Info

+ CPP (20 mg/kg ip)

0a

a Significantly different from saline control, as determined by a %2-test (p < 0.05).

a Significantly different from saline control, as determined by a %2-test (p < 0.05).

The above-described observations demonstrated that bicuculline injected into the frontal cortex enhanced the response to amphetamine administered systemically. The data in Table 7, however, add an additional facet to the role of the GABA system vis-à-vis stereotypy. As shown in Table 7, bicu-culline injected into the frontal cortex in relatively high doses produces stereotypy even in the absence of amphetamine. The bicuculline-induced stereotypy either in the presence or the absence of amphetamine does not produce sensitization, providing further evidence of the distinction between the systems that generate the acute response and those that are required for the induction of sensitization. The data shown in Table 7 also indicate that the bicuculline-induced stereotypy is not blocked by sulpiride, suggesting that the stereotypy does not involve dopamine but is blocked by the NMDA antagonist CPP administered either systemically or into the frontal cortex. These results suggest that stereotypy produced by the stimulants is the result of diminishing the physiological GABA inhibitory control over a tonically active NMDA system in the frontal cortex. This view is further supported by the observations in Table 5, which demonstrated that THIP, a GABAa agonist, injected into the frontal cortex can block the systemic effect of amphetamine. The key role of the GABAA system in the manifestation of stereo-typy is further underscored by the above-described drug studies in the striatum. Stereotypy originating in the striatum appears to result from a GABAergic inhibition of its GABAergic outflow; similarly, in the frontal cortex stereotypy is again the result of the inhibition of a GABAergic system, which physiologically functions to inhibit a tonically active glutamatergic system.

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