Biology subjects

Espinosa, P.

Publications and source records attributed to Espinosa, P..

3 recordsLinked to original sources

bioRxiv2022

Insular cortex to ventral striatum synapses encode valence of social interaction

The nature of social interactions determines engagement or avoidance with conspecifics. Here, we explore the circuit mechanisms that guide approach or avoidance behavior in mice based on the valence of previous social interactions. We identify a novel circuit connecting D1 receptor expressing neurons of the anterior insular cortex (AIC) to D1R expressing neurons of the nucleus accumbens (NAc). These cells become active during social interactions in a valence-dependent manner. Lower frequency patterns encoded appetitive interactions, while aversive interactions led to higher activation. These activity patterns elicited distinct forms of synaptic plasticity in the accumbal target neurons, which were causal for subsequent approach or avoidance behavior. Our results unravel the synaptic mechanisms instructing behavior after the social interaction of opposite valence.

neuroscience↗

bioRxiv2021

Optogenetic stimulation of BLA terminals in the BNST elicits long term synaptic plasticity and restores synaptic alterations induced by adolescent Shank3 downregulation

Anxiety disorders are the most prevalent co-morbidity factor associated with the core domains of Autism Spectrum Disorders (ASD). Investigations on potential common neuronal mechanisms that may explain the co-occurrence of ASD and anxiety disorders are still poorly unexplored. One of the key questions which remained unsolved is the role of Shank3 protein in anxiety behaviors. Here we used shRNA strategy to model Shank3 insufficiency in the bed nucleus of the stria terminalis (BNST). We found that Shank3 downregulation in the BNST induced anxiogenic effects. Associated with these behavioural defects, we showed alteration of glutamatergic synaptic functions in the BNST induced by Shank3 insufficiency during adolescence. In addition, we pointed that adolescence represents a crucial time window to interfere with BNST maturation, a key hub for anxiety control. Together, these results unravelled the crucial role of Shank3 expression in the BNST during adolescence. Our study provided a new insight in the neuronal mechanisms underlying anxiety disorders. We proposed to screen a novel molecular target essential for BNST integrity during adolescence. This result may further help for the diagnosis and the development of therapeutic strategy for anxiety disorders and anxiety disorders implicated in some forms of ASD.

neuroscience↗

bioRxiv2019

Deficit in motor skill learning-dependent synaptic plasticity at motor cortex to Dorso Lateral Striatum synapses in a mouse model of Huntington's disease

Huntington's disease (HD) is a neurodegenerative disease notably characterized by progressive motor symptoms. Although the loss of Medium Spiny Neurons (MSNs) in the striatum has been associated with motor deficits, premanifest patients already present cognitive deficiencies and show early signs of motor disabilities. Here in a YAC128 HD mouse model, we identified impairment in motor skill learning at the age of 11 to 14 weeks. Using optogenetic stimulation, we found that excitatory synaptic transmission from motor cortex to MSNs located in the Dorso Lateral part of the Striatum (DLS) is altered. Using single pellet reaching task, we observed that while motor skill learning is accompanied by a dynamic change in AMPA/NMDA ratio in wild type mice, this form of synaptic plasticity does not occur in YAC128 mice. This study not only proposes new meaningful insight the synaptopathic mechanisms of HD, but also highlights that deficit in motor skill learning dependent synaptic plasticity at motor cortex to DLS synapses represents an early biomarker for Huntington's disease.

neuroscience↗