Cannabidiol preserves astrocyte viability and attenuates injury-induced glial stress responses across zebra finch song control nuclei
- 1Department of Pharmacology and Toxicology, Brody School of Medicine at East Carolina University , , ,
- 2Department of Anatomy and Cell Biology, Brody School of Medicine and East Carolina Diabetes and Obesity Institute at East Carolina University , , ,
Abstract
Chronic neuroinflammation following traumatic brain injury (TBI) increases the risk of affective disorders and early-onset dementias. Existing anti-inflammatory therapies are limited by systemic side effects with chronic use and by poor brain penetration of newer biologics. Cannabidiol (CBD), a non-euphorigenic phytocannabinoid with a favorable safety profile and multi-target neuroprotective actions, is a promising alternative. Using a songbird microlesion model of learned vocal recovery after targeted damage to the premotor nucleus HVC, we previously showed that systemic CBD (10 mg/kg/day) reduces vocal disruption, inflammatory cytokines, oxidative stress, and synaptic loss. Here we tested the hypothesis that these benefits involve astrocytes. CBD (10 mg/kg/day IM for 7 days) preserved astrocyte viability, attenuated injury-induced lysosomal stress, suppressed reactivity markers (C3, S100A10, aromatase), and upregulated key metabolic and antioxidant transcripts (glutamine synthetase and GCLM) across the interconnected song-control nuclei HVC, RA, and Area X. These changes were accompanied by reduced neuronal apoptosis in lesioned HVC. The results identify astrocyte-associated responses as a candidate cellular substrate of CBD’s circuit-wide protective effects and support its translational potential to mitigate secondary injury and communication deficits after TBI.
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BibTeX
@article{marshall2026cannabidiol,
title = {{Cannabidiol preserves astrocyte viability and attenuates injury-induced glial stress responses across zebra finch song control nuclei}},
author = {Dylan A. Marshall and Karen A. Litwa and Ken Soderstrom},
journal = {Frontiers in pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1972787},
url = {https://europepmc.org/article/PMC/PMC13690509},
note = {CC BY},
}
RIS
TY - JOUR
TI - Cannabidiol preserves astrocyte viability and attenuates injury-induced glial stress responses across zebra finch song control nuclei
AU - Dylan A. Marshall
AU - Karen A. Litwa
AU - Ken Soderstrom
PY - 2026
DA - 2026/10/09
JO - Frontiers in pharmacology
DO - 10.3389/fphar.2026.1972787
UR - https://europepmc.org/article/PMC/PMC13690509
AB - Chronic neuroinflammation following traumatic brain injury (TBI) increases the risk of affective disorders and early-onset dementias. Existing anti-inflammatory therapies are limited by systemic side effects with chronic use and by poor brain penetration of newer biologics. Cannabidiol (CBD), a non-euphorigenic phytocannabinoid with a favorable safety profile and multi-target neuroprotective actions, is a promising alternative. Using a songbird microlesion model of learned vocal recovery after targeted damage to the premotor nucleus HVC, we previously showed that systemic CBD (10 mg/kg/day) reduces vocal disruption, inflammatory cytokines, oxidative stress, and synaptic loss. Here we tested the hypothesis that these benefits involve astrocytes. CBD (10 mg/kg/day IM for 7 days) preserved astrocyte viability, attenuated injury-induced lysosomal stress, suppressed reactivity markers (C3, S100A10, aromatase), and upregulated key metabolic and antioxidant transcripts (glutamine synthetase and GCLM) across the interconnected song-control nuclei HVC, RA, and Area X. These changes were accompanied by reduced neuronal apoptosis in lesioned HVC. The results identify astrocyte-associated responses as a candidate cellular substrate of CBD’s circuit-wide protective effects and support its translational potential to mitigate secondary injury and communication deficits after TBI.
SN - 1663-9812
ER -