A5021236252- Neuroscience and Neuropharmacology Research
- Amyotrophic Lateral Sclerosis Research
- Stress Responses and Cortisol
- Tryptophan and brain disorders
- Neurogenetic and Muscular Disorders Research
- Parkinson's Disease Mechanisms and Treatments
- Amino Acid Enzymes and Metabolism
- Cholinesterase and Neurodegenerative Diseases
- Genetic Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- biodegradable polymer synthesis and properties
- Biochemical Acid Research Studies
- Neuroscience and Neural Engineering
- Neurogenesis and neuroplasticity mechanisms
- Photoreceptor and optogenetics research
- Mitochondrial Function and Pathology
- Ion channel regulation and function
- Receptor Mechanisms and Signaling
- Nerve injury and regeneration
- RNA regulation and disease
- Neural dynamics and brain function
- Anesthesia and Neurotoxicity Research
- Spinal Cord Injury Research
- Mesenchymal stem cell research
- Genetics and Neurodevelopmental Disorders
University of Genoa
2015-2024
University of Pisa
2022-2024
University of Milan
2012-2022
European University of Rome
2022
University of Milano-Bicocca
2022
Background Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases. Converging evidence suggested that acute associated with increase of excitatory transmission in certain forebrain areas. Aim this work was to investigate the mechanism whereby increases glutamate release, and if therapeutic drugs prevent effect on release. Methodology/Findings Rats were chronically treated vehicle or employed therapy mood/anxiety disorders (fluoxetine, desipramine, venlafaxine,...
Despite some advances in the understanding of amyotrophic lateral sclerosis (ALS) pathogenesis, significant achievements treating this disease are still lacking. Mesenchymal stromal (stem) cells (MSCs) have been shown to be effective several models neurological disease. To determine effects intravenous injection MSCs an ALS mouse model during symptomatic stage disease, (1 × 106) were intravenously injected mice expressing human superoxide dismutase 1 (SOD1) carrying G93A mutation (SOD1/G93A)...
Depression is a debilitating mental disease, characterized by persistent low mood and anhedonia. Stress represents major environmental risk factor for depression; the complex interaction of stress with genetic factors results in different individual vulnerability or resilience to disorder. Dysfunctions glutamate system have primary role depression. Clinical neuroimaging studies consistently reported alterations volume connectivity cortico-limbic areas, where neurons synapses predominate....
Abstract The Excitatory Amino Acid Transporter 2 (EAAT2) accounts for 80% of brain glutamate clearance and is mainly expressed in astrocytic perisynaptic processes. EAAT2 function finely regulated by endocytic events, recycling to the plasma membrane degradation. Noteworthy, deficits have been associated with neuronal excitotoxicity neurodegeneration. In this study, we show that trafficking impaired leucine-rich repeat kinase (LRRK2) pathogenic variant G2019S, a common cause late-onset...
Stress represents a major risk factor for psychiatric disorders, including post-traumatic stress disorder (PTSD). Recently, we dissected the destabilizing effects of acute on excitatory glutamate system in prefrontal cortex (PFC). Here, assessed single subanesthetic administration ketamine (10 mg/kg) transmission and dendritic arborization PFC footshock (FS)-stressed rats, along with changes depressive, anxious, fear extinction behaviors. We found that ketamine, while inducing mild increase...
Abstract Stress affects the brain and alters its neuroarchitecture function; these changes can be severe lead to psychiatric disorders. Recent evidence suggests that astrocytes microglia play an essential role in stress response by contributing maintenance of cerebral homeostasis. These cells respond rapidly all stimuli reach brain, including stressors. Here, we used a recently validated rodent model post-traumatic disorder which rats categorized as resilient or vulnerable after acute...
J. Neurochem . (2011) 116 , 1028–1042. Abstract Glutamate‐mediated excitotoxicity plays a major role in the degeneration of motor neurons amyotrophic lateral sclerosis and reduced astrocytary glutamate transport, which turn increases synaptic availability amino acid neurotransmitter, was suggested as cause. Alternatively, here we report our studies on exocytotic release possible source excessive transmission. The basal efflux from spinal cord nerve terminals mice‐expressing human soluble...
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons (MN). Importantly, MN degeneration intimately linked to oligodendrocyte dysfunction and impaired capacity precursor cells (OPCs) regenerate the myelin sheath enwrapping protecting neuronal axons. Thus, improving OPC reparative abilities represents an innovative approach counteract loss. A pivotal regulator maturation P2Y-like G protein-coupled receptor 17 (GPR17), whose role...
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with no effective cure. Astrocytes display toxic phenotype in ALS and contribute to motoneuron (MN) degeneration. Modulating astrocytes' neurotoxicity can reduce MN death. Our previous studies showed the beneficial effect of mesenchymal stem cell (MSC) administration SOD1G93A mice, but mechanisms are still unclear. We postulated that effects could be mediated by extracellular vesicles (EVs) secreted MSCs. investigated,...
Amyotrophic lateral sclerosis (ALS) is a late-onset fatal neurodegenerative disease reflecting degeneration of upper and lower motoneurons (MNs). The cause ALS the mechanisms neuronal death are still largely obscure, thus impairing establishment efficacious therapies. Glutamate (Glu)-mediated excitotoxicity plays major role in MN ALS. We recently demonstrated that activation Group I metabotropic Glu autoreceptors, belonging to both type 1 5 receptors (mGluR1 mGluR5), at glutamatergic spinal...
Abstract Stress represents a main risk factor for psychiatric disorders. Whereas it is known that even single trauma may induce disorders in humans, the mechanisms of vulnerability to acute stressors have been little investigated. In this study, we generated new animal model resilience/vulnerability footshock (FS) stress rats and analyzed early functional, molecular, morphological determinants at tripartite glutamate synapses prefrontal cortex (PFC). We found adult male subjected FS can be...
Abstract Background Agomelatine is a melatonergic receptor agonist and 5HT 2C antagonist that has shown antidepressant efficacy. In order to analyze separately the effect of two receptorial components, rats were chronically treated with agomelatine, melatonin (endogenous agonist), or S32006 (5-HT antagonist), then subjected acute footshock-stress. Results Only chronic but not S32006, completely prevented stress-induced increase glutamate release in rat prefrontal/frontal cortex. Conclusions...
Background: Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases.Converging evidence suggested that acute associated with increase of excitatory transmission in certain forebrain areas.Aim this work was to investigate the mechanism whereby increases glutamate release, and if therapeutic drugs prevent effect on release.Methodology/Findings: Rats were chronically treated vehicle or employed therapy mood/anxiety disorders (fluoxetine, desipramine, venlafaxine,...
Abstract Background and Purpose Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive motor neuron (MN) loss consequent muscle atrophy, for which no effective therapies are available. Recent findings reveal that disease progression fuelled early aberrant neuroinflammation the of oligodendrocytes with neuroprotective remyelinating properties. On this basis, pharmacological interventions capable restoring pro‐regenerative local milieu...
The effect of GABA on glutamate release from astrocytes has been studied in healthy mice and a murine transgenic model amyotrophic lateral sclerosis (ALS), using mouse spinal cord gliosomes labeled with [(3)H]d-aspartate ([(3)H]d-ASP). concentration-dependently evoked the [(3)H]d-ASP. was not mimicked by GABA(A) or GABA(B) receptor agonists counteracted antagonists, excluding involvement. However, it prevented transport inhibitor N-(4,4-phenyl-3-butenyl)-nipecotic acid (SKF 89976A),...
Abstract Background Growing compelling evidence from clinical and preclinical studies has demonstrated the primary role of alterations glutamatergic transmission in cortical limbic areas pathophysiology mood disorders. Chronic antidepressants have been shown to dampen endogenous glutamate release rat hippocampal synaptic terminals prevent marked increase overflow induced by acute behavioral stress frontal/prefrontal cortex. Agomelatine, a new antidepressant endowed with MT1/MT2 agonist 5-HT...
Abstract Amyotrophic lateral sclerosis is an adult‐onset neurodegenerative disease that develops because of motor neuron death. Several mechanisms occur supporting neurodegeneration, including mitochondrial dysfunction. Recently, we demonstrated the synaptosomes from spinal cord SOD1 G93A mice, in vitro model presynapses, displayed impaired metabolism at early pre‐symptomatic stages disease, whereas perisynaptic astrocyte particles, or gliosomes, were characterized by mild energy impairment...