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Seo, M. S.

Publications and source records attributed to Seo, M. S..

2 recordsLinked to original sources

Temporal Interference Modulates Medial Temporal and Frontoparietal Activity During Mnemonic Discrimination: A high-resolution whole-brain fMRI investigation

Mnemonic discrimination--the ability to distinguish between existing memories and similar new inputs--supports accurate memory in the face of interference (e.g., remembering where you parked today versus yesterday in the same parking deck). Although hippocampal pattern separation has been emphasized as a key mechanism, recent theoretical frameworks and empirical findings suggest that surrounding medial temporal lobe and cortical regions also contribute by resolving interference. An important source of interference in everyday life is temporal interference: similar events may compete not only because they overlap perceptually, but also because they are separated by intervening experiences (e.g., having to remember your morning parking spot after a full day of work). Here, we investigated how temporal interference impacts mnemonic discrimination and its neural correlates using high-resolution fMRI and a continuous recognition task in which the lag between an items first presentation and its subsequent target or similar lure was systematically manipulated (10, 60, or 140 intervening trials). Behaviorally, increasing lag impaired both mnemonic discrimination and target recognition. At the neural level, lag effects were not observed in hippocampal subfields. Rather, temporal interference modulated activity in extrahippocampal MTL regions including parahippocampal and perirhinal cortex, as well as distributed cortical regions including frontoparietal control areas. Importantly, lag-related modulation was process-specific, with partially dissociable patterns for successful mnemonic discrimination and target recognition. Together, these findings demonstrate that temporal interference engages a distributed MTL-cortical network that supports interference resolution during mnemonic discrimination.

neuroscience↗

The sodium-glucose cotransporter 2 inhibitor tofogliflozin induces vasodilation by activating Kv channels, the SERCA pump, and the sGC/cGMP pathway

OBJECTIVETofogliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor widely used to treat T2DM, but it also exhibits cardio-protective effects. This study investigated the vasodilatory action of tofogliflozin using rabbit femoral artery rings pre-contracted with phenylephrine. APPROACH AND RESULTSThe femoral artery quickly separated from the rabbit and fix it to the organ bath chamber. Subsequently, administer an inhibitor that modulates vascular tension in the rings or remove the endothelium to assess its impact on vasodilation. The results showed the concentration-dependent induction of vasodilation by tofogliflozin, a response that remained unchanged following endothelial removal, pretreatment with the nitric oxide synthase (NOS) inhibitor L-NAME, or the inhibition of low- and intermediate-conductance Ca2+-activated K+ channels (SKCa and IKCa) using apamin in combination with TRAM-34. Furthermore, pretreatment with the voltage-dependent K+ (Kv) channel inhibitor 4-AP reduced the vasodilatory effects of tofogliflozin whereas pretreatment with the ATP-sensitive K+ (KATP) channel inhibitor glibenclamide or the large-conductance Ca2+-activated K+ (BKCa) channel inhibitor paxilline did not. Notably, our findings indicated that Kv7.X, rather than Kv1.5 or Kv2.1, is the primary Kv subtype involved in tofogliflozin-induced vasodilation. The vasodilatory effects of tofogliflozin were also significantly inhibited in femoral arterial rings pretreated with the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump inhibitors thapsigargin and cyclopiazonic acid (CPA). Tofogliflozin-induced vasodilation was unaltered in arterial rings exposed to the adenylyl cyclase inhibitor SQ 22536, the protein kinase A (PKA) inhibitor KT 5720, and the protein kinase G (PKG) inhibitor KT 582 whereas it was effectively reduced by the soluble guanylyl cyclase (sGC) inhibitor ODQ. CONCLUSIONSThese findings suggest that tofogliflozin-induced vasodilation is mediated by the activation of the SERCA pump, the sGC/cGMP pathway, and Kv channels, but not the PKA signaling pathway, other K+ channels, or endothelium-dependent mechanisms.

pharmacology and toxicology↗