| dc.description | Enhanced activity and overexpression of Pannexin 1 (Panx1) channels contribute to neuronal pathologies such as epilepsy and Alzheimer’s disease (AD). The Panx1 channel ablation alters
the hippocampus’s glutamatergic neurotransmission, synaptic plasticity, and memory flexibility.
Nevertheless, Panx1-knockout (Panx1-KO) mice still retain the ability to learn, suggesting that compensatory mechanisms stabilize their neuronal activity. Here, we show that the absence of Panx1
in the adult brain promotes a series of structural and functional modifications in the Panx1-KO
hippocampal synapses, preserving spontaneous activity. Compared to the wild-type (WT) condition,
the adult hippocampal neurons of Panx1-KO mice exhibit enhanced excitability, a more complex
dendritic branching, enhanced spine maturation, and an increased proportion of multiple synaptic
contacts. These modifications seem to rely on the actin–cytoskeleton dynamics as an increase in
the actin polymerization and an imbalance between the Rac1 and the RhoA GTPase activities were
observed in Panx1-KO brain tissues. Our findings highlight a novel interaction between Panx1
channels, actin, and Rho GTPases, which appear to be relevant for synapse stability. | |
