OVLT electrical stimulation increased astrocytic calcium transients in the supraoptic nucleus compared to baseline (peak ΔF/F0 3.00 vs 1.88, p=0.038) via a glutamate-dependent mechanism.
OVLT stimulation robustly increases astrocytic calcium activity in the SON via a glutamate-dependent mechanism, demonstrating a functional role for astrocytes in central osmoregulatory circuitry.
Absolute Event Rate: 3% vs 1.88%
p-value: p=0.038
Extracellular osmolality is tightly regulated to preserve cellular integrity and physiological function. In the central nervous system, osmoreception is mediated by circumventricular organs, particularly the organum vasculosum of the lamina terminalis (OVLT), which senses fluctuations in osmotic pressure and conveys this information to hypothalamic nuclei such as the supraoptic nucleus (SON) and paraventricular nucleus (PVN) thereby regulating the vasopressin (VP) and oxytocin (OT) release. While SON magnocellular neurons have been extensively studied in the context of osmoregulation, the contribution of glial cells, including astrocytes, to OVLT–SON communication remains poorly understood. Given that astrocytes contribute to signaling at the tripartite synapse, we hypothesized that astrocytes might be functionally activated when the OVLT-SON pathways is engaged. To test this, we electrically stimulated the OVLT, mimicking the osmostimulation, while monitoring astrocytic calcium activity in the SON using GCaMP-based imaging. Adult male C57BL/6 mice (8 weeks old) received stereotaxic injections of a GCaMP viral vector (AAV2/5-gfsABC1D-cyto-GCaMP6f) into the SON targeting astrocytes. After 21-28 days, astrocytic activity was recorded before (2 min), during OVLT electrical stimulation (5 min, 5 Hz), and after stimulation (2 min). OVLT stimulation significantly increased astrocytic calcium transients during stimulation, as evidenced by increased peak ΔF/F 0 (baseline: 1.88 ± 0.53 vs stimulation: 3.00 ± 0.74, n = 8, p = 0.038), half-width (baseline: 1086 ± 136 ms vs stimulation: 1421 ± 157 ms, n = 8, p = 0.029), and frequency (baseline: 0.034 ± 0.005 Hz vs stimulation: 0.050 ± 0.007 Hz, n = 8, p = 0.0046). Because many of the OVLT inputs to the SON are glutamatergic, we next examined whether this response was glutamate-dependent. In the presence of ionotropic and metabotropic glutamate receptor antagonists, OVLT stimulation failed to increase peak ΔF/F 0 (baseline: 0.54 ± 0.19 vs stimulation: 1.00 ± 0.24, n = 5, p = 0.4199), half-width (baseline: 1315 ± 406 vs stimulation: 3335 ± 537, n=5, p = 0.1492), or frequency (baseline: 0.016 ± 0.006 vs stimulation: 0.017 ± 0.002, n = 5, p = 0.9797). These findings demonstrate that OVLT stimulation robustly increases astrocytic activity in the SON via a glutamate-dependent mechanism, supporting a role for astrocytes in OVLT–SON osmoregulatory circuitry. Financial Support: FAPESP #2024/22511-1 to KMS, CIHR #PJT-180511 to CB. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Santos et al. (Fri,) reported a other. OVLT electrical stimulation vs. Baseline was evaluated on Astrocytic calcium transients (peak ΔF/F0) (p=0.038). OVLT electrical stimulation increased astrocytic calcium transients in the supraoptic nucleus compared to baseline (peak ΔF/F0 3.00 vs 1.88, p=0.038) via a glutamate-dependent mechanism.