Axonal release of glutamate analog, d-2,3-3H-Aspartic acid and l-14C-proline from segments of sciatic nerve following electrical and magnetic stimulation.

Segments of the mouse sciatic nerve were preloaded with either d-2,3-(3)H-Aspartic acid [nonmetabolizable analog of glutamate] or l-(14)C-proline and the release of these exogenous molecules was evaluated in the fractions of the perfusate following electrical or magnetic stimulation. The electrical stimulation (10Hz, 10Am, 20s) induced an instantaneous increase in the release of both molecules, although the release of d-2,3-(3)H-Aspartic acid was much greater. Moreover, contrary to l-(14)C-proline, the release of d-2,3-(3)H-Aspartic acid was Ca(2+)-dependent. While magnetic stimulation (15mT, 0.16Hz, 30min) also induced the release of d-2,3-(3)H-Aspartic acid in a Ca(2+)-dependent way, the release of l-(14)C-proline was negligible. These results indicate that axons can release glutamate in a specific, calcium-dependent way. This release may contribute to interaxonal interactions.