6533b7d3fe1ef96bd1261539

RESEARCH PRODUCT

Expression of PSA-NCAM and synaptic proteins in the amygdala of psychiatric disorder patients.

Carlos CrespoEmilio VareaJavier Gilabert-juanJosé Miguel Blasco-ibáñezUlisses MartíJuan NacherEsther Castillo-gómezRamon Guirado

subject

AdultMalemedicine.medical_specialtyGlutamate decarboxylaseSynaptophysinNeural Cell Adhesion Molecule L1NeuropathologyAmygdalamental disordersNeuropilmedicineHumansBipolar disorderPsychiatryBiological PsychiatryAgedNeuronsbiologyGlutamate DecarboxylaseMood DisordersMiddle Agedmedicine.diseaseAmygdalaPsychiatry and Mental healthmedicine.anatomical_structurenervous systemGene Expression RegulationSchizophreniaPhosphopyruvate HydratasePostmortem ChangesVesicular Glutamate Transport Protein 1Synaptophysinbiology.proteinAcetylcholinesteraseSchizophreniaSialic AcidsNeural cell adhesion moleculeFemalePsychologyCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroscience

description

Neuroimaging has revealed structural abnormalities in the amygdala of different psychiatric disorders. The polysialylated neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity, which expression is altered in schizophrenia, major depression and in animal models of these disorders, may participate in these changes. However, PSA-NCAM has not been studied in the human amygdala. To know whether its expression and that of presynaptic markers, was affected in psychiatric disorders, we have analyzed post-mortem sections from the Stanley Neuropathology Consortium, which includes controls, schizophrenia, bipolar and major depression patients. PSA-NCAM was expressed in neuronal somata and neuropil puncta, many of which corresponded to interneurons. Depressed patients showed decreases in PSA-NCAM expression in the basolateral and basomedial amygdala; synaptophysin and GAD67 were also decreased, while VGLUT-1 was increased, in different nuclei. Increases in PSA-NCAM expression were found in the lateral nucleus of bipolar patients; synaptophysin and GAD67 were reduced, and VGLUT-1 increased, in their basolateral and lateral nuclei. The expression of synaptophysin and GAD67 was downregulated in the basolateral nucleus of schizophrenics. These results indicate that inhibitory and excitatory amygdaloid circuits are affected in these disorders and that abnormal PSA-NCAM expression in depressive and bipolar patients may underlie these alterations.

10.1016/j.jpsychires.2011.10.011https://pubmed.ncbi.nlm.nih.gov/22099865