Past events

In my talk I will present a generalized view of dendritic function in neocortical pyramidal neurons summarizing a decade of research. Later I will present two yet unpublished works. The first will describe dendritic integration in layer 4 spiny stellate neurons and the role of dendritic spikes in-vivo. The second work will present coding of texture in layer 2-3 neurons in the rat barrel cortex using two photon imaging methods.

Adolescence is a period of major physical, hormonal and psychological change. It is also characterized by a significant increase in the incidence of psychopathologies and this increase is gender-specific. Likewise, stress during adolescence is associated with the development of psychiatric disorders later in life. Here, we study the immediate impact of psychogenic stress before and during puberty (postnatal days 28-42) on behavior (novelty seeking, risk taking, anxiety and depression) and hypothalamus-pituitary-adrenocortical (HPA) axis activation and brain metabolism during late adolescence (postnatal days 45-51). Peri-pubertal stress: a) decreased anxiety-like behavior and increased risk taking and novelty seeking behaviors during late adolescence; b) did not affect depressive-like behavior; c) decreased fear memories (freezing in response to a tone associated with electrical shock) only in females; d) did not affect brain activation on basal conditions (home cage) but increase activation of hippocampus, basal amygdala, cingulated and motor cortices when the animals underwent recall of a tone associated to electrical shock; and e) did not affect acute HPA response to stress (blood corticosterone and glucose). Interestingly, when controlling for the basal anxiety of the mothers, animals exposed to peri-pubertal stress showed a significant decrease in corticosterone levels right after an acute stressor. The results from this study suggest that exposure to mild stressors during the peri-pubertal period induces a broad spectrum of behavioral and brain activation changes in late adolescence, which seems to exacerbate the independence-building behaviors naturally happening during this transitional period (increase in curiosity, sensation-seeking and risk taking behaviors).

What are the sources of trial-to-trial variability in neural responses in early sensory cortical areas and how does this variability affect perceptual decisions? In this talk I will describe results from two studies that aim to address these questions. In the first study, we examined co-variations between behavioral choices of monkeys performing a threshold visual detection task and neural population responses recorded simultaneously from their V1. We found that fluctuations in V1 responses to the same visual stimulus are correlated with fluctuations in perceptual decisions. Our results provide insight regarding the decoding mechanisms that mediate behavior based on V1 responses and suggest that most choice-related variability is already present in V1. Top-down modulations from higher visual cortical areas are one potential source for these decision related signals in V1. The goal of the second study was to characterize two forms of top-down effects in V1: modulations by spatial uncertainty and by stimulus relevance. We found that V1 responses are unaffected by spatial uncertainty, suggesting that target sensitivity is not a limited resource that can be improved by focal attention in V1. Conversely, V1 responses were significantly modulated by stimulus relevance. These modulations are likely to contribute to spatial gating of task-irrelevant information. However, the spatial and temporal characteristics of this top-down signal suggest that it is not a major source of choice-related variability in V1. Our results are therefore consistent with a predominantly bottom-up source of decision related activity in V1.

It is widely believed that memories are encoded and stored in the pattern and strength of synaptic connections. Individual synapses, the elementary units of information transfer, encode and store new information in response to the environmental changes through structural and functional reorganization. The key mechanisms that normally maintain plasticity of synapses and initiate synapse loss in neurodegenerative diseases remain elusive. To target this question, we developed an integrative approach to correlate structure and function at the level of single synapses in hippocampal circuits. Utilizing FRET spectroscopy, optical imaging, electrophysiology and molecular biology we explore the casual relationship between the pattern of ongoing neuronal activity, structural rearrangements within the synaptic signaling complexes and plasticity of single synapses and whole networks. Our results suggest that ongoing background synaptic activity critically determines the number and plasticity of synapses in hippocampal circuits.