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10.1016/j.celrep.2017.05.002 http://scihub22266oqcxt.onion/10.1016/j.celrep.2017.05.002 C5457478!5457478 !28538174     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28538174 &cmd=llinks): Failed to open stream: HTTP request failed! 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Schizophrenia-Related Microdeletion Impairs Emotional Memory through MicroRNA-Dependent Disruption of Thalamic Inputs to the Amygdala |pdf=|usr=}}{{28538174 }} gab.com Text Schizophrenia-Related Microdeletion Impairs Emotional Memory through MicroRNA-Dependent Disruption of Thalamic Inputs to the Amygdala JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28538174 #FOAvip Individuals with 22q11.2 deletion syndrome (22q11DS) are at high risk of developing psychiatric diseases such as schizophrenia. Individuals with 22q11DS and schizophrenia are impaired in emotional memory, anticipating, recalling, and assigning a correct context to emotions. The neuronal circuits responsible for these emotional memory deficits are unknown. Here, we show that 22q11DS mouse models have disrupted synaptic transmission at thalamic inputs to the lateral amygdala (thalamo-LA projections). This synaptic deficit is caused by haploinsufficiency of the 22q11DS gene Dgcr8, which is involved in microRNA processing, and is mediated by the increased dopamine receptor Drd2 levels in the thalamus and by reduced probability of glutamate release from thalamic inputs. This deficit in thalamo-LA synaptic transmission is sufficient to cause fear memory deficits. Our results suggest that dysregulation of the Dgcr8-Drd2 mechanism at thalamic inputs to the amygdala underlies emotional memory deficits in 22q11DS. Twit Text FOAVip Schizophrenia-Related Microdeletion Impairs Emotional Memory through MicroRNA-Dependent Disruption of Thalamic Inputs to the Amygdala ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28538174 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28538174 #FOAvip English Wikipedia <ref>{{Cite pmid|28538174 }}</ref> Schizophrenia-Related Microdeletion Impairs Emotional Memory through MicroRNA-Dependent Disruption of Thalamic Inputs to the Amygdala #MMPMID28538174 Eom TY ; Bayazitov IT ; Anderson K ; Yu J ; Zakharenko SS Cell Rep 2017[May]; 19 (8 ): 1532-1544 PMID28538174 show ga Individuals with 22q11.2 deletion syndrome (22q11DS) are at high risk of developing psychiatric diseases such as schizophrenia. Individuals with 22q11DS and schizophrenia are impaired in emotional memory, anticipating, recalling, and assigning a correct context to emotions. The neuronal circuits responsible for these emotional memory deficits are unknown. Here, we show that 22q11DS mouse models have disrupted synaptic transmission at thalamic inputs to the lateral amygdala (thalamo-LA projections). This synaptic deficit is caused by haploinsufficiency of the 22q11DS gene Dgcr8, which is involved in microRNA processing, and is mediated by the increased dopamine receptor Drd2 levels in the thalamus and by reduced probability of glutamate release from thalamic inputs. This deficit in thalamo-LA synaptic transmission is sufficient to cause fear memory deficits. Our results suggest that dysregulation of the Dgcr8-Drd2 mechanism at thalamic inputs to the amygdala underlies emotional memory deficits in 22q11DS. |*Chromosome Deletion [MESH] |*Emotions [MESH] |*Memory [MESH] |Amygdala/*physiopathology [MESH] |Animals [MESH] |Behavior, Animal [MESH] |Chromosomes, Mammalian/genetics [MESH] |Fear [MESH] |Gene Knockdown Techniques [MESH] |Glutamates/metabolism [MESH] |Mice [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Neurons/metabolism [MESH] |RNA-Binding Proteins/metabolism [MESH] |Receptors, Dopamine D2/metabolism [MESH] |Schizophrenia/*genetics/*physiopathology [MESH] |Synapses/metabolism [MESH] |Synaptic Transmission [MESH]Schizophrenia-Related Microdeletion Impairs Emotional Memory through (epmc).pdf DeepDyve Pubget Overpricing