Publications by authors named "Domenico Pimpinella"

Autism spectrum disorders (ASDs) comprise developmental disabilities characterized by impairments of social interaction and repetitive behavior, often associated with cognitive deficits. There is no current treatment that can ameliorate most of the ASDs symptomatology; thus, identifying novel therapies is urgently needed. Here, we used the Neuroligin 3 knockout mouse (NLG3), a model that recapitulates the social deficits reported in ASDs patients, to test the effects of systemic administration of IGF-2, a polypeptide that crosses the blood-brain barrier and acts as a cognitive enhancer.

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  • Epilepsy commonly occurs alongside Alzheimer's disease (AD) and often appears before noticeable memory decline, suggesting a potential link worth studying in early AD stages.
  • Research on Tg2576 mice showed that repeated seizures led to memory impairment and increased amyloid-β (Aβ) levels specifically in those with pre-symptomatic AD, indicating a connection between seizures and AD pathology.
  • The antiepileptic drug lamotrigine was effective in reversing the neuronal changes and memory deficits caused by seizures, suggesting it could help mitigate the progression of AD in its early stages.
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In Neurodevelopmental Disorders, alterations of synaptic plasticity may trigger structural changes in neuronal circuits involved in cognitive functions. This hypothesis was tested in mice carrying the human R451C mutation of gene (NLG3 KI), found in some families with autistic children. To this aim, the spike time dependent plasticity (STDP) protocol was applied to immature GABAergic Mossy Fibers (MF)-CA3 connections in hippocampal slices from NLG3 KI mice.

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Animal species are named social when they develop the capability of complex behaviors based on interactions with conspecifics that include communication, aggression, mating and parental behavior, crucial for well-being and survival. The underpinning of such complex behaviors is social memory, namely the capacity to discriminate between familiar and novel individuals. The Medial Septum (MS), a region localized in the basal forebrain, is part of the brain network involved in social memory formation.

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  • Acetylcholine (ACh) plays a vital role in learning and memory, specifically in social memory within the CA2 region of the hippocampus.
  • Inhibiting cholinergic neurons from the medial septum/diagonal band of Broca impairs mice's ability to recognize new social interactions, highlighting ACh's importance in social novelty discrimination.
  • Activation of nicotinic ACh receptors (nAChRs) increases excitation in CA2 principal cells, indicating that these receptors are key for social memory by regulating inhibition in this area.
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  • GABAergic transmission is essential for regulating neuronal activity and is linked to cognitive functions, with the scaffold protein gephyrin playing a crucial role in anchoring GABA receptors at synapses.
  • The balance between excitation and inhibition (E/I balance) is vital for proper brain function, and disruptions in this balance can lead to disorders like epilepsy and schizophrenia.
  • The article utilizes a computational model to analyze how blocking gephyrin affects inhibitory postsynaptic currents (IPSCs) and suggests methods for correlating experimental changes in synaptic events with underlying cellular pathways.
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Autism spectrum disorders (ASDs) comprise a heterogeneous group of neuro-developmental abnormalities with a strong genetic component, characterized by deficits in verbal and non-verbal communication, impaired social interactions, and stereotyped behaviors. In a small percentage of cases, ASDs are associated with alterations of genes involved in synaptic function. Among these, relatively frequent are mutations/deletions of genes encoding for neuroligins (NLGs).

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  • - The study investigates how chronic treatment with β-amyloid (Aβ), associated with Alzheimer’s disease, influences glutamatergic transmission in neurons, revealing significant activation of the prokineticin (PK) system in this process.
  • - An increase in ionic current through AMPA receptors was observed in neurons treated with Aβ, which was reversed by the prokineticin antagonist PC-1, indicating that PK plays a key role in Aβ's effects.
  • - The findings suggest that targeting the prokineticin system with antagonists like PC-1 may offer potential new therapeutic strategies to reduce neuronal damage and slow Alzheimer’s disease progression.
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