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ALONSO, M.

Publications and source records attributed to ALONSO, M..

2 recordsLinked to original sources

Olfactory learning potentiates long-range cortical GABAergic inputs onto adult-born neurons.

Adult neurogenesis in the olfactory bulb (OB) contributes to structural and functional plasticity, influencing olfactory perception, learning, and memory. Adult-born granule cells (abGCs) exhibit unique morphological, electrophysiological, and synaptic properties compared to their neonatally born counterparts, suggesting a specialized role in olfactory processing. In the OB, such processing relies both on sensory inputs from the olfactory epithelium as well as top-down cortical feedback, which encompass both glutamatergic and GABAergic projections from the olfactory cortex back to the OB. While abGCs are known to integrate both bottom-up sensory inputs and top-down cortical projections, the specific connectivity and functional influence of cortical GABAergic inputs on abGCs remain largely unexplored. In this study, we investigated whether activity of cortical GABAergic projections is modulated by olfactory learning, how they impact olfactory behavior and whether these connections selectively influence mature abGCs. Using in vivo fiber photometry following odor-reward associative conditioning, we found odor- and reward-dependent activity of cortical GABAergic projections during learning session. Furthermore, their functional role was revealed using optogenetic activation which impaired both the acquisition and the reversal of an odor-reward association. Ex vivo patch-clamp recordings demonstrated that olfactory learning potentiates cortical GABAergic inputs specifically onto abGCs, and morphological analysis confirmed that learning increases the number of cortical GABAergic synapses. These findings highlight a novel mechanism by which top-down inhibitory control from the olfactory cortex selectively targets abGC activity during olfactory learning. Our results provide new insights into the functional specialization of abGCs and their role in adaptive olfactory behaviors.

neuroscience↗

Basolateral amygdala circuits supporting negative emotional bias in a mouse model for depression

Negative emotional bias is an essential hallmark of depression reflected by negative shift in hedonic valence assignment to emotional stimuli. Pleasant cues become less attractive and unpleasant ones more aversive. Given the crucial role of amygdala in valence coding, we hypothesize that specific basolateral amygdala (BLA) circuits alterations might support negative emotional bias associated with depressive states. Using a translational assay, we evaluate odor valence assignment in an animal model for depression chronically administered by corticosterone (CORT). We show spontaneous negative bias in depressive-like mice that attribute more negative valences for both attractive and aversive odors, mimicking thus the bias observed in depressed bipolar patients. Combining CTB and rabies-based tracing with ex vivo measurements of neuronal activity and chemogenetics experiments, we find that the CORT treatment reduces BLA-to-nucleus accumbens (NAc) neuronal activity and increases BLA-to-central amygdala activity, circuits respectively known to be involved in positive and negative valence encoding. Alterations in presynaptic connectivity of BLA-projecting neurons accompany these activity shifts. Interestingly, inputs from the paraventricular thalamus nucleus (PVT) towards BLA-to-NAc neurons are reduced in CORT-treated mice. Finally, chemogenetically activating the BLA-to-NAc circuit attenuates the negative bias in CORT-treated mice as well as the depressive-like phenotype, similarly than Fluoxetine antidepressant treatment. Altogether, we demonstrate that depressive states are associated with negative emotional bias both in human and mice. This bias is supported by activity shifts of specific BLA circuits along with durable presynaptic connectivity changes, but it could be alleviated by antidepressant drug or activity manipulation of altered BLA circuit.

neuroscience↗