Dihydrokainic acid

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). 

AMPA receptors. This difference in quantal content is temperature-sensitive, being reduced at 37°C as compared to room temperature (Asztely et al., 1997). The authors suggest that the temperature effect could be due to glutamate transporters more efficiently preventing spillover at 37 C. This interpretation is strengthened by the finding that the temperature effect is sensitive to dihydrokainic acid, a glutamate uptake blocker. 

Whereas L-glutamic acid exhibits a substantial affinity for the kainate site with a Ki of 700 nM, D-glutamic acid has a 60-fold lower affinity notably, l- and D-glutamic acid and dihydrokainic acid all exhibit shallow... 

Also in cultured neuroendocrine pinealocytes K+-induced release of Asp was both Ca +-dependent and sensitive to botulinum toxin (Yatsushiro et al., 1997). To rule out involvement of exchange mechanisms in the K" -induced release of Asp the authors used dihydrokainate, which is a non-transported inhibitor (see above) of the excitatory amino acid carrier (GLTl) found in the pinealocytes (Yamada et al., 1997). This treatment did not affect the K+-induced release, but inhibited Na" -dependent sequestration of Asp into the pinealocytes. In addition they showed that the pinealocytes, which contain both the L-form the D-form of Asp, released only L-Asp upon membrane depolarization. This makes it further... 

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