{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T01:00:03Z","timestamp":1776387603395,"version":"3.51.2"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1990,12,1]],"date-time":"1990-12-01T00:00:00Z","timestamp":660009600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1990,12]]},"abstract":"<jats:p>1. Modulation of the hyperpolarization\u2010activated cation current, Ih, by noradrenaline (NA) and serotonin (5\u2010HT) was examined in guinea\u2010pig and cat medial and lateral geniculate relay neurones using the in vitro slice technique. 2. In the absence of pharmacological antagonists, local application of NA resulted in a slow depolarization and decrease in apparent input conductance, a response which was blocked by local or bath application of the alpha 1\u2010adrenoceptor antagonist prazosin. Application of NA after pharmacological block of alpha 1\u2010 and alpha 2\u2010adrenoceptors, or application of 5\u2010HT in all conditions, induced a 1\u20103 mV slow depolarization which was associated with a pronounced increase in apparent input conductance. This response to NA and 5\u2010HT persisted during blocked synaptic transmission and was present in both the guinea\u2010pig and cat medial and lateral geniculate nuclei. 3. The increase in membrane conductance elicited by NA was mimicked by the beta\u2010specific agonist isoprenaline and blocked by the beta\u2010antagonists propranolol and atenolol, indicating that it is mediated by beta\u2010adrenoceptors. The response to 5\u2010HT was blocked by the 5\u2010HT1 and 5\u2010HT2 antagonist methysergide, but not by the 5\u2010HT2 antagonist ritanserin. Applications of either the 5\u2010HT1A agonist ipsapirone or the partial agonist 8\u2010hydroxy\u2010dipropylaminotetralin (8\u2010OHDPAT) were without effect. 4. Current versus voltage relationships obtained under voltage clamp revealed NA and 5\u2010HT to cause a voltage\u2010dependent inward shift at membrane potentials negative to approximately \u201060 mV. This response appeared to be shared by NA and 5\u2010HT since maximal application of 5\u2010HT greatly reduced or abolished the response to NA. 5. Application of NA and\/or 5\u2010HT during hyperpolarizing voltage steps in voltage clamp resulted in a marked increase in amplitude of the hyperpolarization\u2010activated cation current, Ih. In addition, the rate of activation of Ih was strongly increased during activation of beta\u2010adrenoceptors. 6. The activation curve of the conductance underlying Ih (Gh) was shifted by 4\u20106 mV on the voltage axis with NA and\/or 5\u2010HT. The positive shift of Gh activation in the voltage domain resulted in an increase in the amplitude of Gh which is active at resting, and more hyperpolarized, membrane potentials. The subsequent increase in resting membrane conductance decreased the responsiveness of thalamic neurones to hyperpolarizations of all durations. 7. Local or bath application of caesium blocked both Ih and the increase in membrane conductance in response to NA and 5\u2010HT. By contrast, barium blocked neither Ih nor the responses to NA and 5\u2010HT.(ABSTRACT TRUNCATED AT 400 WORDS)<\/jats:p>","DOI":"10.1113\/jphysiol.1990.sp018332","type":"journal-article","created":{"date-parts":[[2014,12,18]],"date-time":"2014-12-18T06:19:15Z","timestamp":1418883555000},"page":"319-342","source":"Crossref","is-referenced-by-count":305,"title":["Noradrenergic and serotonergic modulation of a hyperpolarization\u2010activated cation current in thalamic relay neurones."],"prefix":"10.1113","volume":"431","author":[{"given":"D A","family":"McCormick","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H C","family":"Pape","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1990,12]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1990.sp018332","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1990.sp018332","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,23]],"date-time":"2023-10-23T02:37:40Z","timestamp":1698028660000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1990.sp018332"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1990,12]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,12]]}},"alternative-id":["10.1113\/jphysiol.1990.sp018332"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1990.sp018332","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1990,12]]}}}