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Ziko, I.

Publications and source records attributed to Ziko, I..

2 recordsLinked to original sources

Serotonergic circuit architecture underlies sex dimorphism in anxiogenic states

The serotonergic system underpins anxiety-like behavior vital for the adaptive response to a new environment. However, our understanding of the neural circuitry underlying the diversity of anxiety-like behaviors across individuals is limited. Whilst previous studies have characterized diverse features related to the neurochemical substrate of serotonergic neurotransmission and behavioral presentation between males and females, no investigations have fully addressed the sexual dimorphism in the structural and functional connectivity of serotonergic circuits. Here, using functional FosTRAP connectivity analysis, we found sex-dependent functional differences in the serotonergic neurons of the dorsal raphe nucleus (DRN), such as enriched connectivity to the amygdala in females, compared to male mice. We also discovered previously unidentified morpho-functional sex-specific differences in DRN serotonergic circuitry that reflects the disparity in behavior presentation. To understand the molecular basis of serotonergic circuit architecture differences between sexes, we leveraged on single-cell RNA sequencing dataset from DRN serotonergic cells taking sex as a biological variable and spotted some gene candidates involved in neural circuit wiring. Altering the expression of the receptor tyrosine kinase Erbb4 in serotonergic circuits, altered the axonal connectivity to downstream targets and shifted sex-specific behavior which. Overall, this study provides an essential foundation to delineate the molecular basis and connectivity pattern mechanisms underlying the serotonergic system-dependent sex-specific behaviors. Since alterations in serotonin function play a vital role in adaptive behavior, as well as various pathologies including chronic anxiety and depression, this study may advance our understanding of sex-biases in presentation and treatment response of neuropsychiatric disorders.

neuroscience↗

Alpha Synuclein Induced Immune Response Triggers Parkinson's Disease Like Symptoms

Increasing evidence suggests that Parkinsons disease is an autoimmune disorder, with findings of elevated peripheral blood mononuclear cell in patients, and antigenic properties of -synuclein driving both the innate and adaptive immunity. Yet, how the interaction of -synuclein and a specific immune response participates to Parkinsons disease ontogenesis has remained unanswered. Here, we reveal that autoimmune response to an -synuclein antigen underlies Parkinsons disease. We demonstrate that autoimmunity mediated by CD4+T cell activation with -synuclein -syn61-75 antigen is required to lead to immune cell infiltration and localized inflammation in the substantia nigra, triggering dopaminergic cell neurodegeneration and deficits in locomotion and gait kinematics. This study offers the first immune-induced mouse model that recapitulates all features of Parkinsons disease to study the mechanisms triggering disease onset. It provides the basis for temporally tracking symptom development, exploring preventive strategies and prodromal therapeutic interventions in Parkinsons Disease. In briefPeripheral -synuclein immunization causes Parkinsons disease-like symptoms in mice. Highlights- Both CD4+ T cells and -synuclein are essential for Parkinsons disease ontogenesis. - Peripheral injection of -syn61-75 induces significant CD4+ T cell infiltration in the mouse brain. - -syn61-75 immunization is associated with inflammation, -synuclein aggregation and dopaminergic cell loss in the substantia nigra pars compacta. - Levodopa-sensitive motor symptoms are detected 8 weeks following -syn61-75 immunization in mice. - This study offers a novel autoimmune -synuclein induced mouse model of Parkinsons disease.

neuroscience↗