IRIS
BONIFACINO, TIZIANA
 Distribuzione geografica
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Continente #
EU - Europa 9.643
Totale 9.643
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Nazione #
IT - Italia 9.643
Totale 9.643
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Città #
Genova 6.178
Genoa 1.407
Rapallo 1.170
Vado Ligure 854
Bordighera 34
Totale 9.643
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Nome #
Genetic inactivation of mGlu5 receptor improves motor coordination in the Grm1crv4 mouse model of SCAR13 ataxia 164
Acute stress increases depolarization-evoked glutamate release and presynaptic SNARE complex accumulation in prefrontal/frontal cortex. The dampening action of antidepressants. 162
In-vivo effects of knocking-down metabotropic glutamate receptor 5 in the SOD1G93A mouse model of amyotrophic lateral sclerosis. 161
Blockade of stress-induced increase of glutamate release in the rat prefrontal/frontal cortex by agomelatine involves synergy between melatonergic and 5-HT2C receptor-dependent pathways 157
In-vivo genetic ablation of metabotropic glutamate receptor type 5 slows down disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis 155
Characterization of the Mitochondrial Aerobic Metabolism in the Pre- and Perisynaptic Districts of the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis 144
Altered mechanisms underlying the abnormal glutamate release in amyotrophic lateral sclerosis at a pre-symptomatic stage of the disease 143
Exocytosis regulates trafficking of GABA and glycine heterotransporters in spinal cord glutamatergic synapses: a mechanism for the excessive heterotransporter-induced release of glutamate in experimental amyotrophic lateral sclerosis. 138
Altered Mechanisms Underlying the Abnormal Glutamate Release in Amyotrophic Lateral Sclerosis at a Pre-Symptomatic Stage of the Disease. 133
Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF trafficking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine 131
Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes 130
The endocannabinoid system in rat gliosomes and its role in the modulation of glutamate release 125
Enriched experience and recovery from amblyopia in adult rats: impact of motor, social and sensory components. 122
Acute stress rapidly increases the readily releasable pool of glutamate vesicles in prefrontal and frontal cortex through non-genomic action of corticosterone 122
Group I metabotropic glutamate autoreceptors induce abnormal glutamate exocytosis in a mouse model of amyotrophic lateral sclerosis 122
Colocalization of neurotransmitter transporters on the plasma membrane of the same nerve terminal may reflect cotransmission. 121
Fluoxetine in adulthood normalizes GABA release and rescues hippocampal synaptic plasticity and spatial memory in a mouse model of Down Syndrome. 120
Abnormal exocytotic release of glutamate in a mouse model of amyotrophic lateral sclerosis 116
Differential expression of metabotropic glutamate and GABA receptors at neocortical glutamatergic and GABAergic axon terminals 115
Role of calpain-1 in the early phase of experimental ALS 112
Knocking down metabotropic glutamate receptor 1 improves survival and disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis 110
Abnormal exocytotic release of glutamate in a mouse model of amyotrophic lateral sclerosis. 107
Stress and corticosterone increase the readily releasable pool of glutamate vesicles in synaptic terminals of prefrontal and frontal cortex 105
Enhanced Function and Overexpression of Metabotropic Glutamate Receptors 1 and 5 in the Spinal Cord of the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis during Disease Progression 105
Glutamate release from astrocytic gliosomes under physiological and pathological conditions 103
Intravenous mesenchymal stem cells improve survival and motor functions in symptomatic mutant SOD1/G93A mice 101
Abnormal and precocious exocytotic glutamate release in a mouse model of amyotrophic lateral sclerosis 99
Increased [3H]D-aspartate release and changes in glutamate receptor expression in the hippocampus of the mnd mouse. 99
Ketamine modulates glutamate release, BDNF trafficking and dendrite morphology in rats vulnerable to chronic mild stress 99
Metabotropic glutamate receptor 5 as a potential target in ALS 99
mGluR1 and mGluR5 knock-down improves survival, motor skills and disease progression in amyotrophic lateral sclerosis mouse model 98
Acute stress rapidly increases the readily releasable pool of glutamate vesicles in prefrontal and frontal cortex through non-genomic action of corticosterone. 97
GroupI metabotropic glutamate autoreceptors induce abnormal glutamate exocytosis in a mouse model of amyotrophic lateral sclerosis 97
Synaptic mechanisms underlying the excessive and precocious glutamate release in the spinal cord of sod1g93a mice. 97
Knocking-down mGluR1 and mGluR5 in the SOD1/G93A mouse model of amyotrophic lateral sclerosis ameliorates survival and disease progression 97
Fluoxetine treatment promotes functional recovery in a rat model of cervical spinal cord injury 96
Intravenous Mesenchymal Stem Cells Improve Survival and Motor Function in Experimental Amyotrophic Lateral Sclerosis 93
Knocking-down mGlu1 receptors prolongs survival and ameliorates disease progression in the SOD1/G93A mouse model of ALS. 92
Acute stress and corticosterone increase the readily releasable pool of glutamatergic vesicles in rat synaptosomes of prefrontal/frontal cortex via mineralocorticoid and glucocorticoid receptors 91
Altered glucose catabolism in the presynaptic and perisynaptic compartments of SOD1G93A mouse spinal cord and motor cortex indicates that mitochondria are the site of bioenergetic imbalance in ALS 91
Targeting Group I Metabotropic Glutamate Receptors in Amyotrophic Lateral Sclerosis 90
Abnormal glutamate release in a mouse model of amyotrophic lateral sclerosis 87
GROUP I METABOTROPIC GLUTAMATE RECEPTORS AND NEUROTOXICITY IN AMYOTROPHIC LATERAL SCLEROSIS 86
Abnormal glutamate release in a mouse model of amyotrophic lateral sclerosis 84
Group I metabotropic glutamate receptors tune excitotoxicity in amyotrophic lateral sclerosis 84
Effect of miRNAs shuttled by exosomes derived from primed-MSCs on activated-microglia phenotype and possible implication in amyotrophic lateral sclerosis. 84
GLUTAMATE NEUROTRANSMISSION IS MODIFIED IN THE SOD1/G93A MOUSE MODEL OF ALS 83
Acute ketamine restores deficits in glutamate release and related molecular mechanisms induced by chronic mild stress in vulnerable rats 83
Astrocyte contribution to the excessive glutamate release in the spinal cord of the SOD1G93A mouse model of amyotrophic lateral sclerosis 82
Targeting group i metabotropic glutamate receptors in experimental als. 82
miRNAs shuttled by exosomes derived from primed-MSCs affect the activated-microglia phenotype and possibly support the therapeutic effects of MSC administration in SOD1G93A mice 81
Ketamine restores changes in glutamate release, dendrite morphology and BDNF trafficking in the hippocampus of rats vulnerable to chronic mild stress 81
Reducing the expression of mGlu1 and mGlu5 receptors ameliorates survival and disease progression in SOD1G93A mice 80
Excessive glutamate release and undelying synaptic mechanisms in a mouse model of amyotrophic lateral sclerosis 80
Amyotrophic lateral sclerosis and excitotoxicity: role of Group I metabotropic glutamate receptors 79
Knocking down mglu1 receptors prolongs survival and improves symptomatology in a mouse model of amyotrophic lateral sclerosis 79
The Modulation of Glutamate Release by Group I Metabotropic Glutamate Auto-Receptors in ALS 78
Group I metabotropic glutamate receptors in ALS: knocking-down mGlu1 receptors ameliorates survival and disease progression in SOD1/G93A mice. 77
G93A mutated SOD1-linked murine ALS produces abnormal exocytotic release of glutamate 75
Altered Mechanisms Underlying the Abnormal Glutamate Release in Amyotrophic Lateral Sclerosisat a Pre-Symptomatic Stage of the Disease. 75
Altered synaptic mechanisms and excessive glutamate release in amyotrophic lateral sclerosis 75
Genetic and pharmacological effects of mGlu5 receptor blockade in the SOD1G93A mouse model of amyotrophic lateral sclerosis 74
Partial deletion of mGluR1 receptors prolongs life span and ameliorates motor skills and biochemical and cellular parameters in a mouse model of experimental ALS 73
Non conventional activity of the endocannabinoid system at glutamate release in rat cortical astrocytes 73
Mesemchymal stem cells systemically administered in symptomatic mutant SOD1-G93A mice ameliorate survival and motor abilities 73
Group I metabotropic glutamate receptors induce excessive glutamate release in the spinal cord of sod1g93a mice 73
Neuroprotective Effect of AM404 Against NMDA-Induced Hippocampal Excitotoxicity 73
Reducing excitotoxicity knocking down mGluR1: prolonged survival and improved symptomatology of SOD1/G93A mouse model of ALS 72
In vitro Evidence of Abnormal Glutamate to Glutamine Conversion in Astrocytes harvested from a Mouse Model of Amyotrophic Lateral Sclerosis: a potential Experimental Application of N-13-ammonia 72
Alterations of Synaptic Mechanisms and Excessive Glutamate Release in the Spinal Cord of SOD1G93A Mice 72
Acute stress rapidly increases the readily releasable pool of glutamate vesicles in prefrontal and frontal cortex through corticosterone non-genomic action 71
In-vitro activation of GAT1 transporters expressed in spinal cord gliosomes stimulates glutamate release that is abnormally elevated in the SOd1/G93A(+) mouse model of amyotrophioc lateral sclerosis. 71
Intravenous mesenchymal stem cells administration induces survival and symptom amelioration in mutant SOD1 G93A mice 71
Group I metabotropic glutamate receptors modulate glutamate exocytosis in a mouse model of als 70
Altered expression of the GPR17 receptor in the spinal cord of SOD1G93A mice, a model of amyotrophic lateral sclerosis 70
Inactivation of the Grm5 gene improves motor coordination defects in the Grm1crv4 mouse model of SCAR13 ataxia 69
Abnormal Upregulation of GPR17 Receptor Contributes to Oligodendrocyte Dysfunction in SOD1 G93A Mice 69
Abnormal glutamate release induced by group I metabotropic glutamate receptors in experimental ALS. 68
Intravenous mesenchymal stem cells administration induces survival and symptom amelioration in mutant SOD1 G93A mice 68
The modulation of Glutamate release by Group I metabotropic Glutamate auto-receptors in ALS 66
Group I metabotropic glutamate receptors in ALS: mGluR1 and mGluR5 autoreceptors induce excessive glutamate release in SOD1/G93A mice. 64
Alterations of Synaptic Mechanisms and Excessive Glutamate Release in the Spinal Cord of SOD1G93A Mice 64
Knocking-down mGluR1 and mGluR5 in the SOD1/G93A mouse model of amyotrophic lateral sclerosis ameliorates survival and disease progression 63
The modulation of Glutamate release by pre-synaptic Group I metabotropic Glutamate receptors in ALS 63
Effects of BND-11624 at ionotropic and metabotropic glutamatergic receptors regulating neurotransmitter release in the rat CNS 63
Genetic inactivation of metabotropic glutamate 5 (mGlu5) receptor ameliorates motor coordination in the Grm1crv4 mouse model of SCAR13 ataxia 63
Synaptic mechanisms underlying the excessive and precocious glutamate release in the spinal cord of SOD1G93A experimental mice 62
Genetic and pharmacological effects by blocking mGlu5 Receptor in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis 62
Acute stress increases the readily releasable pool of glutamate vesicles in cortical areas 61
Knocking-down mGluR1 and mGluR5 in SOD1G93A mice ameliorates survival and disease progression 61
Molecular mechanisms supporting abnormal glutamate release in the spinal cord of a mouse model of Amyotrophic Lateral Sclerosis. 60
Reducing mglur5 expression attenuates the reactive phenotype of astrocytes cultured from the spinal cord of late symptomatic SOD1G93A mice 59
Intravenously administered mesenchymal stem cells improve lifespan and motor skills in a mouse model of ALS. 58
Knocking-down Group I metabotropic glutamate receptors ameliorates survival and disease progression in SOD1G93A mice. 57
Molecular mechanism underlying excessive and precocious glutamate release in the spinal cord of the SOD1G93A mouse model of amyotrophic lateral sclerosis. 56
Synaptic Mechanisms Sustaining The Excessive And Precocious Glutamate Release In The Spinal Cord Of SOD1G93A Mice 56
Abnormal and precocious exocytotic release of glutamate in the spinal cord of a mouse model of amyotrophic lateral sclerosis. 55
A multistationary loop model of ALS unveils critical molecular interactions involving mitochondria and glucose metabolism 55
Synaptic mechanisms of the abnormal release of glutamate in the spinal cord of pre-symptomatic SOD1G93A mice 54
Mechanisms underlying the predictive power of high skeletal muscle uptake of FDG in amyotrophic lateral sclerosis 54
Totale 8.912
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Categoria #
all - tutte 33.710
article - articoli 15.487
book - libri 370
conference - conferenze 17.853
curatela - curatele 0
other - altro 0
patent - brevetti 0
selected - selezionate 0
volume - volumi 0
Totale 67.420
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Totale Lug Ago Sett Ott Nov Dic Gen Feb Mar Apr Mag Giu
2019/20201.818 0 0 0 0 139 253 324 128 173 450 272 79
2020/2021771 46 85 65 41 59 64 67 89 63 66 56 70
2021/20221.332 21 85 62 127 50 107 83 322 84 126 68 197
2022/20231.440 137 147 21 164 212 201 15 104 214 12 183 30
2023/20241.113 36 124 33 135 80 235 95 43 46 61 74 151
2024/2025982 189 237 82 246 228 0 0 0 0 0 0 0
Totale 10.152