To direct stimulation circuit CSTC be assigned, in addition, as mentioned above HNT this behavior by various NMDA antagonists Campbell et al McGrath et al Rft. The working group dam To ftigt Mice pr Sented a DICT corticallimbic glutamatergic neurons ZD4054 Zibotentan CGN model Hyperaktivit t and tic symptoms of Zwangsst changes, The model has developed over ICCS tt Zwangsst Changes and tried to account for the R glutamate, dopamine and serotonin in the direct and indirect ways ICCS Nordstrom and Burton. Although the model was developed DICT, direct evidence of glutamatergic dysfunction in OCD by Rosenberg and colleagues in their series of studies by Rosenberg et al above, SRM was collected. Their results were in line with its previous expectations, and led them out, they were reversible with treatment, mediation glutamatergically thalamocorticalstriatal dysfunction in OCD Rosenberg et al.
Their first results obtained Glx ht in the caudate nucleus, together with the results of high glutamate CSF in patient with OCD Chakrabarty et al, seemed taken in accordance with the general model of glutamatergic CGN Hyperaktivit t in OCD in the circuits of the ICCS. But have mainly GDC-0449 Rosenberg and others found that concentrations were not consistently glx HIGEN f, But showed a regional specificity. Based on these findings, as Rosenberg and al.hypothesized OCDwas tonicphasic with a St Tion of glutamate in the CSTC circuits confinement Lich reduce the toxic levels of glutamate in the ACC connected, as evidenced by decreased Glx, which in turn leads to a phasic Hyperaktivit t covered in the striatum and the orbitofrontal cortex than in the two regions increased ht Glx Rosenberg et al.
Although there is growing evidence for glutamatergic dysfunction in OCD, until recently there were no studies that help explained Utern the nature of this dysfunction nnte k. As of Pittenger et al. Emphasized k nnte There are many m Possible causes for the observed VER Nderten concentrations of glutamate in MRS studies Lich Andor Andor postsynaptic mechanisms Including pr Synaptic neurons VER Be changed glial cell function. However, there is now evidence from two studies of candidate genes and animal models that Funktionsst Changes of postsynaptic glutamate signaling mechanism is most likely candidate at the molecular level to Changes in the order explained leave Ren as the transmission of glutamate WBK a current chart view and discuss this hypothesis and see Feng Ting.
First, the gene is replicated in most OCD found an association with social balance sheet, the glutamate transporter EAATEAAC primarily on the postsynaptic membrane and perisynaptic coded words. Another candidate gene with some evidence for the association is GRINB code NMDAB subunit expressed in fa predominates in the same cell site and interacts with SLCA Scimemi et al. Second, in both models and knockout animals that DLGAP SLTRK Ver Changes of genes involved in the postsynaptic scaffolding and signaling by glutamate can produce amazing Similar compulsive behaviors. In addition, two mouse models of direct detection of the expression of glutamate receptors and VER MODIFIED Known electrophysiological Ver Changes, the glutamate signaling w Provided while. Closing Lich are emerging findings in OCD is consistent with h Ufenden notes in the autistic spectrum Tues