{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:49:04Z","timestamp":1790617744562,"version":"4.1.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["15GRNT25710176"],"award-info":[{"award-number":["15GRNT25710176"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Institutes of Health, National Heart, Lung and Blood Institute","award":["P01 HL088052-07"],"award-info":[{"award-number":["P01 HL088052-07"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2018,5,1]]},"abstract":"<jats:p>\n                    Blackburn MB, Andrade MA, Toney GM. Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation. J Appl Physiol 124: 1233\u20131243, 2018. First published December 19, 2017; doi: 10.1152\/japplphysiol.00743.2017 .\u2014 Acute intermittent hypoxia (AIH) repetitively activates the arterial chemoreflex and triggers a progressive increase of sympathetic nerve activity (SNA) and phrenic nerve activity (PNA) referred to as sympathetic and phrenic long-term facilitation (S-LTF and P-LTF), respectively. Neurons of the hypothalamic paraventricular nucleus (PVN) participate in the arterial chemoreflex, but their contribution to AIH-induced LTF is unknown. To determine this, anesthetized rats were vagotomized and exposed to 10 cycles of AIH, each consisting of ventilation for 3 min with 100% O\n                    <jats:sub>2<\/jats:sub>\n                    followed by 3 min with 15% O\n                    <jats:sub>2<\/jats:sub>\n                    . Before AIH, rats received bilateral PVN injections of artificial cerebrospinal fluid (aCSF; vehicle) or the GABA-A receptor agonist muscimol (100 pmol in 50 nl) to inhibit neuronal activity. Thirty minutes after completing the AIH protocol, during which rats were continuously ventilated with 100% O\n                    <jats:sub>2<\/jats:sub>\n                    , S-LTF and P-LTF were quantified from recordings of integrated splanchnic SNA and PNA, respectively. PVN muscimol attenuated increases of SNA during hypoxic episodes occurring in later cycles (6\u201310) of AIH ( P &lt; 0.03) and attenuated post-AIH S-LTF ( P &lt; 0.001). Muscimol, however, did not consistently affect peak PNA responses during hypoxic episodes and did not alter AIH-induced P-LTF. These findings indicate that PVN neuronal activity contributes to sympathetic responses during AIH and to subsequent generation of S-LTF.\n                  <\/jats:p>\n                  <jats:p>NEW &amp; NOTEWORTHY Neural circuits mediating acute intermittent hypoxia (AIH)-induced sympathetic and phrenic long-term facilitation (LTF) have not been fully elucidated. We found that paraventricular nucleus (PVN) inhibition attenuated sympathetic activation during episodes of AIH and reduced post-AIH sympathetic LTF. Neither phrenic burst patterning nor the magnitude of AIH-induced phrenic LTF was affected. Findings indicate that PVN neurons contribute to AIH-induced sympathetic LTF. Defining mechanisms of sympathetic LTF could improve strategies to reduce sympathetic activity in cardiovascular and metabolic diseases.<\/jats:p>","DOI":"10.1152\/japplphysiol.00743.2017","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T02:40:39Z","timestamp":1514169639000},"page":"1233-1243","source":"Crossref","is-referenced-by-count":17,"title":["Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation"],"prefix":"10.1152","volume":"124","author":[{"given":"Megan B.","family":"Blackburn","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary Ann","family":"Andrade","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Texas Health Science 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