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Astrocytic oxytocin receptors mediate behavioral stress response through Gαi signaling in the central amygdala

ABSTRACT: Anticipated reactions to stressful situations are vital for the survival and well-being of organisms, and abnormal reactions are involved in stress-related disorders. The neuropeptide oxytocin is a key modulator ensuring well-adapted stress responses. Oxytocin acts on both neurons and astrocytes, but the molecular and cellular mechanisms mediating stress response remain poorly understood. Here, we focus on the amygdala, a crucial hub that integrates and processes sensory information through oxytocin-dependent mechanisms. Using an acute stress paradigm in mice, genetic and pharmacological manipulations combined with molecular, morphological, electrophysiological and behavioral approaches, we reveal that oxytocinergic modulation of the freezing response to stress is mediated by transient, Gαi-dependent retraction of astrocytic processes, followed by enhanced neuronal sensitivity to extracellular potassium in the amygdala. Our findings elucidate a pivotal role for oxytocin-dependent signaling in astrocytes that is required for proper anticipated behavioral response to stressful situations.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Amygdala

SUBMITTER: Syed Azmal Ali

LAB HEAD: Prof. Dr. Jeroen Krijgsveld

PROVIDER: PXD053856 | Pride | 2025-12-09

REPOSITORIES: Pride

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			Action	DRS
	20231213_FS1_Azmal_DIA_Amag-Fear_Rep1.raw	Raw
	20231213_FS1_Azmal_DIA_Amag-Fear_Rep4.raw	Raw
	20231213_FS1_Azmal_DIA_Amag_Control_Rep1.raw	Raw
	20231213_FS1_Azmal_DIA_Amag_Control_Rep2.raw	Raw
	20231213_FS1_Azmal_DIA_Amag_Control_Rep3.raw	Raw

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Project description:Prolonged stress has adverse consequences for neurons in the hippocampus (HIPP). The amygdala (AMY) is a brain region that is similar to HIPP across many measures, suggesting that chronic stress might modulate AMY and HIPP function in similar ways. However, studies addressing this issue have produced surprising results. For example, a regimen of chronic stress shown to produce atrophy in HIPP neurons caused dendritic branching in AMY neurons. These and other data have revealed that excessive stress induces fundamentally opposing processes in the AMY and HIPP, such that AMY function is facilitated by levels of stress that produce deleterious effects in HIPP. The mechanisms that contribute to the opposing responses of these brain regions to chronic stress are unknown. Such knowledge may suggest novel directions for pharmacological interventions to protect the HIPP from stress-mediated damage.,We will determine gene expression patterns in the hippocampus and amygdala under basal and stressful conditions, with a particular interest in those genes that are differentially regulated across the two regions. ,We hypothesize that genes that are oppositely regulated in the amygdala and hippocampus after stress mediate the opposing functional consequences of chronic stress in these two brain regions. Moreover, genes which are differentially expressed in these regions under basal conditions may underlie the distinct responses of these regions to stress.,Rats will receive either 30sec of handling (Control group; n=15) or 3hr of immobilization stress (Stress group; n=15) each day for 14 consecutive days. This stress paradigm has previously been shown to produce opposing effects on dendritic morphology and region-dependent behaviors for the hippocampus versus amygdala. Twenty-four hours after the last stress or handling session, the rats will be overanaesthetized, and the brain will be removed and placed in ice-cold buffer. Tissue will be rapidly dissected from the basolateral complex of the amygdala and the CA3 region of the hippocampus of both hemispheres, flash frozen in liquid nitrogen, and stored at -80C until further processing. The tissue from each brain region will be pooled across groups, yielding four samples (Control-Hippocampus, Control-Amygdala, Stress-Hippocampus, and Stress-Amygdala). Total RNA will be extracted using standard methods, and sent to the centers. Each sample will be run in triplicate, utilizing a total of 12 Affymetrix Rat Genome U34A gene chips. A triplicate array assay of pooled samples has previously been shown to both substantially increase the sensitivity of detecting genes of interest and reduce the variability associated with individual microarrays. In addition, the large number of rats used in each group will reduce the variability in gene expression associated with individual responses to chronic stress, as well as variability due to slight anatomical differences in the tissue extracted from each rat.

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Astrocytic oxytocin receptors mediate behavioral stress response through Gαi signaling in the central amygdala

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