Stress causes divergent patterns of structural and physiological plasticity in the hippocampus versus amygdala. However, a majority of earlier studies focused primarily on neurons. Despite growing evidence for the importance of glia in health and disease, relatively little is known about how stress affects astrocytes. Further, previous work focused on hippocampal astrocytes. Hence, we examined the impact of chronic immobilization stress (2 h/d, 10 d), on the number and structure of astrocytes in the rat hippocampus and amygdala. We observed a reduction in the number of glial fibrillary acidic protein (GFAP)-positive astrocytes in the basal amygdala (BA), 1 d after the end of 10 d of chronic stress. Detailed morphometric analysis of individual dye-filled astrocytes also revealed a decrease in the neuropil volume occupied by these astrocytes in the BA, alongside a reduction in the volume fraction of fine astrocytic protrusions rather than larger dendrite-like processes. By contrast, the same chronic stress had no effect on the number or morphology of astrocytes in hippocampal area CA3. We also confirmed previous reports that chronic stress triggers dendritic hypertrophy in dye-filled BA principal neurons that were located adjacent to astrocytes that had undergone atrophy. Thus, building on earlier evidence for contrasting patterns of stress-induced plasticity in neurons across brain areas, our findings offer new evidence that the same stress can also elicit divergent morphological effects in astrocytes in the hippocampus versus the amygdala.
Astrocytes are glial cells that interact with neuronal synapses via their
distal processes, where they remove glutamate and potassium (K
+
) from
the extracellular space following neuronal activity. Astrocyte clearance of both
glutamate and K
+
is voltage-dependent, but astrocyte membrane
potential (V
m
) has been thought to be largely invariant. As a result,
these voltage-dependencies have not been considered relevant to astrocyte
function. Using genetically encoded voltage indicators to enable the measurement
of V
m
at peripheral astrocyte processes (PAPs) in mice, we report
large, rapid, focal, and pathway-specific depolarizations in PAPs during
neuronal activity. These activity-dependent astrocyte depolarizations are driven
by action potential-mediated presynaptic K
+
efflux and electrogenic
glutamate transporters. We find that PAP depolarization inhibits astrocyte
glutamate clearance during neuronal activity, enhancing neuronal activation by
glutamate. This represents a novel class of sub-cellular astrocyte membrane
dynamics and a new form of astrocyte-neuron interaction.
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