A5046898516- Neuroscience and Neuropharmacology Research
- Botulinum Toxin and Related Neurological Disorders
- Neurological disorders and treatments
- Retinal Development and Disorders
- Neural dynamics and brain function
- Visual perception and processing mechanisms
- Hereditary Neurological Disorders
- Cellular transport and secretion
- Transcranial Magnetic Stimulation Studies
- Neurogenesis and neuroplasticity mechanisms
- Lipid Membrane Structure and Behavior
- Alzheimer's disease research and treatments
- Advanced Neuroimaging Techniques and Applications
- Photoreceptor and optogenetics research
- Nerve injury and regeneration
- Glaucoma and retinal disorders
- Functional Brain Connectivity Studies
- Spinal Dysraphism and Malformations
- Olfactory and Sensory Function Studies
- Biochemical and Structural Characterization
- Prion Diseases and Protein Misfolding
- Genetics and Neurodevelopmental Disorders
- Ophthalmology and Visual Impairment Studies
- Neuroscience and Neural Engineering
- Pain Mechanisms and Treatments
Neuroscience Institute
2015-2024
National Research Council
2013-2024
National Academies of Sciences, Engineering, and Medicine
2012-2020
Istituti di Ricovero e Cura a Carattere Scientifico
2019
University of Milan
2019
University of Würzburg
2019
UiT The Arctic University of Norway
2019
Northwestern University
2019
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2019
University of Minho
2019
The striking differences between the clinical symptoms of tetanus and botulism have been ascribed to different fate parental neurotoxins once internalised in motor neurons. Tetanus toxin (TeNT) is known undergo transcytosis into inhibitory interneurons block release neurotransmitters spinal cord, causing a spastic paralysis. In contrast, botulinum (BoNTs) acetylcholine at neuromuscular junction, therefore inducing flaccid Whilst overt experimental evidence supports sorting TeNT axonal...
Botulinum neurotoxin type A (BoNT/A) is a metalloprotease that blocks synaptic transmission via the cleavage of SNAP-25 (synaptosomal-associated protein 25 kDa). BoNT/A successfully used in clinical neurology for treatment several neuromuscular pathologies and pain syndromes. Despite its widespread use, relatively little known on intracellular trafficking neurons. Using visual pathway as model system, here we show catalytically active capable undergoing anterograde axonal transport...
Early life experiences can affect brain development, contributing to shape interindividual differences in stress vulnerability and anxiety-like behavior. In rodents, high levels of maternal care have long-lasting positive effects on the behavior offspring response; post-weaning rearing an enriched environment (EE) or massage counteract negative separation prenatal stressors. We recently found that insulin-like growth factor 1 (IGF-1) is a key mediator early EE development. Whether enrichment...
The widely used botulinum neurotoxin A (BoNT/A) blocks neurotransmission via cleavage of the synaptic protein SNAP-25 (synaptosomal-associated 25 kDa). Recent evidence demonstrating long-distance propagation proteolysis has challenged idea that BoNT/A remains localized to injection site. However, extent which distant neuronal networks are impacted by retrograde trafficking unknown. Importantly, no studies have addressed whether translates into structural and functional changes in intoxicated...
Key points Transcription factors at the basis of plasticity in adult visual system are unknown. Enhanced levels NPAS4 transcription factor parallel cortical life. Overexpression restores cortex. down‐regulation prevents plastic outcome caused by fluoxetine (FLX) adulthood. regulates expression genes Abstract There is evidence that developmental‐like can be reactivated Although activity‐dependent underlying process reactivation currently unknown, recent studies point towards as a candidate...
Botulinum neurotoxin Type A (BoNT/A) is an effective treatment for several movement disorders, including spasticity and dystonia. BoNT/A acts by cleaving synaptosomal-associated protein of 25 kDa (SNAP-25) at the neuromuscular junction, thus blocking synaptic transmission weakening overactive muscles. However, not all therapeutic benefits are explained peripheral neuroparalysis, suggesting action on central circuits. Currently, specific targets activity remain unclear. Here, we show that...
Neural circuits in the cerebral cortex are shaped by experience during “critical periods” early life. For example, visual is immature at time of eye opening and gradually develops its functional properties a sensitive period. Very few reports have addressed role intrinsic neural activity cortical maturation. Here we exploited bacterial enzyme botulinum neurotoxin E (BoNT/E) to produce unilateral, reversible blockade rat BoNT/E highly selective protease that interferes with transmitter...
Ocular dominance (OD) plasticity triggered by monocular eyelid suture is a classic paradigm for studying experience-dependent changes in neural connectivity. Recently, rodents have become the most popular model studies of OD plasticity. It therefore important to determine how determined rodent primary visual cortex. In particular, cortical cells receive considerable inputs from contralateral hemisphere via callosal axons, but role these connections controlling eye preference remains...
The therapeutic potential of botulinum neurotoxin type A (BoNT/A) has recently been widely recognized. BoNT/A acts to silence synaptic transmission via specific proteolytic cleavage an essential neuronal protein, SNAP25. advantages BoNT/A-mediated silencing include very long duration, high potency and localized action. However, there is a fear possible side-effects due its diffusible nature which may lead neuromuscular blockade away from the injection site. We developed "protein-stapling"...
Clostridial neurotoxins reversibly block neuronal communication for weeks and months. While these proteolytic hold great promise clinical applications the investigation of brain function, their paralytic activity at neuromuscular junctions is a stumbling block. To redirect clostridial to populations other than motor neurons, we used new self-assembling method combine botulinum type A protease with tetanus binding domain, which natively targets central neurons. The two parts were produced...
Objective: Amblyopia is a neurodevelopmental disorder characterized by visual acuity and contrast sensitivity loss, refractory to pharmacological optical treatments in adulthood. In animals, the corpus callosum (CC) contributes suppression of responses amblyopic eye. To investigate role interhemispheric pathways patients, we studied response cortex transcranial Direct Current Stimulation (tDCS) applied over primary area (V1) contralateral "lazy eye." Methods: Visual (logMAR) was assessed...
In chronic neurodegenerative diseases associated with aggregates of misfolded proteins (such as Alzheimer's, Parkinson's and prion disease), there is an early degeneration presynaptic terminals prior to the loss neuronal somata. Identifying mechanisms that govern synapse paramount importance, cognitive decline strongly correlated in these disorders. However, very little known about processes link presence a protein synapses. It has been suggested process follows simple linear sequence which...
Oligophrenin-1 (Ophn1) encodes a Rho GTPase activating protein whose mutations cause X-linked intellectual disability (XLID) in humans. Loss of function Ophn1 leads to impairments the maturation and excitatory inhibitory synapses, causing deficits synaptic structure, plasticity. Epilepsy is frequent comorbidity patients with Ophn1-dependent XLID, but cellular bases hyperexcitability are poorly understood. Here we report that male mice knock-out (KO) for display hippocampal epileptiform...
Binocularity is a key property of primary visual cortex (V1) neurons that widely used to study synaptic integration in the brain and plastic mechanisms following an altered experience. However, it not clear how inputs from two eyes converge onto binocular neurons, their interaction modified by unbalanced drive. Here, using evoked potentials recorded juvenile rat V1, we report evidence for suppressive mechanism which contralateral eye activity inhibits responses ipsilateral eye. Accordingly,...