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A developmental analysis of clonidine's effects on cardiac rate and ultrasound production in infant rats
Author(s) -
Blumberg Mark S.,
Sokoloff Greta,
Kent Kristen J.
Publication year - 2000
Publication title -
developmental psychobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 93
eISSN - 1098-2302
pISSN - 0012-1630
DOI - 10.1002/(sici)1098-2302(200004)36:3<186::aid-dev2>3.0.co;2-v
Subject(s) - clonidine , bradycardia , heart rate , ultrasound , agonist , medicine , anesthesia , endocrinology , blood pressure , receptor , radiology
Under controlled conditions, infant rats emit ultrasonic vocalizations during extreme cold exposure and after administration of the α 2 adrenoceptor agonist, clonidine. Previous investigations have determined that, in response to clonidine, ultrasound production increases through the 2nd‐week postpartum and decreases thereafter. Given that sympathetic neural dominance exhibits a similar developmental pattern, and given that clonidine induces sympathetic withdrawal and bradycardia, we hypothesized that clonidine's developmental effects on cardiac rate and ultrasound production would mirror each other. Therefore, in the present experiment, the effects of clonidine administration (0.5 mg/kg) on cardiac rate and ultrasound production were examined in 2‐, 8‐, 15‐, and 20‐day‐old rats. Age‐related changes in ultrasound production corresponded with changes in cardiovascular variables, including baseline cardiac rate and clonidine‐induced bradycardia. This experiment is discussed with regard to the hypothesis that ultrasound production is the acoustic by‐product of a physiological maneuver that compensates for clonidine's detrimental effects on cardiovascular function. © 2000 John Wiley & Sons, Inc. Dev Psychobiol 36: 186–193, 2000