The glutamatergic system has been identified as an important mediator of risky choice. However, previous studies have focused primarily on ionotropic glutamate receptors (e.g., NMDA receptors). Little research has examined the contribution of metabotropic glutamate receptors (mGluRs) on risky choice. The goal of the current experiment was to determine the effects of mGluR 1 and mGluR 5 antagonism on risky choice as assessed in probability discounting (PD). Male Sprague Dawley rats (n = 24) were trained in PD, in which consistently choosing a large, probabilistic reward (LR) reflects risky choice. For half of the rats, the odds against (OA) receiving the LR increased across blocks of trials, whereas the OA decreased across the session for half of the rats. Following training, rats received injections of the mGluR1 antagonist JNJ 16259685 (JNJ; 0, 0.1, 0.3, or 1.0 mg/kg; i.p) and the mGluR5 antagonist MTEP (0, 1.0, 3.0, or 10.0 mg/kg; i.p.). Regardless of which schedule was used, JNJ and MTEP decreased preference for the LR when its delivery was guaranteed. In contrast to delay discounting, in which blocking the mGluR 1 has been shown to alter impulsive choice, these results show that the Group I mGluR family does not selectively alter risky choice. Instead, blocking these receptors appears to impair discriminability of reinforcers of varying magnitudes in PD. Keywordsrisky choice; probability discounting; sensitivity to probabilistic reinforcement; discriminability of reinforcer magnitude; metabotropic glutamate receptor; rat Probability discounting (PD) is often used to measure risky choice in animals (see [1] for a recent review). Recent evidence has implicated the glutamatergic system as being an important mediator of PD. The N-methyl-D-aspartate (NMDA) receptor antagonists MK-801 and ketamine differentially alter performance in this task, as MK-801 decreases sensitivity to probabilistic reinforcement (i.e., increases risky choice), whereas ketamine

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