Nested compressed co-representations of multiple sequential experiences during sleep.

Animals encounter and remember multiple experiences daily. During sleep, hippocampal neuronal ensembles replay past experiences and preplay future ones. Although most previous studies investigated p/replay of a single experience, it remains unclear how the hippocampus represents many experiences without major interference during sleep.

Efficient mapping of the thalamocortical monosynaptic connectivity in vivo by tangential insertions of high-density electrodes in the cortex.

The thalamus provides the principal input to the cortex and therefore understanding the mechanisms underlying cortical integration of sensory inputs requires to characterize the thalamocortical connectivity in behaving animals. Here, we propose tangential insertions of high-density electrodes into mouse cortical layer 4 as a method to capture the activity of thalamocortical axons simultaneously with their synaptically connected cortical neurons. This technique can reliably monitor multiple parallel thalamic synaptic inputs to cortical neurons, providing an efficient approach to map thalamocortical connectivity in both awake and anesthetized mice.

Retinal input integration in excitatory and inhibitory neurons in the mouse superior colliculus in vivo.

The superior colliculus (SC) is a midbrain structure that receives inputs from retinal ganglion cells (RGCs). The SC contains one of the highest densities of inhibitory neurons in the brain but whether excitatory and inhibitory SC neurons differentially integrate retinal activity in vivo is still largely unknown. We recently established a recording approach to measure the activity of RGCs simultaneously with their postsynaptic SC targets in vivo, to study how SC neurons integrate RGC activity.

Retinal waves align the concentric orientation map in mouse superior colliculus to the center of vision.

Neurons in the mouse superior colliculus (SC) are arranged in a concentric orientation map, which is aligned to the center of vision and the optic flow experienced by the mouse. The origin of this map remains unclear. Here, we propose that spontaneous retinal waves during development provide a scaffold to establish the concentric orientation map within the SC and its alignment to the optic flow.

Absence of the Fragile X messenger ribonucleoprotein alters response patterns to sounds in the auditory midbrain.

Among the different autism spectrum disorders, Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability. Sensory and especially auditory hypersensitivity is a key symptom in patients, which is well mimicked in the mouse model. However, the physiological mechanisms underlying FXS's acoustic hypersensitivity in particular remain poorly understood.

High-density electrode recordings reveal strong and specific connections between retinal ganglion cells and midbrain neurons.

The superior colliculus is a midbrain structure that plays important roles in visually guided behaviors in mammals. Neurons in the superior colliculus receive inputs from retinal ganglion cells but how these inputs are integrated in vivo is unknown. Here, we discovered that high-density electrodes simultaneously capture the activity of retinal axons and their postsynaptic target neurons in the superior colliculus, in vivo.

Tangential high-density electrode insertions allow to simultaneously measure neuronal activity across an extended region of the visual field in mouse superior colliculus.

Background: The superior colliculus (SC) is a midbrain structure that plays a central role in visual processing. Although we have learned a considerable amount about the function of single SC neurons, the way in which sensory information is represented and processed on the population level in awake behaving animals and across a large region of the retinotopic map is still largely unknown. Partially because the SC is anatomically located below the cortical sheet and the transverse sinus, which render the measure of neuronal activity from a large population of neurons in the SC technically difficult to perform.

Orientation selectivity enhances context generalization and generative predictive coding in the hippocampus.

We learn and remember multiple new experiences throughout the day. The neural principles enabling continuous rapid learning and formation of distinct representations of numerous sequential experiences without major interference are not understood. To understand this process, here we interrogated ensembles of hippocampal place cells as rats explored 15 novel linear environments interleaved with sleep sessions over continuous 16 h periods.

Strengthened Temporal Coordination within Pre-existing Sequential Cell Assemblies Supports Trajectory Replay.

A central goal in learning and memory research is to reveal the neural substrates underlying episodic memory formation. The hallmark of sequential spatial trajectory learning, a model of episodic memory, has remained equivocal, with proposals ranging from de novo creation of compressed sequential replay from blank slate networks to selection of pre-existing compressed preplay sequences. Here, we show that increased millisecond-timescale activation of cell assemblies expressed during de novo sequential experience and increased neuronal firing rate correlations can explain the difference between post-experience trajectory replay and robust preplay.

Preconfigured patterns are the primary driver of offline multi-neuronal sequence replay.

Spontaneous neuronal ensemble activity in the hippocampus is believed to result from a combination of preconfigured internally generated dynamics and the unique patterns of activity driven by recent experience. Previous research has established that preconfigured sequential neuronal patterns (i.e.

Generative Predictive Codes by Multiplexed Hippocampal Neuronal Tuplets.

Rapid internal representations are continuously formed based on single experiential episodes in space and time, but the neuronal ensemble mechanisms enabling rapid encoding without constraining the capacity for multiple distinct representations are unknown. We developed a probabilistic statistical model of hippocampal spontaneous sequential activity and revealed existence of an internal model of generative predictive codes for the regularities of multiple future novel spatial sequences. During navigation, the inferred difference between external stimuli and the internal model was encoded by emergence of intrinsic-unlikely, novel functional connections, which updated the model by preferentially potentiating post-experience.

Activity-Dependent Plasticity of Astroglial Potassium and Glutamate Clearance.

Recent evidence has shown that astrocytes play essential roles in synaptic transmission and plasticity. Nevertheless, how neuronal activity alters astroglial functional properties and whether such properties also display specific forms of plasticity still remain elusive. Here, we review research findings supporting this aspect of astrocytes, focusing on their roles in the clearance of extracellular potassium and glutamate, two neuroactive substances promptly released during excitatory synaptic transmission.

Astroglial calcium signaling displays short-term plasticity and adjusts synaptic efficacy.

Astrocytes are dynamic signaling brain elements able to sense neuronal inputs and to respond by complex calcium signals, which are thought to represent their excitability. Such signaling has been proposed to modulate, or not, neuronal activities ranging from basal synaptic transmission to epileptiform discharges. However, whether calcium signaling in astrocytes exhibits activity-dependent changes and acutely modulates short-term synaptic plasticity is currently unclear.

The neuroglial potassium cycle during neurotransmission: role of Kir4.1 channels.

Neuronal excitability relies on inward sodium and outward potassium fluxes during action potentials. To prevent neuronal hyperexcitability, potassium ions have to be taken up quickly. However, the dynamics of the activity-dependent potassium fluxes and the molecular pathways underlying extracellular potassium homeostasis remain elusive.

Astroglial potassium clearance contributes to short-term plasticity of synaptically evoked currents at the tripartite synapse.

Astroglial processes enclose ∼60% of CA1 hippocampal synapses to form the tripartite synapse. Although astrocytes express ionic channels, neurotransmitter receptors and transporters to detect neuronal activity, the nature, plasticity and impact of the currents induced by neuronal activity on short-term synaptic plasticity remain elusive in hippocampal astrocytes. Using simultaneous electrophysiological recordings of astrocytes and neurons, we found that single stimulation of Schaffer collaterals in hippocampal slices evokes in stratum radiatum astrocytes a complex prolonged inward current synchronized to synaptic and spiking activity in CA1 pyramidal cells.

Dual electrophysiological recordings of synaptically-evoked astroglial and neuronal responses in acute hippocampal slices.

Astrocytes form together with neurons tripartite synapses, where they integrate and modulate neuronal activity. Indeed, astrocytes sense neuronal inputs through activation of their ion channels and neurotransmitter receptors, and process information in part through activity-dependent release of gliotransmitters. Furthermore, astrocytes constitute the main uptake system for glutamate, contribute to potassium spatial buffering, as well as to GABA clearance.

Transcriptome profile reveals AMPA receptor dysfunction in the hippocampus of the Rsk2-knockout mice, an animal model of Coffin-Lowry syndrome.

Coffin-Lowry syndrome (CLS) is a syndromic form of mental retardation caused by loss of function mutations in the X-linked RPS6KA3 gene, which encodes RSK2, a serine/threonine kinase acting in the MAPK/ERK pathway. The mouse invalidated for the Rps6ka3 (Rsk2-KO) gene displays learning and long-term spatial memory deficits. In the current study, we compared hippocampal gene expression profiles from Rsk2-KO and normal littermate mice to identify changes in molecular pathways.