Effects of intrastriatal blockade of glutamatergic transmission on the acquisition of T-maze and radial maze tasks.

Prefrontal cortex and neostriatum constituting the prefrontal system are connected by glutamatergic neurones. The involvement of this corticostriatal projection in control of maze performance of rats was investigated. Glutamatergic transmission mediated by N-methyl-D-aspartate (NMDA) receptors was blocked by intrastriatal injections of dl-2-amino-5-phosphonovaleric acid (AP-5) (50 nmole in 0.5 microliters). In experiment 1, intrastriatal AP-5 was found to increase the number of errors during acquisition of a delayed alternation task in a T-maze. In experiment 2, the effect of intrastriatal AP-5 on acquisition of different 8 arm maze tasks was investigated. AP-5 did not affect the number of reentries on spontaneous and reinforced alternation; pre- and postdelay errors on delayed alternation were not altered. Therefore, intrastriatal NMDA receptor blockade impairs acquisition of a delayed alternation in a T-maze, while intrastriatal blockade of NMDA receptors does not affect acquisition of different 8 arm maze tasks. The impairment in the T-maze task appears not to be due to deficient acquisition of spatial information per se, since 8 arm maze performance is intact. Instead, repeated delays in the T-maze task seem to be the critical component that gives difficulties in acquisition. These difficulties in bridging successive temporal discontiguities were attributed to an increased susceptibility to external and internal interfering stimuli during delays. Thus, striatal NMDA receptors within the prefrontal system may be involved in correct response retention over the duration of delays.