ePoster

REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (RTMS) MODULATES HIPPOCAMPAL ASTROCYTES, GABA-GLUTAMATE SYSTEM, AND BEHAVIOR IN A POSTNATAL MK-801 MODEL OF SCHIZOPHRENIA: A SEX-DEPENDENT STUDY.

David Meneses San Juanand 1 co-author

Ramon de la Fuente Muñíz National Institute of Psychiatry

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-500

Presentation

Date TBA

Board: PS01-07AM-500

Poster preview

REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (RTMS) MODULATES HIPPOCAMPAL ASTROCYTES, GABA-GLUTAMATE SYSTEM, AND BEHAVIOR IN A POSTNATAL MK-801 MODEL OF SCHIZOPHRENIA: A SEX-DEPENDENT STUDY. poster preview

Event Information

Poster Board

PS01-07AM-500

Abstract

Schizophrenia (SZ) involves glutamatergic/GABAergic alterations. Postnatal MK-801, an NMDA antagonist, models negative symptoms (social isolation, anhedonia, hypolocomotion). Astrocytes, implicated in SZ, regulate GABA-glutamate transmission. Repetitive Transcranial Magnetic Stimulation (rTMS) may have therapeutic potential. We hypothesized rTMS reverses behaviors by modulating hippocampal astrocytes and the GABA-glutamate system. Male/female FVB/N mice were divided into: NaCl+Sham, MK-801+Sham, NaCl+rTMS, MK-801+rTMS. MK-801 (0.1 mg/kg) was administered neonatally (P7-14). Behaviors were assessed in adolescence (P51-54) and adulthood (P103-105). rTMS (10 Hz) was applied in adulthood (P110-140). Hippocampal astrocyte (GFAP) and interneuron (parvalbumin) density, and GABA/glutamate levels were analyzed. Neonatal MK-801 induced anhedonia, hypolocomotion, and social isolation, effects more prominent in males from adolescence. It reduced astrocyte density in the hilus (both sexes) and interneurons (males only), while increasing extracellular glutamate and intracellular GABA. rTMS reversed MK-801-induced hypolocomotion and social isolation in males, restored astrocyte density, increased interneuron density, and partially (males) or fully (females) reversed glutamate/GABA alterations. In conclusion, 10 Hz rTMS exerts a therapeutic effect in an SZ model, possibly mediated by astrocytes and the GABA-glutamate system, with sex-dependent influences.

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