The mGluR2 receptor agonist, DCG-IV, has been hypothesised to promote memory formation by disinhibiting mitral cell activity in the accessory olfactory bulb (AOB), leading to increased feedback inhibition from granule cells. We tested a key aspect of this hypothesis by recording DCG-IV effects on mitral cell activity in the AOB of urethane anaesthetised mice. Animals received 1 μl infusion of artificial cerebro-spinal fluid or 10, or 100 pmol of DCG-IV into the AOB. A recording electrode was located in the mitral cell layer and a reference electrode in the granule cell layer. There was no single unit activity in the latter. Single unit activity in the mitral cell layer was recorded before, during and after drug infusion. Local infusions of DCG-IV not only did not disinhibit mitral cells but actually reduced their firing frequency. The effect appeared during the infusion and was dose-dependent. The 10 pmol DCG-IV-induced decrease in spike rate was deeper and lasted longer than 100 pmol effect. Trends to return to the preinfusion levels were observed in both groups by the end of 60-min post-infusion period. Thus, this study failed to find a disinhibitory effect of DCG-IV on mitral cells that had been predicted on the basis of in vitro data. These findings challenge the established hypothesis that the memory inducing effects of DCG-IV are mediated by mitral cell disinhibition.
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