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New paper online:

We are pleased to announce a release of nice study led by our collaborator Prof. Christian Müller. It was pleasure to contribute, thanks Christian!

Neutral sphingomyelinase mediates the co-morbidity trias of alcohol abuse, major depression and bone defects

Neutral sphingomyelinase (NSM) and its coding gene SMPD3 is a single source for multiple pathways interlinking alcohol abuse—depression/anxiety—bone disorder (DH dorsal hippocampus, Nac nucleus accumbens).
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New paper online.

Our study about regulation of synaptic vesicle recycling at excitatory synapses by Amyloid beta and alpha7 nicotinic acetylcholine receptors is online.

Anni et al., (2021) demonstrated that Aβ1-42 and Aβ1-16, but not Aβ17-42, increased size of the recycling pool of synaptic vesicles (SV). This presynaptic effect was driven by enhancement of endogenous cholinergic signalling via α7 nicotinic acetylcholine receptors, which led to activation of calcineurin, dephosphorylation of synapsin 1 and consequently resulted in reorganization of functional pools of SV increasing their availability for sustained neurotransmission. These results identify synapsin 1 as a molecular target of Aβ and reveal an effect of physiological concentrations of Aβ on cholinergic modulation of glutamatergic neurotransmission.
Anni et al., CMLS, 2021Download

Congratulations Dani and thanks to the whole team!

We discussed this topic extensively at our symposium at the 14th meeting of German neuroscience society in the symposium S26  Regulation of synaptic vesicle recycling: from physiology to disease.

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What a day!

Yesterday, after the work, we took our backpacks and climbed over the hill to look over town of Erlangen. Then we spent nice evening in the beer-garden in Atzelsberg.

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New paper

Zoicas et all described new mouse model of depression where acid sphyngomyelinase (Smpd1) was overexpressed exclusively in the forebrain. Thanks for nice collaboration Iulia and Cosima!

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New paper is online

Our work on the role of CtBP1 in retrieval of synaptic vesicles is online.

Ivanova et al. demonstrate a dual role of CtBP1 in synaptic transmission. Nuclear CtBP1 restricts synaptogenesis and vesicular release probability, whereas presynaptic CtBP1 promotes compensatory endocytosis via activation of the lipid enzyme PLD1. Phosphorylation by Pak1 controls the redistribution of CtBP1 from active zones toward endocytic sites linking presynaptic exo- and endocytosis.