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Maria Amalia Di Castro

Researcher at Sapienza University of Rome

Publications -  13
Citations -  458

Maria Amalia Di Castro is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Hippocampal formation & Excitatory postsynaptic potential. The author has an hindex of 9, co-authored 12 publications receiving 329 citations. Previous affiliations of Maria Amalia Di Castro include Pasteur Institute.

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GABAA currents are decreased by IL-1β in epileptogenic tissue of patients with temporal lobe epilepsy: implications for ictogenesis.

TL;DR: The novel finding that pathophysiological concentrations of IL-1β decreased the I(GABA) amplitude in specimens from patients with TLE with or without HS, but not in control tissues is reported, suggesting that this cytokine contributes to seizure generation in human TLE by reducing GABA-mediated neurotransmission.
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Electrophysiological Properties of CA1 Pyramidal Neurons along the Longitudinal Axis of the Mouse Hippocampus

TL;DR: Findings indicate an increased probability of both GABA and glutamate release and a reduced plasticity in the ventral compared to more dorsal regions of the hippocampus, and variations in neuronal excitability, subthreshold membrane properties and neurotransmitter responses along the longitudinal axis.
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Fractalkine (CX3CL1) enhances hippocampal N-methyl-d-aspartate receptor (NMDAR) function via d-serine and adenosine receptor type A2 (A2AR) activity

TL;DR: CX3CL1 transiently potentiates NMDAR function though mechanisms involving A2AR activity and the release of d-serine, and mass spectrometry analysis demonstrates that stimulation of microglia and astrocytes with CX3 CL1 or VT7 increases d-Serine release in the extracellular medium.
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Chemokines: Key Molecules that Orchestrate Communication among Neurons, Microglia and Astrocytes to Preserve Brain Function

TL;DR: The evidence that chemokines modulate neuroprotective processes upon different noxious stimuli and participate to orchestrate neurons-microglia-astrocytes action to preserve and limit brain damage is summarized.
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The chemokine CXCL16 modulates neurotransmitter release in hippocampal CA1 area.

TL;DR: It is demonstrated for the first time that CXCL16 exerts a modulatory activity on inhibitory and excitatory synaptic transmission in CA1 area and it is found that CxCL16 increases the frequency of the miniature inhibitory synaptic currents and the paired-pulse ratio of evoked IPSCs, suggesting a presynaptic modulation of the probability of GABA release.