Figure 2
From: GluD1, linked to schizophrenia, controls the burst firing of dopamine neurons
GluD1 is co-expressed with mGlu1/5 in DA neurons. (a) Fluorescence micrographs of the SNc and VTA showing diffuse GluD1 immunostaining of somata and processes of DAT-positive DA neurons. Immunostaining almost disappeared in GluD1−/− mice. Scale bar: 100 μm. (b) Electron micrographs of the SNc showing immunoparticles for GluD1 (arrowheads) and TH (arrows), as detected using a double-labeling post-embedding immunogold method. GluD1 immunoparticles were detected along the postsynaptic density of dendritic shafts (Den) of TH-labeled DA neurons, establishing asymmetrical synapses with axon terminal (at). No GluD1 immunoparticles were detected in GluD1−/− mice, as highlighted by open arrowhead pointing to postsynaptic density of a TH-labeled neuron. Scale bars: 0.5 μm. (c) Characterization of a DA neuron from the SNc typically exhibiting long duration action potentials and spontaneous pacemaker firing at low rate. This biocytin-filled neuron (Bio) was TH-immunopositive (scale bar: 20 μm). (d) RT-PCR analysis of a single DA neuron detected expression of TH, mGlu1, mGlu5, GluD1 and GluD2 upon agarose gel electrophoresis of PCR products (ΦX HaeIII molecular weight marker). Summary of single-cell RT-PCR data obtained in SNc DA neurons is given below the agarose gel picture. (e,f) The mGlu1/5 antagonist AIDA (150 μM) prevented the DHPG-induced current and the sEPSC triggered by local electrical stimulation in DA neurons. AIDA, 1-aminoindan-1,5-dicarboxylic acid; DA, dopamine; RT-PCR, real-time PCR; sEPCS, slow excitatory postsynaptic current; SN, substantia nigra; SNc, SN pars compacta; VTA, ventral tegmental area.
