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Cardiovascular Effects Of Acute Optogenetic Modulation Of Oxytocin‐PVN Neurons
Author(s) -
Mohammed Mazher,
Tan Yalun,
Harrison Caitlin Baumer,
Scott Karen A,
Sumners Colin,
Kloet Annette,
Krause Eric G.
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.691.12
Subject(s) - optogenetics , medicine , blood pressure , heart rate , oxytocin , endocrinology , chemistry , biology , neuroscience
The actions of oxytocin (OT), a neuropeptide that is largely synthesized in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus, has been implicated in a variety of homeostatic processes. Recent studies have demonstrated that chronic activation of OT neurons in the PVN prevents hypertension that is a consequence of intermittent hypoxia/hypercapnia. The present study combines genetically‐modified mice with in vivo optogenetics to determine the cardiovascular consequences of selective inhibition or excitation of OT neurons residing in the PVN. Male mice engineered to direct the expression of Cre recombinase to the OT gene had adenoassociated virus synthesizing an inhibitory opsin (Switch), an excitatory opsin (ChR2), or enhanced yellow fluorescent protein (eYFP) bilaterally injected into the PVN. Subsequently, mice were implanted with fiber optics targeting the PVN. One month later, mice were anesthetized with isoflurane and were implanted with a Millar catheter into their left common carotid artery for continuous recording of blood pressure and heart rate. Relative to the eYFP control group, OT‐Cre mice expressing Switch exhibited reduced blood pressure (−24±6 mmHg) and heart rate (−21±9 BPM) in response to optogenetic inhibition when compared with the eYFP group (4±2 mmHg and 5±4 bpm; n=3, p<0.05). In contrast, in the ChR2‐injected group, blue light stimulation (1 min; 30 Hz; 20ms pulse width) significantly increased blood pressure by 15±2 mmHg while decreasing heart rate by −27±10 bpm when compared to controls (0±1mmHg and 9±5 bpm; n=5, p<0.01. Neuroanatomical experiments revealed that neurons in the PVN that synthesize OT send dense axonal projections to the median eminence, the nucleus of the solitary tract, and the rostral ventral lateral medulla. Collectively, the results suggest that OT synthesizing neurons in the PVN mediate cardiovascular function possibly by affecting autonomic outflow and/or the activity of neuroendocrine axes. Support or Funding Information NIH Funding supported the present study This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .