Past events

Inhibitory neurons are critically important for the adaptation of neural circuits to sensory experience, but the molecular mechanisms by which experience controls the connectivity between different types of inhibitory neurons to regulate cortical plasticity are largely unknown. In this talk, I will present studies demonstrating that sensory experience induces in cortical vasoactive intestinal peptide (VIP)-expressing neurons a gene program that is markedly distinct from that induced in excitatory neurons and other subtypes of inhibitory neuron. I will show that is Igf1 one of several activity-regulated genes that are specific to VIP neurons, that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto these neurons and that VIP neuron-derived IGF1 regulates visual acuity in an experience-dependent manner, likely by promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons. I will discuss how our findings support a model by which experience-induced transcriptional networks regulate the synaptic connectivity of each type of neuron according to a circuit-wide homeostatic logic and I will propose that the analysis of the genomic mechanisms regulating these transcriptional networks will allow us to evaluate the extent to which cell-type-specific homeostatic mechanisms contribute to the function of cortical circuits.

In all sensory modalities the response of cortical cells to repeated stimulus is highly variable from trial to trial and it is often correlated in nearby cells. Spiking mechanisms are highly reliable, suggesting that correlated variability of cortical response results from fluctuations in shared synaptic inputs, as we showed in our previous studies. However, the origin of correlated synaptic activities in the cortex is under dispute. Whereas some studies suggest that correlated variability originates from thalamic inputs, others claim that it emerges in the cortex due to recurrent local activity. By combining optogenetic silencing and paired intracellular recordings in the barrel cortex of anesthetized mice as well as using paired LFP-intracellular recordings in awake mice, we revealed the origin of synchronized ongoing and sensory evoked cortical activities.

: I will review a set of biologically inspired NeuroImaging methods (i.e. methods that take into consideration the brain topography, neuronal adaptation and population receptive fields, brain functional connectivity and so on), that we developed and/or refined to shed light on maps and computations in the human brain. Starting from retinotopy, we used partial correlations resting-state functional connectivity analysis to show that the large-scale topographical biases in all 3 dimensions of retinotopy are preserved in individuals without any visual experience. I will discuss how this result challenges classical views of retinotopy as the key organizational principle for computations in the visual system, and further suggest plasticity principles beyond classical Hebbian learning. Next, we use virtual environments to show that key retinotopic regions (mainly in the dorsal visual stream) are recruited not only during vision-based navigation but even when early-blind and sighted-blindfolded learn to navigate these same environments using audition. I will then show how such approaches can be applied to study the whole-body somatosensory-motor system, and demonstrate that topographical gradients are far more widespread than previously known. These findings help to bridge gaps between animal and human studies, and have clinical relevance to improve and refine deep-brain-stimulation and imaging-based diagnostics. Finally, I will briefly present the development of crossmodal adaptation and multiphase spectral analysis to study topographical binding and crossmodal integration. Based on all of these results I will discuss the intriguing hypothesis that our brain is topographically organized for high-order cognitive functions as well, and discuss our plans to combine the aforementioned approaches with the use of the high-field imaging (7T) that is required to test it. I will conclude by summarizing the wide set of tools that enable us to investigate and gain novel insights into the nature of the Topographical Multisensory Human Brain mind. (Most relevant papers for the talk: Striem-Amit et al. Neuron 2012; Cerbral Cortex 2012; Curr Biol 2014; Brain 2015; Zeharia et al. PNAS 2012; J Neurosci 2015; Saadon-Grosman et al. PNAS 2015; Murray, et al. Trends Neurosci 2016 (cond. accepted); Maidenbaum et al. (in preparation)); Siuda-Krzywicka et al. Elife 2016; Sabbah et al. NeuroImage 2016 (accepted).

Perception of external objects involves sensory acquisition via the relevant sensory organs. A widely-accepted assumption is that the sensory organ is the first station in a serial chain of processing circuits leading to an internal circuit in which a percept emerges. This open-loop scheme, in which the interaction between the sensory organ and the environment is not affected by its downstream neuronal processing, is strongly challenged by behavioral and anatomical data. I will present a hypothesis in which the perception of external objects is a closed-loop dynamical process encompassing loops that integrate the organism and its environment and converging towards organism-environment steady-states. I will discuss the consistency of closed-loop perception (CLP) with empirical data, show that it can be synthesized in a robotic setup, and discuss possible empirical ways to discriminate between open- and closed-loop schemes for perception.