{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T16:00:12Z","timestamp":1779379212209,"version":"3.53.1"},"reference-count":83,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T00:00:00Z","timestamp":1775692800000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100002923","name":"Consejo Nacional de Investigaciones Cient\u00edficas y T\u00e9cnicas","doi-asserted-by":"publisher","award":["PIP\u20102230"],"award-info":[{"award-number":["PIP\u20102230"]}],"id":[{"id":"10.13039\/501100002923","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Two\u2010pore domain potassium (K2P) channels control resting membrane potential of neurons and contribute to pain hypersensitivity when their expression or function is reduced. Tandem of P\u2010domains in a Weak Inwardly rectifying K\n                    <jats:sup>+<\/jats:sup>\n                    channel 1 (TWIK1) is broadly expressed in the nervous system, yet little is known about its regulation in dorsal root ganglion (DRG) neurons. Because components of the renin\u2013angiotensin system (RAS) modulate sensory excitability, we investigated whether Angiotensin\u2010II (Ang II) and its receptors, AT1R and AT2R, regulate TWIK1 expression. Using primary DRG cultures, we found that Ang II significantly increased TWIK1 mRNA and protein at 1\u20132\u2009days in vitro. Quantitative immunocytochemistry revealed receptor\u2010specific effects: TWIK1 up\u2010regulation at 1\u2009day was primarily AT2R\u2010dependent, whereas AT1R contributed to a lesser extent. TWIK1 expression declined by 2\u2009days but remained sensitive to receptor blockade. To test physiological relevance, we injected Ang II intradermally into the hindpaw of adult rats. Repeated\u2014but not single\u2014Ang II injections produced a modest reduction of TWIK1 in large L5 DRG neurons and in NF200\u2010positive cutaneous terminals. This decrease was accompanied by mild mechanical hypersensitivity without changes in cold sensitivity. These in vivo effects align with preferential AT1R expression in medium and large DRG neurons and with the in\u00a0vitro finding that TWIK1 down\u2010regulation is most evident when AT1R remains active. These results identify TWIK1 as a downstream target of Ang II signaling in sensory neurons and suggest that RAS\u2010dependent modulation of K2P channels may influence neuronal excitability and contribute to pain\u2010related processes.\n                  <\/jats:p>","DOI":"10.1002\/jnr.70127","type":"journal-article","created":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T04:26:01Z","timestamp":1775795161000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Angiotensin\u2010\n                    <scp>II<\/scp>\n                    Type 1 and Type 2 Receptors Differentially Regulate\n                    <scp>TWIK1<\/scp>\n                    Potassium Channel Expression in Wistar Rat Sensory Neurons"],"prefix":"10.1002","volume":"104","author":[{"given":"Emanuel David","family":"Peralta","sequence":"first","affiliation":[{"name":"Laboratory of Neurobiology of Pain, Faculty of Medical Sciences IHEM\u2010CONICET 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