic voltammetry of the electrode in PBS pH 7.0 shows the dioxygen reduction peak close to 0 V (vs. Ag/AgCl). Rotating disk electrode experiments indicate a four‐electron transfer mechanism of dioxygen reduction. The chemically modified electrode is recommended as a potential oxygen sensor working at a relatively low potential.

Lysophosphatidic acid (LPA) is a bioactive phospholipid that affects hippocampal excitatory synaptic transmission.

Here we provide in vitro evidence that LPA elicits intracellular calcium concentration ([Ca2+]i) transients by LPA2 receptor activation in primary cultured hippocampal mouse neurons. Downstream and via Gi-coupling, this led to phospholipase C (PLC) activation, inositol (1,4,5) trisphosphate (IP3)-induced Ca2+ release (IICR) and voltage gated Ca2+ channel activation. In addition, we found that LPA elevated [Ca2+]i, not only in the soma but also in presynaptic terminals. This altered the frequency of spontaneous vesicle release specifically in excitatory synapses. However, against our expectations, LPA reduced the frequency of miniature excitatory postsynaptic currents. This was due to a depletion of releasable vesicles resulting from a slowed recycling. SynaptopHluorin based measurements indicated a transient augmentation of release followed by prolonged persistence of vesicles at the membrane. Concordant to our previous findings on ex vivo brain slices, LPA increased spontaneous glutamatergic vesicle release in Banker style astrocytic co-cultures. Our results indicate that pro-excitatory LPA effects critically depend on stable vesicle pools.

Taken together, our data further support membrane derived phospholipids as active modulators of excitatory synaptic transmission.