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Glangetas, C.

Publications and source records attributed to Glangetas, C..

4 recordsLinked to original sources

A subset of dorsal raphe dopamine neurons is critical for survival-oriented vigilance.

Defensive behaviors are essential for survival, with risk assessment enabling organisms to evaluate and respond to potential threats. The dorsal raphe nucleus (DRN), a key neuromodulatory center, is crucial for encoding motivational salience and regulating arousal and sleep-wake states through its diverse neuronal populations, including dopaminergic neurons (DRNDA). While the roles of DRNDA neurons have been studied, their specific contributions to threat evaluation are less understood. Recent research identifies a distinct subset of DRNDA neurons that express vasoactive intestinal peptide (VIP) and project to the central amygdala (CeA) and the oval nucleus of the bed nucleus of the stria terminalis (ovBNST). Together, these two regions comprise the central extended amygdala, a key network regulating adaptive responses to threats. We hypothesized that distinct DRNDA subpopulations exert diverging effects on sleep-wake regulation and that DRNVIP neurons play a pivotal role in coordinating activity between the CeA and ovBNST, thereby influencing risk assessment and defensive response. To test this hypothesis, we used a combination of in situ hybridization, immunochemistry, whole-brain mapping, electrophysiology, and cell-specific genetic tools in mice and non-human primates. Our findings reveal that DRNVIP neurons form a key DRNDA neuronal subset, uniquely positioned to regulate the central extended amygdala through a feedback loop. These neurons receive inputs from Protein Kinase C delta (PKC-{delta}) neurons in the ovBNST and CeA and send glutamate-releasing projections back to these regions, modulating PKC-{delta} neuron excitability. Selective ablation of DRNVIP neurons increases activity in both the BNST and CeA, disrupting active-phase sleep architecture and impairing risk assessment and defensive behaviors. Together, these findings suggest DRNVIP neurons control specific phases of sleep and orchestrate the central extended amygdalas role in risk assessment and defensive responses. HIGHLIGHTSO_LIDRNVIP neurons form a subset of DRNDA neurons in mice and non-human primates. C_LIO_LIDRNVIP receive inputs from Protein Kinase C delta (PKC-{delta}) neurons in the ovBNST and CeA and project back to both. C_LIO_LIBy releasing glutamate, DRNVIP neurons regulate PKC-{delta} neuron excitability in the ovBNST and CeA. C_LIO_LIAblating DRNVIP neurons increases BNST and CeA activity, disrupts active-phase sleep architecture, and impairs threat responses. C_LI IN BRIEFDRNVIP neurons, a key subset of DRNDA neurons in mice and primates, are strategically positioned to influence the central extended amygdala via feedback loops. They regulate PKC-{delta} neuron excitability in the ovBNST and CeA through glutamate release, with their ablation heightening activity in these regions and altering active-phase sleep architecture, risk assessment and defensive behaviors.

neuroscience↗

Encoding social preference by interhemispheric neurons in the Insula

The Insula is a multisensory relay that participates in socio-emotional processing through multiple projections to sensory, cognitive, emotional, and motivational regions. Interestingly, the Insula interhemispheric projection to the contralateral Insula is a strong but understudied projection. Using cutting-edge neuroanatomy, ex vivo and in vivo electrophysiology associated with specific circuit manipulation, we unraveled the nature and role of Insula interhemispheric communication in social and anxiety processing in mice. In this study, we 1) characterized the anatomical and molecular profile of the interhemispheric neurons of the Insula, 2) highlighted that stimulation of this neuronal subpopulation triggers excitation in the Insula interhemispheric circuit 3) uncovered their engagement in social processing. In conclusion, this study demonstrates that interhemispheric neurons of the Insula constitute a unique class of Insula neurons and proposes new meaningful insights into the neuronal mechanisms underlying social behavior.

neuroscience↗

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↗

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↗