id_814. ACTION POTENTIAL PROPERTIES OF HIPPOCAMPAL CA1 PYRAMIDAL NEURONS IN XKR8 KNOCKOUT MICE DURING POSTNATAL DEVELOPMENT
Igor Nagula1, Emilija Kavalnyte1, Kornelija Vitkute1, Daiva Dabkeviciene3, Urte Neniskyte1,2, Aidas Alaburda1
1 Vilnius University Life Sciences Center, Department of Neurobiology and Biophysics, Sauletekio al. 7, Vilnius, Lithuania
2 Vilnius University Life Sciences Center, VU-EMBL Partnership Institute, Sauletekio al. 7, Vilnius, Lithuania
3 National Cancer Institute, Santariskiu st. 1, Vilnius, Lithuania
INTRODUCTION: The first three postnatal weeks are characterized by morphological and electrophysiological maturation of hippocampal neurons, driven by the incorporation of ion channels and receptors and coinciding with peak synaptogenesis. Phosphatidylserine, a neuronal "eat me" signal translocated by the Xkr8 scramblase, is one of the signals that regulate synaptic pruning. The Xkr8 scramblase is highly expressed in mouse brains after birth, and its deficiency leads to excessive excitatory nerve terminals, altered neuronal bouton morphology, and increased cortico-cortical and cortico-spinal projections. Although altered synaptic activity has been reported in Xkr8-deficient mice, its impact on intrinsic membrane properties has not been systematically investigated.
AIM(S): Here, we investigated action potential (AP) properties of hippocampal CA1 pyramidal neurons in Xkr8 knockout and wild-type mice across postnatal development in males and females
METHOD(S): Whole-cell patch-clamp recordings were performed in acute mouse brain slices, and AP amplitude, width, and threshold were analyzed.
RESULTS: Three-way ANOVA (Age × Genotype × Sex) revealed a significant main effect of age on AP amplitude, width, and threshold (P<0.001). Importantly, significant Age × Genotype interactions were detected for all these properties (P≤0.01), indicating genotype-dependent alterations in developmental trajectories. No genotype-related interactions with sex were observed, although a main effect of sex was detected for AP width and threshold.
CONCLUSIONS: Together, these findings indicate that Xkr8 deficiency modifies the maturation pattern of intrinsic membrane properties across postnatal development.