Release by heteroexchange

Fleck et al., 1993). This result was also obtained under conditions mimicking high neuronal activity (Szerb, 1988). Also in the intact striatum using the microdialysis technique, a selective increase in Asp release after chemical depolarization (with GABA antagonists or NMDA) of the neocortex has been demonstrated (Palmer et al., 1989). Such selectivity suggests that Asp is released independently of Glu both in brain slices and the intact brain. 

Furthermore, in the intact striatum dihydrokainic acid increased the extracellular level of both Asp and Glu during K+ depolarization (Herrera-Marschitzet al., 1996). If heteroexchange was responsible for the depolarization-induced increase in extracellular Asp one would expect the Asp levels to be decreased by dihydrokainic acid (but see Fallgren and Paulsen, 1996). 

Essential as evidence for exocytotic Asp release would be a demonstration of Asp in synaptic vesicles and of a vesicular uptake system for Asp. In contrast to Glu, no study has so 

IS ASPARTATE RELEASED FROM A SEPARATE POOL OF NERVE ENDINGS  

Neighboring ultrathin sections from hypoglycemic CAl hippocampus (same block as in Fig. 4) showing co-localization of L-Asp (A) and l-G1u (B) immunogold particles in a terminal (atl) with asymmetrical synaptic specialization (arrows) on a spine (s). Note that the terminal has high levels of both immunoreactivities, whereas the spines and dendritic shafts (d) are very weakly labeled. Scale bar = 0.2 pm. (Modified from Gundersen et al., 1998.) 

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