REVIEW: Glucocorticoids Orchestrate Adult Hippocampal Plasticity: Growth Points and Translational Aspects*

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Natalia V. Gulyaeva^1,2

¹Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 117485 Moscow, Russia

²Research and Clinical Center for Neuropsychiatry of Moscow Healthcare Department, 115419 Moscow, Russia

*The article is published as a part of the Special Issue “Biochemical Aspects of Different Levels of Neuroplasticity: Molecules, Genes, Synapses, Cells, Cognitive Processes” (Vol. 88, Nos. 3-4).

Received March 27, 2023; Revised April 10, 2023; Accepted April 10, 2023

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The review analyzes modern concepts about the control of various mechanisms of the hippocampal neuroplasticity in adult mammals and humans by glucocorticoids. Glucocorticoid hormones ensure the coordinated functioning of key components and mechanisms of hippocampal plasticity: neurogenesis, glutamatergic neurotransmission, microglia and astrocytes, systems of neurotrophic factors, neuroinflammation, proteases, metabolic hormones, neurosteroids. Regulatory mechanisms are diverse; along with the direct action of glucocorticoids through their receptors, there are conciliated glucocorticoid-dependent effects, as well as numerous interactions between various systems and components. Despite the fact that many connections in this complex regulatory scheme have not yet been established, the study of the factors and mechanisms considered in the work forms growth points in the field of glucocorticoid-regulated processes in the brain and primarily in the hippocampus. These studies are fundamentally important for the translation into the clinic and the potential treatment/prevention of common diseases of the emotional and cognitive spheres and respective comorbid conditions.

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KEY WORDS: neuroplasticity, hippocampus, glucocorticoids, hypothalamic-pituitary-adrenal axis, synaptic plasticity, stress, neurogenesis, neuroinflammation, glutamatergic transmission, proteases, BDNF, insulin resistance, depression, Alzheimer’s disease, aging

DOI: 10.1134/S0006297923050012

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