Fig. 8: A proposed mechanistic model of LID in Drosophila. | Communications Biology

Fig. 8: A proposed mechanistic model of LID in Drosophila.

From: Discovery of levodopa-induced dyskinesia-associated genes using genomic studies in patients and Drosophila behavioral analyses

Fig. 8

a Schematic illustration of PD pathogenesis. Dampened DA production in the presynaptic terminals leads to depression of postsynaptic D1-like receptor-ADCY2 signaling causing motor deficits. b Schematic illustration of acute L-DOPA-mediated amelioration of PD. Acute L-DOPA administration normalizes presynaptic DA production and the postsynaptic signaling is restored, resulting in normal motor behaviors. c Schematic illustration of LID pathogenesis. Chronic L-DOPA administration causes excessive DA conversion in the presynaptic terminals and the excessive DA abnormally boosts of postsynaptic D1-like receptor-ADCY2 signaling, leading to LID. DA, dopamine; D1-like, D1-like family receptors; DDC, DOPA decarboxylase.

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