https://scholar.dgist.ac.kr/handle/20.500.11750/9977 2026-10-10T20:26:08Z https://scholar.dgist.ac.kr/handle/20.500.11750/60877 Title: TWIK-1 plays distinct roles in spinal and peripheral sensory circuits controlling mechanical sensitivity and neuropathic hypersensitivity Author(s): Seo Young Yang; Tery Yun; Yunjeong Lee; Jae Hyuk Jeon; Seojung Kim; Eun Yeong Lim; Junhee Park; Kim, Yong Geon; Jonghoon Jung; Woo, Jin-Nyeong; Yan Zhang; Hyeonwi Son; John Shannonhouse; Juhyun Kim; Eunsil Cho; Young Hoon Sung; Eun-Mi Hwang; Byung-Chang Suh; Pojeong Park; Mi-Ryoung Song; Myungin Baek; Jaekwang Lee; Yu Shin Kim; Jae-Yong Park; Hyosang Lee Abstract: Ion channels are essential for sensing somatic stimuli, and their dysregulation can cause chronic conditions such as neuropathic pain. Although the potassium channel Twik-1 has been linked to sensory processing, its specific roles in the somatosensory system under normal and disease conditions remain unclear. Here, we demonstrate that systemic deletion of Twik-1 selectively reduces innocuous tactile and noxious mechanosensation evoked by both static and dynamic mechanical stimuli and facilitates recovery from mechanical hypersensitivity after peripheral nerve injury. Conditional deletion of Twik-1 in spinal cord neurons, pan-inhibitory neurons, or spinal inhibitory interneurons consistently disrupts innocuous tactile and noxious mechanical sensitivity, while sparing responses to high-intensity mechanical stimulation as well as noxious heat and cold. Notably, these manipulations do not affect nerve injury-induced mechanical hypersensitivity. In contrast, selective deletion of Twik-1 in dorsal root ganglion (DRG) neurons preserves baseline somatosensory and nociceptive functions, including innocuous tactile and noxious mechanical sensitivity, but impairs the persistence of mechanical hypersensitivity after nerve injury. This reduction in hypersensitivity is accompanied by decreased aberrant excitability in injured DRG neurons and distinct transcriptional changes. Together, these results suggest that Twik-1 facilitates innocuous tactile and noxious mechanosensation through spinal inhibitory circuits under baseline conditions, while supporting the maintenance of neuropathic pain via its functions in primary sensory neurons. 2026-05-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60414 Title: Shared and Divergent Transcriptional Programs of Oligodendrocyte Differentiation Across Vertebrate Species Revealed by scRNA-seq Analysis Author(s): Yun, Tery; Park, Junhee; Baek, Myungin Abstract: A myelination is essential for neural function in the vertebrate central nervous system, yet the molecular details of how the oligodendrocyte differentiation program has evolved remain poorly understood. Here, we performed a cross-species single-cell transcriptomic analysis of oligodendrocyte lineage cells in the spinal cord of five vertebrate species: fugu, mudskipper, chicken, mouse, and human. Pseudotime trajectory analysis revealed a shared oligodendrocyte progenitor cell (OPC) to committed oligodendrocyte precursor (COP) to myelin-forming oligodendrocyte (MOL) differentiation trajectory across all species, and CAME-based cross-species mapping confirmed the homology of OPC and MOL identities, while COP showed reduced mapping in teleosts compared with amniotes. Among stage-specific DEGs, highly shared genes (≥4 species) were organized into four co-expression modules encompassing cell projection organization, myelination, synapse assembly, and ribonucleoprotein biogenesis, with evolutionary core genes (all 5 species) enriched for oligodendrocyte differentiation and Wnt signaling. Strikingly, amniote-exclusive genes were enriched for synaptic vesicle transport, cell projection organization, predominantly at the OPC stage. This asymmetry indicates that amniotes have expanded the oligodendrocyte differentiation program at the progenitor stage, potentially linked to the myelination demands of terrestrial locomotor circuits. Our findings provide insights into how the oligodendrocyte differentiation program has been shaped by both deep evolutionary conservation and lineage-specific adaptation. 2026-04-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/59927 Title: Kv7 Channels as an Important Contributor to Alcohol-Induced Modulation of Neuronal Excitability in Neonatal Rat Superior Cervical Ganglion Author(s): Jeong, Da-Jeong; Woo, Jin-Nyeong; Yun, Tery; Baek, Myungin; Suh, Byung-Chang Abstract: Normal alcohols (n-alcohols) exhibit contrasting effects on neuronal excitability; specifi- cally, ethanol enhances neuronal firing, while hexanol suppresses it. Both compounds are known to inhibit sodium currents, yet the mechanisms behind their differing effects remain unclear. Our previous studies demonstrated that Kv7 channels are modulated differently by alcohol chain length, prompting investigation into their role in these contrasting effects. We conducted whole-cell patch clamp recordings on neonatal (P5-P7) rat superior cervical ganglion neurons to assess alcohol impacts on action potential firing and ionic currents, utilizing tetrodotoxin (TTX), XE991, and retigabine (RTG). Ethanol (100 mM) increased action potential frequency, whereas hexanol (3 mM) decreased it, despite both inhibiting sodium currents by 12% and 45%, respectively. Notably, ethanol inhibited Kv7 currents by 16%, while hexanol enhanced them by 29%. TTX alone did not affect firing frequency until sodium current inhibition exceeded 76%, indicating moderate sodium channel blockade cannot fully explain the effects of alcohol. XE991 increased firing frequency and depo- larized the resting membrane potential, while retigabine produced opposite effects. The combination of TTX with Kv7 modulators replicated the effects observed with each alco- hol. These findings suggest Kv7 channel modulation plays an important role in the chain length-dependent effects of alcohol on neuronal excitability. 2025-10-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/58331 Title: Electrical Stimulation of the M1 Activates Somatostatin Interneurons in the S1: Potential Mechanisms Underlying Pain Suppression Author(s): Park, Junhee; Kim, Yong Geon; Kim, Taehyeon; Baek, Myungin Abstract: Chronic pain affects millions globally, yet no universally effective treatment exists. The primary motor cortex (M1) has been a key target for chronic pain therapies, with electrical stimulation of the M1 (eMCS) showing promise. However, the mechanisms underlying M1-mediated analgesic effects are not fully understood. We investigated the role of the primary somatosensory cortex (S1) in M1-mediated analgesia using a neuropathic pain mouse model. In this model, neuropathic pain is associated with increased spontaneous activity of layer V pyramidal neurons (LV-PNs) in the S1, partly attributed to the reduced activity of somatostatin-expressing inhibitory neurons (SST+ INs), which normally suppress LV-PNs. While manipulation of either LV-PNs or SST+ INs has been shown to alleviate pain, the role of S1 in M1-mediated analgesia has not been identified. Using multichannel silicon probes, we applied eMCS to neuropathic mice and observed significant analgesia. Histological analyses revealed that eMCS activated SST+ INs and suppressed hyperactivity of LV-PNs in the S1, suggesting that eMCS suppresses pain by modulating S1 neuronal circuits, alongside other pain-related regions. Notably, eMCS induced long-lasting analgesia, persisting for at least 2 d poststimulation. These findings implicate S1 as a critical mediator of eMCS-induced analgesia and suggest eMCS as a potential durable therapeutic strategy for chronic pain. 2025-03-31T15:00:00Z