Topic: L-type calcium channels

Alzheimer's disease (AD) is a major neurodegenerative disease characterized by a marked decline in the activity of the alpha-ketoglutarate dehydrogenase complex (AKGDHC), a key metabolite of the tricarboxylic acid (TCA) cycle. Earlier studies have shown that the calcium salt of AKG, CaAKG, increases the healthspan and lifespan in C57BL/6 mice by reducing inflammatory cytokines. Here, we demonstrate that CaAKG attenuates long-term potentiation (LTP) in an animal model of AD, APP/PS1 mice. CaAKG application during strong tetanisation converts early-LTP to late-LTP, stable for 4 hours in the CA1

α2δ proteins serve as auxiliary subunits of voltage-gated calcium channels (CaV) and regulate the formation and differentiation of synapses. To comparatively study the neuronal localization of the four α2δ isoforms (α2δ-1 to -4), we previously established hemagglutinin (HA) tagging, which allows the surface detection with anti-HA antibody labeling. However, localizing α2δ proteins in synaptic membranes is limited because the synaptic cleft is densely packed with trans-synaptic and extracellular matrix proteins. Thus, classical antibodies have restricted access to extracellular epitopes. Here,

Pathogenic variants in the CACNA1F gene, encoding retinal Cav1.4 L-type calcium channels can lead to a spectrum of altered functional channel activity, affecting the transmission of visual signals from photoreceptors to bipolar cells. Here, we investigated the effect of the Cav1.4 C-terminal truncation variant R1827X (RX) - lacking an intramolecular mechanism, necessary for continuous calcium influx- in mouse retinas and compared the phenotype to the apparent Cav1.4 gain-of-function variant I745T (IT). Whereas the significant decrease in the Cav1.4 protein can be attributed to a loss of photor

The dorsal lateral geniculate nucleus (dLGN) has long been held to act as a basic relay for visual information travelling from the retina to cortical areas, but recent findings suggest a largely underestimated functional plasticity of dLGN neurons. However, the cellular mechanisms supporting this functional plasticity have not been yet explored. In particular, it remains to elucidate whether intrinsic neuronal excitability change upon visual stimuli. We show here that monocular deprivation for 10 days reduces the intrinsic excitability of dorsal LGN relay cells. Furthermore, dLGN neurons exhib