| 18298662 |
Luccini E, Romei C, Raiteri L: Glycinergic nerve endings in hippocampus and spinal cord release glycine by different mechanisms in response to identical depolarizing stimuli. J Neurochem. 2008 Mar 12.
Studies on hippocampal glycine release are extremely rare. We here investigated release from mouse hippocampus glycinergic terminals selectively pre-labelled with [(3) H] glycine through transporters of the GLYT2 type. Purified synaptosomes were incubated with [(3) H] glycine in the presence of the GLYT1 blocker NFPS to abolish uptake ( approximately 30%) through GLYT1. The non-GLYT1-mediated uptake was entirely sensitive to the GLYT2 blocker Org25543. Depolarization during superfusion with high-K (+) (15-50 mmol/L) provoked overflows totally dependent on external Ca (2+), whereas in the spinal cord the 35 or 50 mmol/L KCl-evoked overflow (higher than that in hippocampus) was only partly dependent on extraterminal Ca (2+). In the hippocampus, the Ca (2+)-dependent 4-aminopyridine (1 mmol/L)-evoked overflow was five-fold lower than that in spinal cord. The component of the 10 mumol/L veratridine-induced overflow dependent on external Ca (2+) was higher in the hippocampus than that in spinal cord, although the total overflow in the hippocampus was only half of that in the spinal cord. Part of the veratridine-evoked hippocampal overflow occurred by GLYT2 reversal and part by bafilomycin A (1)-sensitive exocytosis dependent on cytosolic Ca (2+) generated through the mitochondrial Na (+)/Ca (2+) exchanger. As glycine sites on NMDA receptors are normally not saturated, understanding mechanisms of glycine release should facilitate pharmacological modulation of NMDA receptor function. |
0(0,0,0,0) |