Anti-Metabotropic Glutamate Receptor (C-terminal) polyclonal antibody

Glutamate receptors are well-known actors in the central and peripheral nervous systems, and altered glutamate signaling is implicated in several neurological and psychiatric disorders. It is increasingly recognized that such receptors may also have a role in tumor growth. Here we provide direct evidence of aberrant glutamate signaling in the development of a locally aggressive bone tumor, chondromyxoid fibroma (CMF). We subjected a series of CMFs to whole-genome mate-pair sequencing and RNA sequencing and found that the glutamate receptor gene GRM1 recombines with several partner genes through promoter swapping and gene fusion events. The GRM1 coding region remains intact, and 18 of 20 CMFs (90%) showed a more than 100-fold and up to 1,400-fold increase in GRM1 expression levels compared to control tissues. Our findings unequivocally demonstrate that direct targeting of GRM1 is a necessary and highly specific driver event for CMF development.

Stressing events in the early period of life affect neuronal plasticity and cognitive functions in adulthood. A key role in the mechanisms of formation of memory and attention is played by the glutamatergic system. However, there has been virtually no systematic study on the effect of early postnatal stress on the expression of glutamatergic system genes in various regions of the brain in mice. In this study, we used two types of early postnatal stress: prolonged separation of pups from mothers (for 3 hours per day) and shortterm separation (15 minutes per day) during the first 2 weeks of life. We used an object recognition test to evaluate attention and memory to assess cognitive abilities in adults. We found that prolonged maternal separation reduced the ability to recognize a novel object and also disrupted motor and exploratory activities in adult animals, while short-term separation did not affect the studied parameters. We assessed the expression of the major genes of the glutamatergic system (AMPA receptor subunits Gria1, Gria2; NMDA subunits Grin1, Grin2a, and Grin2b; metabotropic receptor subunits Grm1, Grm2, and Grm3; glutamate transporters Vglut2, Eaat2, and Rab4a) in the frontal cortex, hippocampus, and hypothalamus. In the group with prolonged maternal separation, we found a decrease in the expression of Grin2b in the hypothalamus in comparison with the control, which led to a decrease in the mRNA ratio of this subunit to Grin2a mRNA, and possibly to a change in the ratio of these subunits in the NMDA receptor. In spite of the revealed cognitive impairments, we did not find significant changes in the expression of genes in the frontal cortex and hippocampus. Shortterm daily separation from mothers did not lead to changes in cognitive abilities and expression of genes of the glutamatergic system in mice. Thus, our results show that prolonged maternal separation may lead to a redistribution of the receptor subunits in the hypothalamus, which can modify the activity of the HPAA and determine the response to stress in these mice.