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DYSREGULATION OF THE AGRP–PVH CIRCUIT DISRUPTS SYMPATHETIC CONTROL OF BONE MARROW IN EXPERIMENTAL MULTIPLE SCLEROSIS
Eleonora Cornacchiaand 10 co-authors
University of Genoa, Department of Neurosciences, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI)
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-445
Presentation
Date TBA
Board: PS02-07PM-445
Event Information
Poster Board
PS02-07PM-445
Poster
View posterAbstract
The hypothalamus is a central hub for autonomic regulation and integrates signals that shape sympathetic nervous system (SNS) activity. Bone marrow (BM) hematopoiesis is tightly controlled by SNS output and is disrupted in Multiple Sclerosis (MS). Here, we dissect the hypothalamic circuits that regulate SNS transmission to the BM in experimental MS, focusing on AgRP neurons, a population known to influence autonomic and metabolic homeostasis. Using AgRP‑TRPV1 and AgRP‑ires‑CRE mouse lines, we combined chemogenetic manipulations, viral tracing (AAV‑EGFP), in vivo electrophysiology, c‑FOS immunostaining and single-cell RNAscope in the preclinical model of MS, the experimental autoimmune encephalomyelitis (EAE). We show that AgRP neurons become chronically hyperactive in EAE through vagal inputs. This state induces a loss of GABAergic AgRP projections to the paraventricular hypothalamus (PVH), a major sympathetic output node, resulting in elevated bone‑marrow norepinephrine and dysregulated hematopoiesis. In naïve mice, chemogenetic activation of AgRP neurons suppresses PVH activity and lowers norepinephrine, indicating that the AgRP–PVH pathway normally restrains sympathetic tone. AgRP hyperactivation in EAE is accompanied by local astrocytic reactivity and selective involvement of somatostatin-positive (Sst+) AgRP subset. Chemogenetic inhibition of AgRP neurons delays disease onset, reduces severity, and normalizes bone‑marrow output. These findings indicate that a maladaptive AgRP–PVH-BM circuit contributes to abnormal immune cell generation in EAE.
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