Psychiatry related information on Grm6

• We report here that mGluR6-deficient mice have unaltered locomotor activity in a daily light-dark cycle and exhibit light-stimulated induction of Fos immunoreactivity in the suprachiasmatic nucleus [1].

High impact information on Grm6

• Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGluR6) in retinal ON bipolar cells, we generated knockout mice lacking mGluR6 expression [2].
• The results demonstrate that mGluR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information [2].
• The combination of several different morphological analyses indicates that ON bipolar cells, as well as several distinct amacrine cells, in mGluR6 knock-out mice are normally distributed and correctly extend their terminals to defined retinal laminae [3].
• The mGluR6 5' upstream transgene sequence directs a cell-specific and developmentally regulated expression in retinal rod and ON-type cone bipolar cells [4].
• We generated transgenic mice, using 9.5 kilobase pairs of the 5' upstream sequence from the mouse metabotropic glutamate receptor subtype 6 (mGluR6) gene fused to the beta-galactosidase (lacZ) reporter gene, and investigated the promoter function of the cell-specific and developmentally regulated expression of mGluR6 [4].

Biological context of Grm6

• Impairment of pupillary responses and optokinetic nystagmus in the mGluR6-deficient mouse [1].
• Recovery of rod-mediated a-wave during light-adaptation in mGluR6-deficient mice [5].
• CREB-induced transcriptional activation depends on mGluR6 in rod bipolar cells [6].
• A comparison of the gene structure of mGluR4 with the highly homologous mGluR6 receptor subtype reveals that both of the genes contain ten exons with similar exon/intron boundaries [7].

Anatomical context of Grm6

• Recording light evoked field potentials from the superior colliculus of mGluR6-deficient mice at scotopic and mesopic backgrounds, we found a characteristic ON response that differs from the ON response of wild-type mice [8].
• Quantitative analysis of the hybridization signal obtained from the autoradiographic films revealed decreased expression levels of the mGluR6 mRNA at early stages of photoreceptor degeneration (P17) [9].
• Paradoxically, we find ON responses in retinal ganglion cells of mGluR6-null mice, but they occur at long latency [10].
• In mGluR6-null mice, long-latency ON responses are observed in the visual cortex, indicating that they can be conducted reliably to higher visual areas [10].

Other interactions of Grm6

• This receptor is most related to mGluR4, mGluR7, and mGluR6 (74%, 74%, and 70% identical amino acid residues, respectively) [11].

Analytical, diagnostic and therapeutic context of Grm6

• Ablation of mGluR6 in the ON-bipolar cells by gene targeting results in a loss of ON responses but unchanged OFF responses in visual transmission [1].
• The expression of the gene encoding mGluR6 was studied by in situ hybridization in the retina, using an [(35)S]dATP-labeled oligonucleotide probe [9].

References