ePoster

NEURONAL CASPASE-3 MODULATES SYNAPTIC CALCIUM SIGNALING AND HIPPOCAMPAL PLASTICITY

José Antonio Rodríguez-Gómezand 16 co-authors

Instituto de Biomedicina de Sevilla, IBIS/Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla

FENS Forum 2026 (2026)

Barcelona, Spain

Board PS06-09PM-262

Presentation

Date TBA

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Board: PS06-09PM-262

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Poster Board

PS06-09PM-262

Poster

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Abstract

Although Caspase-3 (Casp3) is classically known as an executioner of apoptosis, growing evidence indicates that it also fulfills non-apoptotic functions in neurons. Using two neuron-specific conditional knockout mouse models (CamKIIα-Cre and Thy1-Cre), we show that Casp3 contributes to hippocampal plasticity and cognitive function. Mice lacking neuronal Casp3 exhibited impaired object recognition and working memory despite normal locomotion and anxiety-like behavior. These deficits were accompanied by increased dendritic spine density, altered spine maturation, and marked disruption of long-term potentiation and long-term depression at Schaffer collateral-CA1 synapses. Mechanistically, Casp3 loss or inhibition attenuated stimulus-evoked calcium influx and reduced CaMKIIα phosphorylation. Together, these findings support a role for basal Casp3 activity in the modulation of postsynaptic calcium signaling during synaptic plasticity.

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