- Neurotransmitter Receptor Influence on Behavior
- Neuroscience and Neuropharmacology Research
- Treatment of Major Depression
- Receptor Mechanisms and Signaling
- Tryptophan and brain disorders
- Memory and Neural Mechanisms
- Stress Responses and Cortisol
- Neurological disorders and treatments
- Circadian rhythm and melatonin
- Sleep and Wakefulness Research
- Photoreceptor and optogenetics research
- Bipolar Disorder and Treatment
- Nicotinic Acetylcholine Receptors Study
- Functional Brain Connectivity Studies
- Neuroendocrine regulation and behavior
- Chemical synthesis and alkaloids
- Neurogenesis and neuroplasticity mechanisms
- Pharmacological Receptor Mechanisms and Effects
- Neuropeptides and Animal Physiology
- Neuroinflammation and Neurodegeneration Mechanisms
- Psychedelics and Drug Studies
- Transcranial Magnetic Stimulation Studies
- Schizophrenia research and treatment
- Retinal Development and Disorders
- Ion channel regulation and function
Institut Cellule Souche et Cerveau
2016-2025
Inserm
2016-2025
Université Claude Bernard Lyon 1
2015-2024
Pitié-Salpêtrière Hospital
2017
Sorbonne Université
2017
Assistance Publique – Hôpitaux de Paris
2017
Lundbeck (United States)
2016
Lundbeck (Denmark)
2016
Virginia Commonwealth University
2016
University of Michigan–Ann Arbor
2016
Tetanus-induced heterosynaptic depression in the hippocampus is a key cellular mechanism neural networks implicated learning and memory. A growing body of evidence indicates that glial cells are important modulators synaptic functions, but very little known about their role plasticity. We examined depression, knowing tetanization NMDA application caused field responses (fEPSPs) induced Ca 2+ rise cells. Here we report chelating syncytium interfered with NMDA-induced fEPSP suggesting...
We report here the first direct functional evidence of an increase in tonic activation postsynaptic 5-HT1A receptors by antidepressant treatments. Because receptor hyperpolarizes and inhibits CA3 pyramidal neurons dorsal hippocampus, we determined, using vivo extracellular recording, whether selective antagonist WAY 100635 could disinhibit these neurons. Unexpectedly, no disinhibition be detected controls. However, after long-term treatment with tricyclic imipramine, 5-HT reuptake inhibitor...
At the present time, no viable treatment exists for cognitive and olfactory deficits in Down syndrome (DS). We show a DS model (Ts65Dn mice) that these progressive nonreproductive neurological symptoms closely parallel postpubertal decrease hypothalamic as well extrahypothalamic expression of master molecule controls reproduction-gonadotropin-releasing hormone (GnRH)-and appear related to an imbalance microRNA-gene network known regulate GnRH neuron maturation together with altered...
Brief summary: This study identified a new role for GnRH in higher brain function using rodent model of Down Syndrome. It reports the first time an improvement cognitive functions patients with Syndrome treated pulsatile GnRH.
1. The aim of the present study was to investigate putative modulation locus coeruleus (LC) noradrenergic (NA) neurones by 5-hydroxytryptaminergic (5-HT) system use in vivo extracellular unitary recordings and microiontophoresis anaesthetized rats. To this end, potent selective 5-HT1A receptor antagonist WAY 100635 (N-[2-[4(2-methoxyphenyl)-1-piperazinyl]-N-(2-pyridinyl) cyclohexanecarboxamide trihydroxychloride) used. 2. In dorsal hippocampus, both local (by microiontophoresis, 20 nA)...
Mirtazapine ([(+/-)-MIR], Remeron, ORG 3770) is an alpha-2 adrenoceptor antagonist endowed with antidepressant activity in humans. The aim of the present study was to assess effects (+/-)-MIR and its (-)enantiomer [(-)-MIR] on pre- postsynaptic adrenoceptors characterize their putative modulation 5-HT neurotransmission. (25 micrograms/kg i.v.) enhanced effectiveness electrical stimulation ascending pathway by blocking both adrenergic auto- heteroreceptors. (-)-MIR (10 these stimulations due...
Serotonin (5-HT)3 receptors are the only ligand-gated ion channel of 5-HT family. They present both in peripheral and central nervous system localized several areas involved mood regulation (e.g., hippocampus or prefrontal cortex). Moreover, they neurotransmitter systems implicated pathophysiology major depression dopamine GABA). Clinical preclinical studies have suggested that 5-HT3 may be a relevant target treatment affective disorders. receptor agonists seem to counteract effects...
Abstract The therapeutic effect of current antidepressant drugs appears after several weeks treatment and a significant number patients do not respond to treatment. Here, we report the effects multi-modal vortioxetine (Lu AA21004), 5-HT3 5-HT7 receptor antagonist, 5-HT1B partial agonist, 5-HT1A agonist 5-HT transporter (SERT) inhibitor, on rat neurotransmission. Using in vivo electrophysiological recordings dorsal raphe nucleus anaesthetized rats, assessed acute subchronic and/or selective...
Although deep brain stimulation (DBS) shows promising efficacy as a therapy for intractable depression, the neurobiological bases underlying its therapeutic action remain largely unknown. The present study was aimed at characterizing effects of infralimbic prefrontal cortex (IL-PFC) DBS on several pre-clinical markers antidepressant-like response and investigating putative non-neuronal mechanism action. We found that induced an prevented by IL-PFC neuronal lesion adenosine A1 receptor...
Abstract Background Recent clinical trials reveal that serotonergic psychedelics, including the prototypical hallucinogen lysergic acid diethylamide (LSD), present a promising potential for treating psychiatric disorders, treatment-resistant depression. LSD is potent 5-HT receptors ligand endowed with high affinity most of all subtypes and regularly used as valuable pharmacological tool to characterize 5-HT1A 5-HT2A receptor mediations [1]. Notably, crystal structure in complex human 5-HT2B...
Background:Recent studies revealed that bipolar disorder may be associated with deficits of neuroplasticity. Additionally, accumulating evidence has implicated alterations the intracellular signaling molecule protein kinase C (PKC) in mania.