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Microglia and their LAG3 checkpoint underlie the antidepressant and neurogenesis-enhancing effects of electroconvulsive stimulation | Psychology Department

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naom Markovitch

Congratulations to Dr. Noam Markovitch

24 May, 2023

For receiving the best doctoral award in developmental psychology from the APA organization!
Noam's doctorate deals with the understanding of children's differential sensitivity to the effects of the environment on their development. The work's contribution to developmental psychology is very significant, both in theoretical thought and methodological approaches.
Well done Noam!
Noam PhD supervisor, Prof. Ariel Knafo-Noam, has also won the award in the past

 

From acute stress to persistent post-concussion symptoms: The role of parental accommodation and child’s coping strategies

19 April, 2023

An article by PhD candidate Irit Aviv, supervised by Dr. Tammy Pilowsky Peleg and Prof. Hillel Aviezer was selected as the winner of the Eighth Annual TCN/AACN student Project Competition, from among 15 eligible manuscripts

Acute stress following mild Traumatic Brain Injury (mTBI) is highly prevalent and associated with Persistent Post-Concussion symptoms (PPCS). However, the mechanism mediating this relationship is understudied.

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Microglia and their LAG3 checkpoint underlie the antidepressant and neurogenesis-enhancing effects of electroconvulsive stimulation

28 October, 2021
Microglia and their LAG3 checkpoint underlie the antidepressant and neurogenesis-enhancing effects of electroconvulsive stimulation

Despite evidence implicating microglia in the etiology and pathophysiology of major depression, there is paucity of information regarding the contribution of microglia-dependent molecular pathways to antidepressant procedures. In a new study Prof. Raz Yirmia, Dr. Neta Rimmerman and other members of the Laboratory for PsychoNeuroImmunology Research, investigated the role of microglia in a mouse model of depression (chronic unpredictable stress—CUS) and its reversal by electroconvulsive stimulation (ECS), by examining the effects of microglia depletion with the colony stimulating factor-1 antagonist PLX5622. Microglia depletion did not change basal behavioral measures or the responsiveness to CUS, but it completely abrogated the therapeutic effects of ECS on depressive-like behavior and neurogenesis impairment. Treatment with the microglia inhibitor minocycline concurrently with ECS also diminished the antidepressant and pro-neurogenesis effects of ECS. Hippocampal RNA-Seq analysis revealed that ECS significantly increased the expression of genes related to neurogenesis and dopamine signaling, while reducing the expression of several immune checkpoint genes, particularly lymphocyte-activating gene-3 (Lag3), which was the only microglial transcript significantly altered by ECS. None of these molecular changes occurred in microglia-depleted mice. Immunohistochemical analyses showed that ECS reversed the CUS-induced changes in microglial morphology and elevation in microglial LAG3 receptor expression. Consistently, either acute or chronic systemic administration of a LAG3 monoclonal antibody, which readily penetrated into the brain parenchyma and was found to serve as a direct checkpoint blocker in BV2 microglia cultures, rapidly rescued the CUS-induced microglial alterations, depressive-like symptoms, and neurogenesis impairment. These findings suggest that brain microglial LAG3 represents a promising target for novel antidepressant therapeutics.

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