26:T53f,

Invertebrate and vertebrate experimental models, each providing unique advantages for addressing specific questions, offer a multifaceted and multiscale view of plasticity. Integration of the obtained knowledge is crucial for understanding general principles and specific mechanisms of synaptic plasticity. However, this process is hindered by field-specific discrepancies in terminology and concepts. A profound case of such discrepancy is heterosynaptic plasticity, which refers to distinct experimental phenomena and mechanisms and serves different functional roles in invertebrate and vertebrate nervous systems. In Aplysia research, heterosynaptic facilitation originally referred to several phenomena and mechanisms of synaptic plasticity that mediate simple forms of learning. In vertebrate research, heterosynaptic plasticity originally referred to changes at synapses that were not activated during the induction of long-term potentiation in the hippocampus. Ironically, most of the difference between the wordings comes from the meaning attributed to their common part, the heterosynaptic. Here, we consider these differences and discuss how the phenomena and concepts behind the field-specific terminologies are related and can be compared.

27:T52b,

Kv4.2 channels, principal mediators of the neuronal A-type K+ current, are emerging as multifunctional regulators of excitability, plasticity, and synaptic signaling. Beyond their canonical role in shaping backpropagating action potentials, Kv4.2 channels integrate diverse signaling modalities through interactions with calcium channels, scaffolding and auxiliary proteins (DPP6, KChIPs), and posttranslational regulators such as Pin1 and UBE3A. These interactions create a context-dependent network that allows Kv4.2 to function as a molecular break, stabilizing excitability under resting conditions and facilitating plasticity and learning when modulated. Recent advances in molecular and genetic tools are transforming how Kv4.2 can be studied. Next-generation genetically encoded inhibitors, for instance membrane-tethered toxins, offer cell-specific modulation of the channel. Complementary genetically encoded potassium indicators provide important steps toward real-time optical monitoring of potassium dynamics, although improvements remain necessary. After a period of diminished attention, the Kv4.2 channel is reemerging as a significant focus of scientific investigation. Recent breakthroughs, coupled with next-generation technologies, are bound to unravel the complex and multifaceted roles of Kv4.2.

28:T492,

Neural activity in the beta band is increasingly recognized to occur not as sustained oscillations but as transient burst-like events. These beta bursts are diverse in shape, timing, and spatial distribution, but their precise functional significance remains unclear. Here, we review emerging evidence on beta burst properties, functional roles, and developmental trajectories and propose a new framework in which beta bursts are not homogeneous events but reflect distinct patterns of synaptic input from different brain regions targeting different cortical layers. We argue that burst waveform shape carries mechanistic and computational significance, offering a window into the dynamic integration of specific combinations of cortical and subcortical signals. This perspective repositions beta bursts as transient computational primitives, rather than generic inhibitory signals or averaged rhythms. We conclude by outlining key open questions and research priorities, including the need for improved detection methods, investigation into developmental and clinical biomarkers, and translational applications in neuromodulation and brain–computer interfaces.

29:T56b,