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Vasopressin V1a receptor and voluntary locomotion linked with cerebral activation in free‐moving mice
Author(s) -
Masuki Shizue,
Sumiyoshi Eri,
Koshimizu Takaaki,
Tsujimoto Gozoh,
Nose Hiroshi
Publication year - 2013
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.27.1_supplement.943.2
Subject(s) - vasopressin , baroreflex , medicine , endocrinology , mean arterial pressure , blockade , receptor , turnover , heart rate , chemistry , blood pressure , management , economics
We have reported that cerebral activation suppressed baroreflex control of heart rate (BR), followed by voluntary locomotion (VL) at higher probability. We examined if vasopressin V1a receptor (V1aR) in the brain was involved in the responses using free‐moving V1aR knockout (KO, n=8), wild type infused with V1aR blockade into the nucleus tractus solitarii (BLK, n=8), and control mice (CNT, n=8). Sensitivity of BR was determined from spontaneous changes in heart rate and mean arterial pressure (ΔHR/ΔMAP) every 4 s during a total resting period for ~8.8 h of 12 daytime hrs. ΔHR/ΔMAP was adopted in periods where cross‐correlation function (R(t)) between ΔHR and ΔMAP was significant (P<0.05). Cerebral activity was determined from the power density ratio of θ to δ wave band (θ/δ) on EEG every 4 s. We found that spontaneous change in θ/δ was significantly correlated with R(t) during 62±3% of the total resting period in CNT (P<0.05), while only 38±4% in KO and 47±2% in BLK (vs CNT, both P<0.001). When R(t) and ΔHR/ΔMAP were divided into 6 bins according to θ/δ, both were positively correlated with θ/δ in CNT (both P<0.001), while neither was correlated in KO or BLK (all P>;0.05). Moreover, the probability of VL after an increase in θ/δ was 24±4% in KO and 24±6% in BLK, lower than 61±5% in CNT (P<0.001), with no suppression of BR. Thus, central V1aR plays an important role in starting VL after cerebral activation through suppression of BR.