bioRxiv Science⌕ Search

Biology subjects

Sengpiel, F.

Publications and source records attributed to Sengpiel, F..

7 recordsLinked to original sources

Experiences are encoded by brainwide reprogramming of synaptome architecture

Synaptome architecture describes the spatiotemporal distribution of highly diverse excitatory synapses throughout the brain. Whether and how this architecture is impacted by experience is key to understanding its role in learning and memory. We found that environmental enrichment and monocular visual deprivation drive large-scale, type-and subtype-specific reorganisation of excitatory synapses in more than one hundred brain regions. Each experience modifies distinct subsets of synapses, with patterns aligned with protein turnover rates and connectome architecture. These reorganisations occur during development and adulthood, revealing a conserved mechanism of synaptome plasticity across the lifespan. Our findings support a population-selection model in which experience drives adaptation by selectively modifying synapse varieties, generating a distributed trace of past experiences. Our results also point to synaptome architecture as a shared framework integrating experience, lifespan changes, sleep, genetic variation and disease.

neuroscience↗

Disruptions in Primary Visual Cortex Physiology and Function in a Mouse Model of Timothy Syndrome

Timothy syndrome (TS) is a rare genetic disorder caused by mutations in the CACNA1C gene which encodes the L-type calcium channel -1 CaV1.2 subunit. While it is expressed throughout the body the most serious symptoms are cardiac and neurological. Classical TS1 and TS2 mutations cause prolonged action potentials (APs) in cardiomyocytes and in induced neurons derived from pluripotent stem cells taken from TS patients, but effects of TS mutations on neuronal function in vivo are not fully understood. TS is frequently associated with autistic traits, which in turn have been linked to altered sensory processing. Using the TS2-neo mouse model we analysed effects of the TS2 mutation on the visual system. We observed a widening of APs of pyramidal cells in ex vivo patch-clamp recordings and an increase in the density of parvalbumin positive (PV+) cells in the primary visual cortex. Neurons recorded extracellularly in vivo were less likely to respond to visual stimuli of low spatial frequency, but more likely to respond to visual stimuli of mid-to-high spatial frequency, compared to WT mice. These results point to a basic processing abnormality in the visual cortex of TS2-neo mice.

neuroscience↗

Experience dependent plasticity of higher visual cortical areas in the mouse

Introduction ABSTRACT Introduction Materials and Methods Results Discussion CRediT authorship contribution... Funding References Since the pioneering work by Hubel and Wiesel on cats and monkeys in the 1960s and 1970s (Wiesel and Hubel, 1963; Hubel et al., 1977) ocular dominance (OD) plasticity has become one of the classic paradigms for the study of experience-dependent brain plasticity. Occluding one eye by monocular deprivation (MD) shifts responses of visual cortical neurons towards the open eye, in particular during a critical period early in life Hubel Wiesel (Hubel and Wiesel, 1970; Olson and Freeman, 1978). It also results in a substantial loss of visual acuity in the deprived eye ( ...

neuroscience↗

Endogenous recruitment of frontal-sensory circuits during visual discrimination

A long-range circuit linking anterior cingulate cortex (ACC) to primary visual cortex (V1) has been previously proposed to mediate visual selective attention in mice during visually guided behaviour. Here we used in vivo two-photon functional imaging to measure endogenous activity of ACC neurons projecting to layer 1 of V1 (ACC-V1axons) in mice either passively viewing stimuli or performing a go/no-go visually guided task. We observed that while ACC-V1axons were recruited under these conditions, this was not linked to enhancement of neural or behavioural measures of sensory coding. Instead, ACC-V1axon activity was observed to be associated with licking behaviour, modulated by reward, and biased towards task relevant sensory cortex.

neuroscience↗

Abi3 regulates microglial ramification and dynamic tissue surveillance in vivo.

A rare coding variant of Abelson-interactor gene family member 3 (Abi3) is associated with increased risk of late-onset Alzheimers Disease (AD). Although Abi3 is recognised as a core microglial gene, its role in microglia is largely unknown. Here we demonstrate that Abi3 is crucial for normal microglial morphology, distribution, and homeostatic tissue surveillance activity in vivo.

neuroscience↗

Stable encoding of visual cues in the mouse retrosplenial cortex

The rodent retrosplenial cortex functions as an integrative hub for sensory and motor signals, serving roles in both navigation and memory. While retrosplenial cortex (RSC) is reciprocally connected with the sensory cortex, the form in which sensory information is represented in the retrosplenial cortex and how it interacts with behavioural state is unclear. Here, we used 2-photon cellular imaging of neural activity of putative excitatory (CaMKII expressing) and inhibitory (parvalbumin expressing) neurons to measure visual and running evoked activity in RSC and compare it to primary visual cortex (V1). We found that stimulus position and orientation information was preserved between V1 and RSC, and additionally that positional information was organised topographically. Stimulus directional preference was biased towards nasal-temporal flow. Locomotion modulation of activity of single neurons, both in darkness and light, was also more pronounced in RSC than V1, and strongest in parvalbumin-positive neurons. Longitudinal measurements of single neurons showed that these response features were stably maintained over many weeks. These data provide evidence for stable representations of visual cues in retrosplenial cortex which are highly spatially selective. These may provide sensory data to contribute to the formation of memories of spatial information.

neuroscience↗

Mammillothalamic disconnection alters hippocampo-cortical oscillatory activity and microstructure: Implications for diencephalic amnesia

Diencephalic amnesia can be as disruptive as the more commonly known temporal lobe amnesia, yet the precise contribution of diencephalic structures to memory processes remains elusive. We used discrete lesions of the mammillothalamic tract to model aspects of diencephalic amnesia and assessed the impact of these lesions on multiple measures of activity and plasticity within the hippocampus and retrosplenial cortex. Lesions of the mammillothalamic tract had widespread indirect effects on hippocampo-cortical oscillatory activity within both theta and gamma bands. Both within-region oscillatory activity and cross-regional synchrony were altered. The network changes were state-dependent, displaying different profiles during locomotion and paradoxical sleep. Consistent with the associations between oscillatory activity and plasticity, complementary analyses using several convergent approaches revealed microstructural changes, which appeared to reflect a suppression of learning-induced plasticity in lesioned animals. Together, these combined findings suggest a mechanism by which damage to the medial diencephalon can impact upon learning and memory processes, highlighting important role for the mammillary bodies in the co-ordination of hippocampo-cortical activity.

neuroscience↗