Ultrasonic vocalizations emitted by infant rodents are typically characterized as cries of distress. There are two contexts that are known to reliably elicit ultrasound production: extreme cold exposure and administration of clonidine, an alpha 2 adrenoceptor agonist. Noting that these two contexts both entail pronounced decreases in cardiac rate, we have hypothesized that the vocalizations are acoustic by-products of a physiological maneuver, the abdominal compression reaction (ACR), that increases venous return to the heart when return is compromised. As a critical test of this hypothesis, we measured venous pressure near the right atrium in 15-day-old rats after clonidine administration. Consistent with the ACR hypothesis, emission of ultrasound was accompanied by large and reliable increases in venous pressure and, therefore, venous return. These results provide strong, direct support for the ACR hypothesis and, by doing so, underscore the potential pitfalls of anthropomorphic interpretations of the vocalizations of infant rats.

Two experiments explored the cardiovascular consequences of extreme cold exposure and their relationship with ultrasound production in infant rats. Experiment 1 addressed the thermoregulatory and cardiovascular concomitants of ultrasound production during cold exposure in rats pretreated with saline or the ganglionic blocker chlorisondamine (5 mg/kg). For both groups, emission of ultrasound was associated with hypothermia and bradycardia. Experiment 2 explored whether the hypothermia experienced by pups in Experiment 1 is associated with increased blood viscosity, which is an important factor affecting venous return to the heart. Blood viscosity increased significantly as temperature decreased from 38 degrees C to 22 degrees C. These experiments suggest that, during extreme cold exposure, decreased cardiac output and increased blood viscosity combine to diminish venous return. The authors have hypothesized that pups respond to decreased return by recruiting the abdominal compression reaction, a physiological maneuver that propels blood back to the heart, resulting in emission of ultrasound as an acoustic by-product.

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In infant rats, adminislration of the a2 adrenoceptor agonist clonidine simultaneously evokes ultrasound production and bradycardia. In this study the authors examined in 8-day-old rats whether these 2 responses to clonidine are causally related. In Experiment 1 pups were pretreated with saline or prenalterol (0.1 or 1.0 mg/kg), a Pj adrenoceptor agonist that increases cardiac rate, followed by administration of clonidine (1.0 mg/kg). Prenalterol pretreatment suppressed clonidine-induced ultrasound production at both doses. Prenalterol also increased skin temperature, however, suggesting that suppression of ultrasound was modulated in part by increased body temperature. Consistent with this suggestion, in Experiment 2 mild hyperthermia significantly inhibited clonidine-induced ultrasound production. Finally, in Experiment 3 the authors found that the pretreatments used in Experiments 1 and 2 prevent or dampen the effects of clonidine on cardiac rate. These results suggest that clonidine's effect on ultrasound production is mediated by its effects on the cardiovascular system.It has been known for many years that isolating infant rats and exposing them to cold evokes emission of an ultrasonic vocalization (Allin & Banks, 1971;Okon, 1971). This vocalization has received considerable attention over the years and has typically been interpreted as a distress call designed to elicit maternal retrieval to the warmth and comfort of the nest (Noirot, 1972). In addition to cold exposure, administration of the a2 adrenoceptor agonist clonidine evokes high rates of ultrasound production, even at warm air temperatures (Hard, Engel, & Lindh, 1988;Kehoe & Harris, 1989). Week-old rats treated with clonidine also exhibit intense locomotor activity, including crawling and wall climbing