Irene Serra

Instituto Cajal

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Marta Navarrete

Instituto Cajal

C. Martín

Instituto Cajal

Ramón Trullás

Biomedical Research Networking Center on Neurodegenerative Diseases

Petar Podlesniy

Institut d'Investigacions Biomèdiques de Barcelona

Julio Esparza

Instituto Cajal

Margalida Puigròs

Institut d'Investigacions Biomèdiques de Barcelona

Jorge García‐Marqués

Instituto Cajal

Clementine Hofmann

University Medical Center of the Johannes Gutenberg University Mainz

Mazahir T. Hasan

Max Planck Institute for Medical Research

ÁR

Ángel R. Nebreda

Spanish National Cancer Research Centre

Cooperative Institutions

Consejo Superior de Investigaciones Científicas

Instituto Cajal

Universidad Autónoma de Madrid

Instituto de Salud Carlos III

Centro de Biología Molecular Severo Ochoa

University Medical Center of the Johannes Gutenberg University Mainz

Johannes Gutenberg University Mainz

Pompeu Fabra University

Centro de Investigacion Principe Felipe

Weatherford College

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Catching Astrocyte Ensembles: Astrocytic Ensembles Control Cue-motivated Behavior

Research Square (Research Square) (2023)

Marta Navarrete Irene Serra Juan Quintanilla Jorge García‐Marqués

Abstract Astrocytes, dynamic cells that play a crucial role in brain function, have traditionally been overshadowed by the emphasis on neuronal activity in regulating behavior. This is in part due to the lack of tools to experimentally map and manipulate specific subsets of astrocytes based on their functional activity, which hampers our understanding of how astrocyte networks contribute to the organization of behavior. Here, using a tool that can translate astrocytic activity–mediated calcium signals into gene expression in a light-dependent manner, we have identified an active astrocytic ensemble -which refers to active astrocytes working together- associated with cue-motivated behavior in the Nucleus Accumbens (NAc), a central hub in the reward system. We mapped behavior-related astrocytic ensemble activity to the ventral and posterior regions of the NAc. Furthermore, we demonstrated that direct activation of this specific astrocytic ensemble through optogenetics was sufficient to retrieve the direction of labeled reward behavior. Overall, these findings uncover the fine-tuning role of astrocytic ensembles in shaping salient behavior.

Premovement neuronal activity

10.21203/rs.3.rs-3427853/v1

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Citations (1)

L'entrevistat: Sebastià Solé i Cot

Àpoca: butlletí català d'informació notarial (2010)

Irene Serra

Source

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NUCLEUS ACCUMBENS ASTROCYTIC ENSEMBLES SHAPE SYNAPTIC PLASTICITY

IBRO Neuroscience Reports (2023)

Javier Sánchez‐Romero Irene Serra Marta Navarrete

Homosynaptic plasticity

10.1016/j.ibneur.2023.08.436

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CATCHING ACTIVE ASTROCYTE ENSEMBLES: ASTROCYTIC ENSEMBLES SHAPE MOTIVATED BEHAVIOR IN THE NUCLEUS ACCUMBENS

IBRO Neuroscience Reports (2023)

Irene Serra Marta Navarrete

10.1016/j.ibneur.2023.08.439

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Nrg1 haploinsufficiency alters inhibitory cortical circuits

Neurobiology of Disease (2021)

Carmen Navarro-González Héctor Carceller Marina Benito Irene Serra Marta Navarrete

Neuregulin 1 (NRG1) and its receptor ERBB4 are schizophrenia (SZ) risk genes that control the development of both excitatory and inhibitory cortical circuits. Most studies focused on the characterization ErbB4 deficient mice. However, ErbB4 deletion concurrently perturbs the signaling of Nrg1 and Neuregulin 3 (Nrg3), another ligand expressed in the cortex. In addition, NRG1 polymorphisms linked to SZ locate mainly in non-coding regions and they may partially reduce Nrg1 expression. Here, to study the relevance of Nrg1 partial loss-of-function in cortical circuits we characterized a recently developed haploinsufficient mouse model of Nrg1 (Nrg1tm1Lex). These mice display SZ-like behavioral deficits. The cellular and molecular underpinnings of the behavioral deficits in Nrg1tm1Lex mice remain to be established. With multiple approaches including Magnetic Resonance Spectroscopy (MRS), electrophysiology, quantitative imaging and molecular analysis we found that Nrg1 haploinsufficiency impairs the inhibitory cortical circuits. We observed changes in the expression of molecules involved in GABAergic neurotransmission, decreased density of Vglut1 excitatory buttons onto Parvalbumin interneurons and decreased frequency of spontaneous inhibitory postsynaptic currents. Moreover, we found a decreased number of Parvalbumin positive interneurons in the cortex and altered expression of Calretinin. Interestingly, we failed to detect other alterations in excitatory neurons that were previously reported in ErbB4 null mice suggesting that the Nrg1 haploinsufficiency does not entirely phenocopies ErbB4 deletions. Altogether, this study suggests that Nrg1 haploinsufficiency primarily affects the cortical inhibitory circuits in the cortex and provides new insights into the structural and molecular synaptic impairment caused by NRG1 hypofunction in a preclinical model of SZ.

Haploinsufficiency

neuregulin 1

ERBB4

10.1016/j.nbd.2021.105442

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Citations (12)

Ca2+-modulated photoactivatable imaging reveals neuron-astrocyte glutamatergic circuitries within the nucleus accumbens

Nature Communications (2022)

Irene Serra Julio Esparza Laura Delgado C. Martín Margalida Puigròs

Astrocytes are key elements of brain circuits that are involved in different aspects of the neuronal physiology relevant to brain functions. Although much effort is being made to understand how the biology of astrocytes affects brain circuits, astrocytic network heterogeneity and plasticity is still poorly defined. Here, we have combined structural and functional imaging of astrocyte activity recorded in mice using the Ca2+-modulated photoactivatable ratiometric integrator and specific optostimulation of glutamatergic pathways to map the functional neuron-astrocyte circuitries in the nucleus accumbens (NAc). We showed pathway-specific astrocytic responses induced by selective optostimulation of main inputs from the prefrontal cortex, basolateral amygdala, and ventral hippocampus. Furthermore, co-stimulation of glutamatergic pathways induced non-linear Ca2+-signaling integration, revealing integrative properties of NAc astrocytes. All these results demonstrate the existence of specific neuron-astrocyte circuits in the NAc, providing an insight to the understanding of how the NAc integrates information.

Basolateral amygdala

Biological neural network

10.1038/s41467-022-33020-6

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Astrocytic p38α MAPK drives NMDA receptor-dependent long-term depression and modulates long-term memory

Nature Communications (2019)

Marta Navarrete María Isabel Cuartero Rocío Palenzuela Jonathan E. Draffin Ainoa Konomi

Abstract NMDA receptor-dependent long-term depression (LTD) in the hippocampus is a well-known form of synaptic plasticity that has been linked to different cognitive functions. The core mechanism for this form of plasticity is thought to be entirely neuronal. However, we now demonstrate that astrocytic activity drives LTD at CA3-CA1 synapses. We have found that LTD induction enhances astrocyte-to-neuron communication mediated by glutamate, and that Ca 2+ signaling and SNARE-dependent vesicular release from the astrocyte are required for LTD expression. In addition, using optogenetic techniques, we show that low-frequency astrocytic activation, in the absence of presynaptic activity, is sufficient to induce postsynaptic AMPA receptor removal and LTD expression. Using cell-type-specific gene deletion, we show that astrocytic p38α MAPK is required for the increased astrocytic glutamate release and astrocyte-to-neuron communication during low-frequency stimulation. Accordingly, removal of astrocytic (but not neuronal) p38α abolishes LTD expression. Finally, this mechanism modulates long-term memory in vivo.

Long-term depression

10.1038/s41467-019-10830-9

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Citations (82)

Novel Ca2+-modulated Photoactivatable Imaging Reveals Neuron-Astrocyte Glutamatergic Circuitries within the Nucleus Accumbens

Research Square (Research Square) (2021)

Irene Serra Julio Esparza Laura Milena Rueda Delgado C. Martín Margalida Puigròs

Abstract Astrocytes are key elements of brain circuits that are involved in different aspects of the neuronal physiology relevant to brain functions. Although much effort is being made to understand how the biology of astrocytes affects brain circuits, astrocytic network heterogeneity and plasticity is still poorly defined. Here, we have combined structural and functional imaging of astrocyte activity using the Ca 2+ -modulated photoactivatable ratiometric integrator and specific optostimulation of glutamatergic pathways to map the functional neuron-astrocyte circuitries in the nucleus accumbens (NAc). We showed pathway-specific astrocytic responses induced by selective optostimulation of main inputs from the prefrontal cortex, basolateral amygdala, and ventral hippocampus. Furthermore, the differences in basal Ca 2+ dynamics between the NAc shell and core astrocytes were associated with differences in mitochondrial DNA copy number, exhibiting molecular heterogeneity in the regulation of their mitochondrial genomes. Finally, co-stimulation of glutamatergic pathways induced non-linear Ca 2+ -signaling integration, revealing integrative properties of NAc astrocytes. All these results demonstrate the existence of specific neuron-astrocyte circuits in the NAc, a critical insight to the understanding of how the NAc integrates information.

Basolateral amygdala

Biological neural network

10.21203/rs.3.rs-956625/v1

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Astrocyte ensembles manipulated with AstroLight tune cue-motivated behavior

Nature Neuroscience (2025)

Irene Serra C. Martín Javier Sánchez Romero Juan Pablo Quintanilla Danny Ganchala

Neuroscientist

Systems neuroscience

10.1038/s41593-025-01870-0

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A specific prelimbic-nucleus accumbens pathway controls resilience versus vulnerability to food addiction

Nature Communications (2020)

Laura Domingo‐Rodriguez Iñigo Ruı́z de Azúa Eduardo Dominguez Eric Senabre Irene Serra

Abstract Food addiction is linked to obesity and eating disorders and is characterized by a loss of behavioral control and compulsive food intake. Here, using a food addiction mouse model, we report that the lack of cannabinoid type-1 receptor in dorsal telencephalic glutamatergic neurons prevents the development of food addiction-like behavior, which is associated with enhanced synaptic excitatory transmission in the medial prefrontal cortex (mPFC) and in the nucleus accumbens (NAc). In contrast, chemogenetic inhibition of neuronal activity in the mPFC-NAc pathway induces compulsive food seeking. Transcriptomic analysis and genetic manipulation identified that increased dopamine D2 receptor expression in the mPFC-NAc pathway promotes the addiction-like phenotype. Our study unravels a new neurobiological mechanism underlying resilience and vulnerability to the development of food addiction, which could pave the way towards novel and efficient interventions for this disorder.

10.1038/s41467-020-14458-y

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Citations (89)