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Mujmer, K.

Publications and source records attributed to Mujmer, K..

2 recordsLinked to original sources

Perineuronal nets in the bed nucleus of stria terminalis mediate stress-induced anxiety behaviour in adult male mice

Anxiety disorders affect an estimated 301.4 million people globally. However, they remain among the most challenging conditions to treat, with only around half of patients reporting a 50% or greater reduction in their symptoms. The discovery of novel and more effective treatments therefore requires a better understanding of the underlying mechanisms of anxiety at both the circuit and cellular levels. Stress induces aberrant changes in neuronal plasticity across brain regions within the anxiety circuitry including the bed nucleus of the stria terminalis (BNST). One mechanism through which synaptic plasticity is regulated is the organisation of perineuronal nets (PNNs), specialised extracellular matrix structures that are highly sensitive to stress. In rodent models, stress is associated with a reduction in PNN number and/or decreased Wisteria floribunda Agglutinin (WFA) labelling in limbic areas. However, the development of PNNs within the BNST and their role in the stress responsiveness remain largely unknown. In the current study we investigated the spatiotemporal development of PNNs within the BNST of male mice, where they first appear at P30 and continue to mature into adulthood, reaching their highest expression at P210 and specifically within the anteromedial BNST. We further showed that stress-induced anxiety is associated with a reduction in PNN number and significant changes to PNN fine structure including increased leakiness in the anteromedial BNST. Most importantly, enzymatic removal of PNNs by chondroitinase ABC in the mouse anteromedial BNST exacerbated behavioural responses to acute stress as demonstrated by increased anxiety-like behaviour. Collectively, these results highlight an indispensable role for PNNs within the anteromedial BNST in mediating a healthy emotional response to psychosocial stress.

neuroscience↗

Antidepressant fluoxetine engages astrocytic cAMP via purinergic signalling

The use of selective serotonin reuptake inhibitors (SSRIs), the first-line treatment for depression, has increased by about 50% over the past decade, placing them amongst the top 10 most frequently prescribed drug classes globally. Overall, SSRIs are effective in reducing frequency, severity, and duration of depressive episodes for a majority of patients, yet the mechanisms underlying their therapeutic effects are not fully understood. While SSRIs elevate synaptic serotonin, this action alone cannot account for their therapeutic effects. Additionally, SSRIs engage astrocytes, enhancing cyclic adenosine monophosphate (cAMP) signalling which is reported to be downregulated in depression. However, the signalling mechanisms underlying SSRI-induced upregulation of the astrocytic cAMP pathway remain unclear. Here, we identify a cascade of events by which the SSRI fluoxetine elevates intracellular cAMP levels in astrocytes, a process that depends on astrocyte-microglia crosstalk and purinergic signalling. Using FRET-based sensors in primary rat astrocytes, we show that fluoxetine elevates intracellular cAMP by 28% without altering calcium dynamics. cAMP increase was blocked by both serotonin (5-HT) 2B and adenosine 2B (A2B) receptor antagonists. Using the GRAB-ATP1.0 sensor and luminescence assays, we revealed that fluoxetine enhances astrocytic ATP release by 10% in a 5-HT2B receptor-dependent manner. Consistent with microglia-driven conversion of extracellular ATP to adenosine, which engages astrocytic A2B receptors, depletion of microglia in astrocyte cultures diminished fluoxetine-induced cAMP elevations and increased extracellular ATP. Together, these findings reveal that fluoxetine requires glial crosstalk and coordinated purinergic signalling to enhance astrocytic cAMP, a process shown to contribute to the therapeutic effect of SSRIs.

neuroscience↗