A5015556586- Neuroscience and Neuropharmacology Research
- Parkinson's Disease Mechanisms and Treatments
- Neurological disorders and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Receptor Mechanisms and Signaling
- Ion channel regulation and function
- Neurotransmitter Receptor Influence on Behavior
- Alzheimer's disease research and treatments
- Neuroscience and Neural Engineering
- Multiple Sclerosis Research Studies
- Estrogen and related hormone effects
- Menopause: Health Impacts and Treatments
- Genetics and Neurodevelopmental Disorders
- Genetic Neurodegenerative Diseases
- Adenosine and Purinergic Signaling
- Autism Spectrum Disorder Research
- Neurogenesis and neuroplasticity mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Neural dynamics and brain function
- Ion Channels and Receptors
- Memory and Neural Mechanisms
- Nuclear Receptors and Signaling
- Epilepsy research and treatment
- Nitric Oxide and Endothelin Effects
- Trigeminal Neuralgia and Treatments
University of Perugia
2015-2025
Fondazione Santa Lucia
2010-2019
Istituti di Ricovero e Cura a Carattere Scientifico
2009-2019
Ospedale San Giuseppe
2018
Azienda Ospedaliera di Perugia
2006-2014
Ospedale Santa Maria
2012-2014
European Brain Research Institute
2010
Bambino Gesù Children's Hospital
2009
University Gastroenterology
2008
University of Naples Federico II
2007
A(2A) adenosine receptor antagonists are currently under investigation as potential therapeutic agents for Parkinson's disease (PD). However, the molecular mechanisms underlying this effect is still unclear. A functional antagonism exists between and D(2) dopamine (DA) receptors that coexpressed in striatal medium spiny neurons (MSNs) of indirect pathway. Since interaction could also occur other neuronal subtypes, we have analyzed pharmacological modulation relationship murine MSNs direct...
The discovery of the molecular mechanisms regulating abundance synaptic NMDA receptors is essential for understanding how plasticity, as well excitotoxic events, are regulated. However, a complete precise composition receptor complex at hippocampal synapse still missing. Here, we show that 2 h CaMKII inhibition leads to specific reduction NR2B-containing without affecting localization NR2A subunit; this event accompanied by dramatic in induction long-term potentiation (LTP), while depression...
Although patients with Parkinson's disease show impairments in cognitive performance even at the early stage of disease, synaptic mechanisms underlying impairment this pathology are unknown.Hippocampal long-term potentiation represents major experimental model for changes learning and memory is controlled by endogenous dopamine.We found that hippocampal altered both a neurotoxic transgenic plastic alteration associated an impaired dopaminergic transmission decrease NR2A/NR2B subunit ratio...
The aim of the present study was to evaluate role nitric oxide/cyclic guanosine monophosphate pathway in corticostriatal long-term depression induction a model levodopa-induced dyskinesia experimental parkinsonism. Moreover, we have also analysed possibility targeting striatal phosphodiesterases reduce dyskinesia. To synaptic plasticity sham-operated rats and 6-hydroxydopamine lesioned animals chronically treated with therapeutic doses levodopa, recordings from spiny neurons were taken using...
Background Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or A53T missense mutation of presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically preferential vulnerability dopaminergic nigrostriatal projection neurons. Methodology/Principal Findings Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in absence neurodegeneration to understand early...
Cortical spreading depression (CSD) is a key pathogenetic step in migraine with aura. Dysfunctions of voltage-dependent and receptor-operated channels have been implicated the generation CSD pathophysiology migraine. Although known correlation exists between release calcitonin gene-related peptide (CGRP), possibility that CGRP involved has not examined detail. We analyzed pharmacological mechanisms underlying investigated endogenous contributes to this phenomenon. was rat neocortical slices...
Altered synaptic function is considered one of the first features Alzheimer disease (AD). Currently, no treatment available to prevent dysfunction excitatory synapses in AD. Identification key modulators synaptopathy particular significance We here characterized pathways leading TgCRND8 mice and showed that c-Jun N-terminal kinase (JNK) activated at spine prior onset cognitive impairment. The specific inhibition JNK, with its inhibiting peptide D-JNKI1, prevented mice. D-JNKI1 avoided both...
Parkinson's disease is a progressive neurodegenerative disorder characterized by altered striatal dopaminergic signalling that leads to motor and cognitive deficits. also abnormal presence of soluble toxic forms α-synuclein that, when clustered into Lewy bodies, represents one the pathological hallmarks disease. However, oligomers might directly affect synaptic transmission plasticity in models. Accordingly, combining electrophysiological, optogenetic, immunofluorescence, molecular...
Abstract Misfolding and aggregation of α-synuclein are specific features Parkinson’s disease other neurodegenerative diseases defined as synucleinopathies. progression has been correlated with the formation extracellular release aggregates, well their spread from neuron to neuron. Therapeutic interventions in initial stages require a clear understanding mechanisms by which disrupts physiological synaptic plastic activity basal ganglia. For this reason, we identified two early time points...
Cognitive impairment (CI) is a disabling concomitant of multiple sclerosis (MS) with complex and controversial pathogenesis. The cytokine interleukin-17A (IL-17A) involved in the immune pathogenesis MS, but its possible effects on synaptic function cognition are still largely unexplored. In this study, we show that IL-17A receptor (IL-17RA) highly expressed by hippocampal neurons CA1 area exposure to dose-dependently disrupts long-term potentiation (LTP) through activation p38...
Abstract We investigated the involvement of store‐operated channels (SOCs) and transient receptor potential (TRP) in response to activation group I metabotropic glutamate subtype 1 (mGluR1) with agonist (S)‐3,5‐dihydroxyphenylglycine (DHPG, puff application) dopamine neurons rat brain slices. The mGluR1‐induced conductance reversed polarity close 0 mV at more positive potentials when extracellular potassium concentrations were increased, indicating a cationic channel. DHPG currents but not...
Abstract Cognitive impairment is common in multiple sclerosis (MS). Unfortunately, the synaptic and molecular mechanisms underlying MS-associated cognitive dysfunction are largely unknown. We explored presence mechanism of hippocampal during remission phase experimental MS. Experiments were performed a chronic-relapsing autoimmune encephalomyelitis (EAE) model MS, after resolution motor deficits. Immunohistochemistry patch-clamp recordings CA1 area. The hole-board was utilized as...
Ischemic stroke is one of the leading causes morbidity and mortality. Treatment options are limited only a minority patients receive acute interventions. Understanding mechanisms that mediate neuronal injury death may identify targets for neuroprotective treatments. Here we show aberrant activity protein kinase Cdk5 principal cause in rodents during stroke. Ischemia induced either by embolic middle cerebral artery occlusion (MCAO) <i>in vivo</i> or oxygen glucose deprivation brain slices...
Alzheimer disease (AD) is characterized by cognitive impairment that starts with memory loss to end in dementia. Loss of synapses and synaptic dysfunction are closely associated AD patients. Biochemical pathological evidence suggests soluble Aβ oligomers correlate impairment. Here, we used the TgCRND8 mouse model investigate role JNK long term deficits. mice were chronically treated cell-penetrating c-Jun N-terminal kinase inhibitor peptide (D-JNKI1). D-JNKI1, preventing action, completely...