As indicated by the adenosine theory of schizophrenia, the traditionally related hyperdopaminergic state might be auxiliary to a deficiency of capacity of the adenosinergic framework. Such a hypo adenosinergic state may either be because of a decrease of the extracellular degrees of adenosine or changes in the thickness of adenosine A2A receptors (A2ARs) or their level of practical heteromerization with dopamine D2 receptors (D2R). In the current investigation, we give preclinical and clinical proof to this last instrument. Two creature models for the investigation of schizophrenia endophenotypes, specifically the phencyclidine (PCP) mouse model and the A2AR knockout mice, were utilized to set up connections among’s social and atomic examinations. Likewise, another AlphaLISA-based strategy was executed to distinguish local A2AR-D2R heteromers in the mouse and human mind. Schizophrenia is a complex mental issue with a heterogeneous hereditary and neurobiological foundation, which impacts early mental health [1]. The most acknowledged unthinking speculation of schizophrenia depends on a concurrent liberation of glutamatergic and dopaminergic frameworks. A critical and articulated decrease of A2AR-D2R heteromers was next shown in after death caudate core from schizophrenic subjects, despite the fact that both D2R and A2AR were upregulated. At long last, in PCP-treated creatures, sub-constant organization of haloperidol or clozapine neutralized the decrease of striatal A2AR-D2R heteromers. The level of A2AR-D2R heteromer development in schizophrenia may comprise a sign of the sickness, which undoubtedly ought to be additionally concentrated to set up potential relationships with constant antipsychotic therapies.
Ref: https://www.nature.com/articles/s41386-020-00872-9
