Stress changes the brain at many levels, from molecular signalling to behaviour, but neurons are only part of that response. Astrocytes and microglia—two major classes of glial cells—help regulate the chemical, metabolic and immune environment in which neural circuits operate. Their responses may therefore influence how the brain adapts to acute challenges or becomes vulnerable under prolonged stress. This broader view of stress biology was the focus of an open seminar held at Łukasiewicz – PORT on 11 June 2026 by Dr. Valentina Mosienko of the University of Bristol.
For decades, models of depression and anxiety were built largely around neuronal signalling and neurotransmitters. Mosienko’s research asks what changes when non-neuronal cells are treated as active participants in emotional regulation. Astrocytes support neuronal metabolism, shape the extracellular environment and interact closely with synapses, while microglia are the resident immune cells of the central nervous system and respond dynamically to changes in tissue state. Acute and chronic stress can affect glial structure, metabolism and plasticity, making these cells relevant to both adaptation and maladaptive stress responses.
The scientific framework of the seminar linked in vivo and in vitro research on astrocytes and microglia across different stages of life. These two levels of experimentation answer different questions. Studies in living organisms preserve the interactions among brain circuits, hormones, immune signals and behaviour, whereas cell-based systems make it possible to examine defined molecular pathways under controlled conditions. Bringing the two together can help distinguish a cellular response associated with stress from a mechanism that actually contributes to altered brain function.
A life-course perspective also matters. The consequences of stress depend not only on its intensity or duration but on when it occurs and on the biological state of the nervous system at the time. Mosienko’s current research programme includes work on early-life stress and microglial morphology as well as projects focused on astrocyte mechanisms in depression. This line of investigation shifts attention from a simple question—whether stress activates a particular cell type—to a more precise one: how glial cells change their function, metabolism and interactions with other cells under different conditions.
Antidepressant action provided a second major theme. Selective serotonin reuptake inhibitors such as fluoxetine increase serotonin availability, but their therapeutic effects cannot be explained by serotonin alone. Work from Mosienko and colleagues points to additional glial mechanisms. A 2026 preprint from the Bristol group reported that fluoxetine increased cAMP signalling in primary rat astrocytes through a pathway involving purinergic signalling and communication between astrocytes and microglia. An abstract prepared by Mosienko for UK Glia 2026 also described astrocytic metabolism and lactate release as possible components of antidepressant action. These findings remain part of an evolving research picture, but they illustrate why the pharmacology of depression may need to be considered at the level of multicellular brain networks rather than neurons alone.
For translational neuroscience, this wider cellular perspective suggests several possibilities. If stress vulnerability and treatment response partly depend on astrocyte or microglial state, these cells could provide new experimental readouts and, potentially, new therapeutic targets. A more complete cellular model may also help researchers investigate why a drug that changes neurotransmitter signalling rapidly can produce its clinically relevant effects on a different timescale. The aim is not to replace neuronal models, but to place neurons within the cellular ecosystem that sustains and modifies their function.
The seminar brought together stress biology, glial physiology and psychopharmacology, connecting basic cell biology with the challenge of understanding stress-related disorders and improving their treatment. As a forum for scientific exchange, the open seminar format also creates a meeting point for researchers working at different levels—from molecular mechanisms and experimental models to behaviour and therapeutic development.