Topic: Long Term Potentiation

Pleiotropic cytokine IL-6 regulates various processes in the body including neuronal functions. IL-6 can signal through its membrane bound receptor IL-6R, which associates with IL-6 signal transducer gp130 IL-6st/gp130 (classical signaling), or binds to soluble IL-6R to act on any cell that that expresses IL-6st/gp130 (trans-signaling). Alzheimer’s disease related enzyme BACE1 has critically important roles in synaptic function and cleaves IL-6st/gp130 as well as IL-6R.Therefore, we hypothesize that BACE1 could be essential for the alteration of neuron excitability and synaptic plasticity via

In this work, we want to dissect the specific and sex-dependent role of CB1 signalling in different cell types and its impact on hippocampal functions such as navigation or memory. A specific Cre-mediated CB1 deletion on neurons (excitatory and inhibitory), astrocytes, or interneurons in CB1-flox males and females was performed. Viral vectors (AAV-Cre) were injected bilaterally into the hippocampus of these mice. The Barnes maze was used for learning, memory, navigation and the Novel Object Recognition Test (NORT) for recognition memory. Anxiety-like behavioural protocols were also performed b

The stress response is a significant precipitating factor in various psychiatric disorders. Numerous neuropsychiatric disorders are characterized by sex differences in the prevalence, type, and severity of symptoms, which include cognitive dysfunctions mainly supported by the prefrontal cortex (PFC). This study aims to evaluate the sexual dimorphic effects of acute stress on PFC synaptic properties, as well as on both the intrinsic and synaptic properties of PFC-basolateral amygdala (BLA) and PFC-PFC projection neurons. Adult male and female mice were exposed to either restraint stress (RS) or

N6-methyladenosine (m6A) methylation, the most prevalent eukaryotic mRNA modification, is enriched in the mammalian brain and the synaptic transcriptome. m6A methylation is dynamically regulated by enzymes called m6A writers (METTL3/14) and erasers (FTO), that are present in distal neuronal processes. Although recent studies link dynamic m6A methylome changes during synaptic plasticity to memory consolidation, the exact mechanisms in neuronal circuits remain unclear. This study investigates m6A methylation effects on synaptic transmission and plasticity within hippocampal networks, utilizing p

During Long Term Potentiation (LTP) AMPA receptors (AMPARs) are inserted into the plasma membrane. This form of synaptic plasticity is crucial for many aspects of brain function, including learning and memory. Protein 4.1N (EPB41L1) is a neuronally enriched member of the protein 4.1 family. In primary hippocampal cultures, 4.1N is enriched at the discrete sites of synaptic contact, co-localizing with the postsynaptic density proteins, suggesting a potential functional role for 4.1N as a component of the cytoskeletal architecture of excitatory synapses. 4.1N also directly interacts with the Glu

Angelman Syndrome (AS) is a neurodevelopmental disorder with complex symptomatology caused by the loss of maternal allele expression of one single gene in the brain, the ubiquitin E3 ligase UBE3A. Even if the underlying genetic basis of AS has previously been extensively described, the molecular mechanisms regulated by UBE3A ubiquitination in the brain remain highly elusive. Here we provide the first proteomic report of UBE3A-mediated ubiquitination events in a mammalian brain. In order to identify Ube3a substrates, we have combined our previously described bioUb mouse with a new mouse strain