Topic: CA3 pyramidal cells

Understanding synaptic connectivity is crucial for understanding how neuronal networks contribute to specific brain functions. However, current methods can measure the functionality only of a limited number of synaptic connections in sufficient detail. Therefore, we evaluated the applicability of a voltage imaging method in acute rat hippocampal slices to map unitary synaptic connections between CA3 neurons by using Voltron, which can detect both action potentials and small subthreshold events, such as unitary EPSPs. These connections are crucial for major hippocampal memory functions; however

The full-length amyloid precursor protein (APP), a key player in Alzheimer’s disease (AD), is ubiquitously expressed in a large majority of neurons, including GABAergic interneurons (INTs). Recent studies showed evidence of disrupted hippocampal plasticity in conditional APP KO of GABAergic forebrain neurons (Mehr et al, 2020). However, the physiological functions of APP at inhibitory synapses remain to be defined. We to study the role of APP at inhibitory synapses onto CA3 pyramidal cells (PCs) as well as on the overall inhibitory balance within the CA3 network. We combine slice electrophysio

The hippocampus is known to play a major role in the storage and recall of information depending on various forms of activity dependent synaptic plasticity. Mossy fiber synapses between the axons of dentate gyrus (DG) granule cells and CA3 pyramidal cells (Mf-CA3 synapses) display a high dynamic range of presynaptic plasticity which endow these synaptic connections with detonator properties. The pattern of action potential firing, in the form of high frequency bursts in the DG, strongly controls the amplitude of synaptic responses and information transfer to CA3. Presynaptic short-term plastic

Fragile X syndrome is the most common form of inherited intellectual disability and a major cause of autism spectrum disorder. This syndrome is caused by the silencing of the Fmr1 gene, which codes for the RNA-binding protein, FMRP. Most studies have focused on dendritic and postsynaptic mechanisms. Here we aim at characterising the functional involvement of new FMRP targets by exploring the consequences of FMRP loss on presynaptic mechanisms. We focus in particular on a recently identified target, Phosphodiesterase 2A (PDE2A). PDE2A is located in the presynaptic compartment and is highly expr

Establishing synaptic connections between neurons is essential for neuronal circuitry and efficient brain communication While the role of neuronal activity in refining and maintaining synapses is well known, we focus on its role, specifically spontaneous neurotransmitter release, for synapse formation between dentate gyrus axons, the mossy fibres (MF), onto CA3 pyramidal cells in the hippocampus. Neurotransmitter release occurs through two primary modes: action potential induced release and spontaneous fusion of synaptic vesicles. These modes are underpinned by distinct pools of vesicles, exhi

Synaptic transmission is a complex process, which requires activation of presynaptic Ca2+ channels, Ca2+ influx and binding to release sensors. Synaptotagmin 1 (Syt-1) has been previously identified as the primary Ca2+ sensor for fast synchronous transmitter release, while synaptotagmin 7 (Syt-7) was suggested to mediate slower, asynchronous release. However, recent reports have conflicting conclusions on the mechanisms of vesicle release modes, making our understanding of Ca2+ sensing in transmission unclear. To understand the action of synaptotagmins at a central synapse, we performed subcel