CaMKII

The functioning of a synapse depends on its accessibility to proteins and, thus, on the localization of protein sources along the dendrite (Westenbroek 2009, Vacher et al. 2008). Therefore, the behaviour of the synapse highly depends on the availability of proteins and ion channels and any perturbation in the localization and availability of these components would lead to a dysfunction of the synapse. Hence, understanding the localization and distribution of ion channels and proteins in the dendrite in relation to the synapse is crucial. Using super-resolution microscopy, Helm et al., 2021 der

…This mechanism is mediated CaMKII dependent twofold increase of the strength of all inhibitory and all excitatory synapses in the cell. The key function of the amplification mechanism is to promote an already-formed memory to a dominant memory.Aim:Using TRAP2 genetically modified mice, we investigated the long-term retention of traumatic memory through an ampl

…signalling and plasticity molecules CaMKII and DAPK1 and their related pathways.We incubated primary hippocampal cell cultures (div 14-21) with patient-derived monoclonal anti-GluN1 or control antibodies. Thereafter, we induced chemical LTP and/or treated cells with the DAPK1 inhibitor TC-DAPK6. We then analysed NMDARs GluN1

Site-specific synaptic plasticity modifying the strength of a particular, individual synapse is critical to cognitive functions such as memory and learning (Kastellakis et al., 2019; Tazerart et al., 2020). This specificity coexists with the experimental observation that the dendrite-wide spine sizes and weights follow a surprisingly stable, lognormal-like distribution (Hasan et al. 2020; Eggl et al., 2023). How synaptic plasticity can be specific, yet the global synapse distribution stable, is an open question that has motivated several recent studies (Kirschner et al., 2019; Eggl et al., 202

A detailed computational model of synaptic plasticity-related intracellular signalling pathways was used to investigate the molecular mechanisms of long-term potentiation (LTP) in a spine head of a hippocampal CA1 pyramidal neuron. The biochemical model can be used to study the mechanisms of different forms of plasticity, the roles and contributions of the molecular pathways, individual molecular species, and the effects of different induction protocols and various types of neuromodulations. The goal of the present study is to describe the molecular changes underlying different forms of synapt

Lactate is an important metabolite produced by astrocytes and delivered to neurons to support their energy needs in a process known as the astrocyte-neuron lactate shuttle. Emerging research during the past decade has unveiled a role of lactate as a signal capable of orchestrating critical functions ranging from neuroprotection to memory. In previous work, we found that lactate enhanced the amplitude and decay time of NMDA receptor currents (INMDAR) evoked by brief applications of glutamate and glycine. These effects were not observed when neurons were exposed to lactate receptor (HCA1) agonis