Although intracerebral hemorrhage (ICH) and cerebral small vessel disease (cSVD) have long been considered distinct clinical entities, emerging evidence reveals significant overlap in their etiologies and imaging markers. This review aims to explore the relationship between ICH and cSVD, suggesting that ICH may represent an acute manifestation of small vessel disease. ICH is primarily caused by cerebral amyloid angiopathy and hypertension, while cSVD is mainly attributed to cerebral amyloid angiopathy and arteriolosclerosis. Hypertension-induced arteriolosclerosis is one of the most common pathologic changes in cSVD. This overlap in etiology suggests a close relationship between ICH and cSVD. In patients with ICH, multiple imaging markers of cSVD are often observed. Recent studies suggest that enlarged perivascular spaces, one of the imaging markers of cSVD, may serve as a pathway for hematoma expansion. Additionally, diffusion-weighted imaging lesions are frequently observed in patients with ICH. These lesions are likely to be based on underlying cSVD and may evolve into other cSVD markers, such as white matter hyperintensity, lacunar infarctions, or microbleeds. These findings highlight the complex interplay between ICH and cSVD, suggesting that ICH could be considered an acute expression of cSVD rather than an entirely separate entity.

The subgenual (sACC) and pregenual (pACC) anterior cingulate and anterior midcingulate (aMCC) cortices are structurally and functionally distinct subregions of the cingulate cortex with critical roles in pain processing. These regions may be promising therapeutic targets using non-invasive neuromodulation techniques, including transcranial magnetic stimulation (TMS), transcranial electrical stimulation (TES), and low-intensity focused ultrasound (LIFU). In this review, we synthesize emerging evidence on the function and connectivity of these subregions in both acute and chronic pain, highlighting their differential roles in the sensory, affective, and autonomic contributions to pain processing. We compare the strengths and limitations of the different non-invasive neuromodulatory methods for accessing these deep midline structures and examine how technique-specific and target-specific effects influence analgesic outcomes. We also explore the influence of placebo mechanisms and stimulation context on therapeutic effects. Finally, we discuss emerging strategies such as personalized connectivity-based targeting to overcome anatomical and technical limitations to advance precision non-invasive neuromodulation for pain.

Primary somatosensory neurons, glial cells in the peripheral ganglia, and neural circuits in the spinal cord function as dynamic network circuits that transmit information to the brain. Although a variety of methods and techniques have been used to study individual neurons or tissue explants, the number of neurons that can be monitored is limited. Imaging intact primary sensory neurons, such as those in the dorsal root ganglion and trigeminal ganglia, and the spinal cord in vivo using fluorescent calcium markers helps overcome the limitations of previous methods and techniques by allowing researchers to monitor tens to thousands of cells simultaneously. This allows researchers to conduct experiments to elucidate somatosensory mechanisms and responses to axonal injury that were previously difficult or impossible to observe. Using this approach, researchers have studied dynamic neural network circuits, connectivity, responses to soft and deep touch, heat, cold, chemicals, inflammation, and injury, and they have repeatedly imaged individual neurons over long periods of time. Approaches include using calcium-sensitive fluorescent dyes and genetically encoded markers, performing terminal exposure surgeries, using chambers designed to monitor large numbers of cells or repeatedly imaging small numbers of cells, and imaging animals with or without anesthesia. This review discusses the advantages and disadvantages of in vivo calcium imaging for studying somatosensory and axonal injury in peripheral sensory ganglia and the dorsal spinal cord, as well as anticipated future directions.

Phosphoinositides (PIs) are essential regulators of neuronal function, playing pivotal roles in processes such as synaptic transmission, membrane excitability, and long-term synaptic plasticity. The seven PI isoforms, including PI(4)P, PI(4,5)P, and PI(3,4,5)P, exhibit distinct subcellular distributions that are tightly regulated by specific kinases and phosphatases. These isoforms contribute to key neuronal processes by modulating protein interactions and signaling pathways. Recent advances in visualization techniques, such as biosensor-based live imaging and SDS-digested freeze-fracture replica labeling, have provided new insights into the spatial distributions and dynamic behaviors of PI isoforms in neurons, particularly at synapses.However, significant questions remain, such as how specific PI isoforms coordinate signaling events in distinct subcellular compartments and how these lipids influence critical neuronal processes like vesicular trafficking and synaptic plasticity. Addressing these challenges will require the continued development of advanced imaging technologies, which are essential for mapping nanoscale distributions of PIs and their dynamic roles in neuronal processes. Here, I will review current findings, advancements in visualization methodologies, and key research directions. This review will be helpful for understanding the roles of PIs in neuronal physiology, their broad impacts on neuronal signaling, and the technological breakthroughs needed to uncover these complex processes.

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 , which refers to distinct experimental phenomena and mechanisms and serves different functional roles in invertebrate and vertebrate nervous systems. In research, originally referred to several phenomena and mechanisms of synaptic plasticity that mediate simple forms of learning. In vertebrate research, 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 . Here, we consider these differences and discuss how the phenomena and concepts behind the field-specific terminologies are related and can be compared.

Recent electron microscopy reveals that weak synaptic connectivity predominates in the human cerebral cortex, raising the question of how information is transmitted by action potentials in these neural networks. Differences in field potential oscillations (brainwaves) and glia between vertebrates and invertebrates provide a possible answer that can also account for the incomparable increase in the cognitive ability of vertebrates.