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. 2006 Apr 19;26(16):4318–4328. doi: 10.1523/JNEUROSCI.0118-06.2006

Figure 1.

Figure 1.

Activation of group III metabotropic glutamate receptors attenuates rotenone toxicity on TH+ neurons in rat embryonic midbrain neuronal cultures. A–F, Midbrain neuronal cultures were treated for 12 h with vehicle (Veh) (A), rotenone (Rot, 100 nm) (B), rotenone plus l-AP-4 (mGluRIII agonist, 100 μm) (C), rotenone plus tADA (mGluRI agonist, 100 μm) (D), rotenone plus APDC (mGluRII agonist, 100 μm) (E), and rotenone plus l-AP-4 and CPPG (mGluRIII antagonist, 40 μm) (F). Fixed neurons were costained for TH (green), TUNEL (red), and NeuN (blue). Arrowheads, Broken process. *Condensed nuclei of dead glial cells (killed by AraC in the media). #Nucleus of TH− neuron. Scale bar: (in F) A–F, 10 μm. G, Statistical summary of data represented in A–F showed that rotenone toxicity on TH+ neurons was selectively attenuated by activation of group III metabotropic glutamate receptors. tADA (100 μm) and DHPG (200 μm) are mGluRI agonists, APDC (100 μm) and LCCG (200 μm) are mGluRII agonists, l-AP-4 (100 μm) and l-SOP (100 μm) are mGluRIII agonists, and CPPG (40 μm) and MSOP (200 μm) are mGluRIII antagonists. *p < 0.001 (n = 7) versus rotenone alone. H, mGluRIII agonist l-AP-4 (100 μm) significantly reduced the toxicity of rotenone at different concentrations. *p < 0.001 (n = 7) versus rotenone at the corresponding concentration. I, l-AP-4 decreased the toxicity of rotenone (100 nm) in a dose-dependent manner. #p < 0.001 (n = 6) versus 0 μm l-AP-4. Error bars indicate SE.