TY - JOUR
T1 - Inhibitory circuit dysfunction as a potential contributor to cortical reorganization in Glioblastoma progression
AU - Spalletti, Cristina
AU - Scalera, Marta
AU - Mori, Elisabetta
AU - Haddad, Sabrin
AU - Mainardi, Marco
AU - Cangi, Daniele
AU - Pillai, Vinoshene
AU - Parmigiani, Elena
AU - Landi, Silvia
AU - Caleo, Matteo
AU - Vannini, Eleonora
N1 - Publisher Copyright:
© 2025
PY - 2025/9
Y1 - 2025/9
N2 - Glioblastoma (GBM) is a highly aggressive brain tumor that infiltrates surrounding brain tissue, profoundly affecting adjacent cortical areas. This study investigates how GBM reshapes the peritumoral cortex by examining plasticity changes in two GBM mouse models. Using optogenetic stimulation, we observed altered motor mapping and reduced cortical specificity in GBM mice compared to controls. Morphologically, GBM mice showed a reduction in dendritic spines, perineuronal nets, and inhibitory markers. Functionally, inhibitory circuits were markedly impaired, characterized by an increased frequency of spontaneous inhibitory currents and a decrease in their amplitude. Our findings highlight the critical role of inhibitory circuit disruption in driving cortical reorganization and loss of motor map specificity. The reduction of parvalbumin and somatostatin interneurons, degradation of perineuronal nets, and imbalance in the excitation/inhibition ratio contribute to maladaptive plasticity, increasing the risk of hyperexcitability and seizures. These insights offer a basis for developing therapeutic strategies aimed at restoring inhibitory function, mitigating GBM-induced cortical changes, and potentially improving patient outcomes.
AB - Glioblastoma (GBM) is a highly aggressive brain tumor that infiltrates surrounding brain tissue, profoundly affecting adjacent cortical areas. This study investigates how GBM reshapes the peritumoral cortex by examining plasticity changes in two GBM mouse models. Using optogenetic stimulation, we observed altered motor mapping and reduced cortical specificity in GBM mice compared to controls. Morphologically, GBM mice showed a reduction in dendritic spines, perineuronal nets, and inhibitory markers. Functionally, inhibitory circuits were markedly impaired, characterized by an increased frequency of spontaneous inhibitory currents and a decrease in their amplitude. Our findings highlight the critical role of inhibitory circuit disruption in driving cortical reorganization and loss of motor map specificity. The reduction of parvalbumin and somatostatin interneurons, degradation of perineuronal nets, and imbalance in the excitation/inhibition ratio contribute to maladaptive plasticity, increasing the risk of hyperexcitability and seizures. These insights offer a basis for developing therapeutic strategies aimed at restoring inhibitory function, mitigating GBM-induced cortical changes, and potentially improving patient outcomes.
KW - Glioblastoma/physiopathology
KW - Animals
KW - Brain Neoplasms/physiopathology
KW - Mice
KW - Disease Progression
KW - Cerebral Cortex/physiopathology
KW - Interneurons/pathology
KW - Neuronal Plasticity/physiology
KW - Nerve Net/physiopathology
KW - Neural Inhibition/physiology
KW - Male
UR - https://www.scopus.com/pages/publications/105008554828
U2 - 10.1016/j.nbd.2025.106997
DO - 10.1016/j.nbd.2025.106997
M3 - Journal article
C2 - 40490040
SN - 0969-9961
VL - 213
SP - 106997
JO - Neurobiology of Disease
JF - Neurobiology of Disease
M1 - 106997
ER -