FIG. 1.

(A) Schematic representation of the timeline of experimental events. (B) Table of pharmacological agents used during abnormal involuntary movement (AIMs) analysis in rats. (C) Mean and individual AIMs score for vmDA graft‐induced dyskinesias (GID) rats (n = 2). Mean AIMs score for non‐GID rats includes small vmDA grafts and vFB grafts, combined into “non‐GID” dataset (n = 6), in response to saline or drug challenges. AIMs were stable between 30 and 52 weeks post‐graft (both saline datasets, P < 0.05 for non‐GID vs. GID rats). Non‐GID rats demonstrate AIMs in response to l‐dopa, but no change in AIMs is evident in GID rats. For GID rats, 0.3 mg/kg buspirone (5‐HT1A agonist/D2‐like antagonist), fenfluramine (5‐HT reuptake inhibitor), 8‐OH‐DPAT+CP94253 (5‐HT1A/1B agonists), and SB399885 (5‐HT6 antagonist) did not alter expression of the AIMs behaviors (all ps < 0.05 for non‐GID vs. GID). High dose buspirone and eticlopride both abolish AIMs (ps = n.s. for non‐GID vs. GID), without affecting normal locomotion. (D) Mean net rotations to the ipsilateral (positive scale) and contralateral (negative scale) sides for non‐GID and GID rats in response to saline (P < 0.05 for non‐GID vs. GID rats), l‐dopa (P = 0.096) or amphetamine (P < 0.05). In contrast to non‐GID rats, GID rats did not rotate in response to amphetamine, but did rotate spontaneously and in response to l‐dopa. Note: All rats had complete unilateral lesions, as evidenced by their pre‐graft rotational response to amphetamine (non‐GID rats: mean = 12.3 net turns/minute, SEM = 0.95; GID rats: mean = 14.5 net turns/minute, SEM = 1.27) and the loss of nigral TH⁺ neurons (non‐GID rats: mean = 99.5%; loss, SEM = 0.17; GID rats: mean = 99.2% loss, SEM = 0.18). vFB = ventral forebrain control grafts; vmDA = ventral midbrain ventral mesencephalic grafts. Error bars = standard errors of the mean. *P ≤ 0.05, **P ≤ 0.01.