Topic: neuronal apoptosis

Neuronal apoptosis is a mechanism used to clear the cells of oxidative stress or DNA damage and to refine the final number of neurons for a functional neuronal circuit. The tumour suppressor protein p53 is a key regulator of the cell cycle and serves as a checkpoint for eliminating neurons with high DNA damage, aberrant hyperproliferative signals or cellular stress. Meanwhile p53 is largely expressed in progenitors’ cells during development, in adult mice p53 expression is restricted to the neurogenic niches where it regulates cell proliferation and self-renewal. To investigate the functional

Recent studies have highlighted the pivotal role of TRPM2 channel activation in neurological disorders. Nevertheless, its association with epileptic seizures and subsequent neuronal damage remains unclear. This study aims to investigate the impact of inhibiting TRPM2 on 4-AP-induced seizures in mouse brain slices and the resultant neuronal damage in the HT-22 cell line. Electrophysiologically using LFP records the effect of TRPM2 inhibition through the TRPM2 antagonist N-ACA was demonstrated in the entorhinal cortex region after the 4-AP-induced seizure model. Furthermore, to shed light on the

PIANP is a primarily neuronally localised protein which binds to the N-terminal domain of GABA-B receptors as well as the inhibitory immunoglobuline-like type 2 receptor PILRa [1]. In humans, a homozygous loss-of-function mutation of PIANP is associated with features of intellectual disability and global development delay whilst PIANP knockout mice display autism spectrum disorder (ASD)-like behaviour as well as heightened anxiety [2]. As we previously reported, PIANP knockout mice present with a different composition of telencephalic cell layers and increased neuronal apoptosis [2, 3]. Here,