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. 2008 Oct 14;6(10):1–18. doi: 10.1371/journal.pbio.0060249

Figure 4. Retinal PER2::LUC Rhythms Are Not Dependent on Communication via Dopamine, Acetylcholine, GABA, or Glycine.

Figure 4

(A–F) Retinal circadian PER2::LUC expression rhythms persisted upon continuous application of: (A) the TH inhibitor L-AMPT (100 μM) along with the vesicular dopamine uptake inhibitor reserpine (10 μM); (B) the dopamine receptor agonist ADTN (100 μM), in the presence of L-AA (100 μM); (C) the dopamine D1 receptor agonist SKF-38393 (50 μM) along with the D2/D4 receptor agonist quinpirole hydrochloride (50 μM); (D) the dopamine D1 receptor antagonist SCH-23390 (50 μM) along with the D2 receptor antagonist sulpiride (50 μM); (E) the nonselective cholinergic agonist carbamoylcholine chloride (100 μM); and (F) the nicotinic acetylcholine receptor antagonist (+)-tubocurarine (100 μM) along with the muscarinic acetylcholine receptor antagonist atropine (100 μM).

(G) GABA (1 mM) greatly suppressed the amplitude of retinal PER2::LUC rhythms.

(H) Retinal PER2::LUC rhythms persisted during blockade of GABA receptors with the GABAA receptor antagonist SR-95531 (40 μM) along with the GABAB receptor antagonist CGP-35348 (100 μM) and the GABAC receptor antagonist TPMPA (100 μM).

(I and J) Retinal PER2::LUC rhythms persisted upon continuous application of: (I) glycine (3 mM); and (J) the glycine receptor antagonist strychnine hydrochloride (50 μM).

Bars indicate the duration of treatment.