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Neuropeptide Y is the ligand of a family of G-protein coupled receptors (Y1 to Y6). In the thalamus, exogenous and endogenously released NPY can shorten the duration of thalamic oscillations in brain slices from P13 to P15 rats, an in vitro model of absence seizures. Here, we examine which Y receptors are involved in this modulation. Application of the Y1 receptor agonist Leu31Pro34NPY caused a reversible reduction in the duration of thalamic oscillations (−26.6 ± 7.8%), while the Y2 receptor agonist peptideYY(3–36) and the Y5 receptor agonist BWX-46 did not exert a significant effect. No Y receptor agonist affected oscillation period. Application of antagonists of Y1, Y2 and Y5 receptors (BIBP3226, BIIE0246 and L152,806, respectively) produced results consistent with those obtained from agonists. BIBP3226 caused a reversible disinhibition, an effect that increases oscillation duration (18.2 ± 9.7%) while BIIE0246 and L152,806 had no significant effect. Expression of NPY is limited to neurons in the reticular thalamic nucleus (nRt), but Y1 receptors are expressed in both nRt and adjacent thalamic relay nuclei. Thus, intra-nRt or nRt to relay nucleus NPY release could cause Y1 receptor mediated inhibition of thalamic oscillations.