Topic: homeostatic synaptic plasticity

Strongly interconnected neuronal populations are thought to be a substrate for memory in the brain. Dynamic connectivity relies on plasticity rules to adjust synapses, enabling learning and neural circuit formation. Networks with only excitatory synaptic plasticity can become unstable due to runaway excitation, compromising a circuit's ability to store memories. To counter this, homeostatic synaptic plasticity of inhibitory connections provide a matched negative feedback that stabilizes neural activity and any associated learning. In this study, we outline the conditions under which recurrent

The concept of homeostasis is a central principle in many biological systems, and aims at maintaining systems in a functional state. In the brain homeostatic synaptic plasticity is a well-known mechanism to maintain neuronal networks in a functional homeostasis. Despite there has been a lot of research and characterization of this form of plasticity in animal models, it remains unknown, whether it is also expressed in the human brain. In this study, we investigated the impact of treatment with antiepileptic drugs on neurotransmission and functional properties of layer 2/3 pyramidal cells in th

In recent years, a pivotal role of gliotransmission in homeostatic synaptic plasticity has been highlighted and glial-derived ATP arises as a key contributor. However, very little is known about the glial non-vesicular ATP-release pathway and how ATP participates in the modulation of synaptic strength. In this work, we have analyzed the functional changes occurring in neurons upon chronic activity blockade and the role of the purinergic signaling, connexin43 and pannexin1 hemichannels in this process. By using hippocampal dissociated cultures, we showed that blocking connexin43 and pannexin1 h

Recent studies have highlighted the dual role of amyloid beta peptide (Aβ) in both Alzheimer’s disease (AD) and normal brain function. Particularly, Αβ1-40 and Αβ1-42 are key in regulating homeostatic synaptic plasticity in the dentate gyrus. This study aimed to identify specific amyloid fragments (N- and C- terminus fragments of Αβ) involved in synaptic plasticity modulation. Using entorhino-hippocampal tissue cultures, combined with whole-cell patch clamp recordings, light- and electron microscopy and molecular biology techniques, we found that the N-terminal fragment Aβ1-16 is essential for