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M S Blumberg

Publications and source records attributed to M S Blumberg.

At least 19 recordsLinked to original sources

Do infant rats cry?

In the current revival of interest in the emotional and mental lives of animals, many investigators have focused attention on mammalian infants that emit distress vocalizations when separated from the home environment. Perhaps the most intensively studied distress vocalization is the ultrasonic vocalization of infant rats. Since its discovery, this vocalization has been interpreted both as a communicatory signal for the elicitation of maternal retrieval and as the manifestation of emotional distress. In contrast, the authors examined the cardiovascular causes and consequences of the vocalization, and on the basis of this work, they hypothesized that the vocalization is the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that results in increased venous return to the heart. Therefore, the vocalization may be analogous to a sneeze, serving a physiological function while incidentally producing sound.

Adrenergic alpha-Agonists↗

Mesopontine contribution to the expression of active 'twitch' sleep in decerebrate week-old rats.

Myoclonic twitching is a ubiquitous feature of infant behavior that has been used as an index of active sleep. Although the active sleep of infants differs in some ways from the REM sleep of adults, their marked similarities have led many to view them them as homologous behavioral states. Recently, however, this view has been challenged. One avenue for resolving this issue entails examination of the neural substrates of active sleep. If the neural substrates of active sleep were found to be similar to those of REM sleep, then this would support the view that the two states are homologous. Therefore, in the present study, decerebrations were performed in the pons and midbrain to determine whether the mesopontine region is important for the expression of active sleep in infants, just as it is for the expression of REM sleep in adults. It was found that, in comparison to controls, caudal pontine decerebrations reduced myoclonic twitching by 76%, rostral pontine decerebrations reduced twitching by 40%, and midbrain transections had no significant effect on twitching. Moreover, analysis of the temporal organization of twitching indicated that pontine decerebrations predominantly affected high-frequency twitching while leaving unaffected the low-frequency twitching that is thought to be contributed by local spinal circuits at this age. These results indicate that the mesopontine region plays a central role in the expression of active sleep in infant rats.

Adipose Tissue, Brown↗

Spontaneous motor activity in fetal and infant rats is organized into discrete multilimb bouts.

Spontaneous motor activity (SMA) is a ubiquitous feature of fetal and infant behavior. Although SMA appears random, successive limb movements often occur in bouts. Bout organization was evident at all ages in fetal (embryonic day [E] 17-21) and infant (postnatal day [P] 1-9) rats, with nearly all bouts comprising 1-4 movements of different limbs. A computational model of SMA, including spontaneous activity of spinal motor neurons, intrasegmental and intersegmental interactions, recurrent inhibition, and descending influences, produced bouts with the same structure as that observed in perinatal rats. Consistent with the model, bouts were not eliminated on E20 after cervical spinal transection, suggesting that the brain is not necessary to produce bout organization. These investigations provide a foundation for understanding the contributions of SMA to neuromuscular and motor development.

Animals↗

A comparative analysis of huddling in infant Norway rats and Syrian golden hamsters: does endothermy modulate behavior?

In infant rats, huddling improves surface-to-volume ratios and provides metabolic savings during cold exposure. It is unclear, however, whether endothermy is also a necessary component of huddling. In the present experiment, huddles composed of infant Norway rats (2- or 8-day-olds), which produce heat endogenously, or Syrian golden hamsters (8-day-olds), which do not produce heat endogenously, were exposed to decreases in air temperature. Behavioral and physiological responses were monitored throughout the test. Rats, especially at 8 days of age, were better able to thermoregulate using huddling than hamsters, due in part to endogenous heat production. Furthermore, 8-day-old rats exhibited behavioral responses that promote heat retention, suggesting that both physiological and behavioral mechanisms contribute to effective thermoregulation during huddling in the cold.

Adipose Tissue, Brown↗

Distress vocalizations in infant rats: what's all the fuss about?

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.

Abdomen↗

A developmental analysis of clonidine's effects on cardiac rate and ultrasound production in infant rats.

Under controlled conditions, infant rats emit ultrasonic vocalizations during extreme cold exposure and after administration of the alpha(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.

Animals↗

Cardiovascular mediation of clonidine-induced ultrasound production in infant rats.

In infant rats, administration of the alpha2 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 beta1 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.

Adrenergic alpha-Agonists↗

Cardiovascular concomitants of ultrasound production during cold exposure in 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.

Animals↗

Leptin disinhibits nonshivering thermogenesis in infants after maternal separation.

Prolonged maternal separation inhibits endogenous heat production in infant mammals exposed to cold. This inhibition of thermogenesis occurs many hours before energy stores have been fully depleted. The need to protect energy resources during separation-induced starvation may be signaled by declining levels of leptin, a hormone that acts as a "fat signal" and a regulator of energy utilization; in fact, starvation reduces leptin levels in adult mice and infant rats. It is not known, however, whether leptin has a functional role during starvation in infants. Such a role may be found in the regulation of nonshivering thermogenesis by brown adipose tissue (BAT), a specialized organ that provides heat to infant mammals, including humans, during cold exposure. Heat produced by BAT allows the cold-exposed infant to prevent the detrimental effects of hypothermia on physiology and behavior and, ultimately, growth. Here we show that leptin disinhibits BAT thermogenesis during cold exposure in infant rats after 18 h of maternal separation. This finding demonstrates that leptin is more than simply an adipostat for the regulation of body weight; specifically, leptin modulates thermogenesis and energy utilization in the early postnatal period.

Adipose Tissue, Brown↗

Thermoregulatory and cardiac responses of infant spontaneously hypertensive and Wistar-Kyoto rats to cold exposure.

Cardiovascular function during cold exposure is dependent on effective thermoregulation. This dependence is particularly apparent in infants. For example, we have previously demonstrated that in infant rats during cold exposure, cardiac rate is directly related to their ability to produce heat endogenously. The primary source of endogenous heat production for infant rats is brown adipose tissue (BAT). Because of the dependence of cardiac rate on effective thermoregulation in the cold and because hypertension in spontaneously hypertensive rats (SHR) is influenced by the preweanling environment, in this study we examined the thermoregulatory and cardiac rate responses of infant SHR and Wistar-Kyoto rats (WKY) to varying levels of cold exposure. In experiment 1, 7- to 8-day-old SHR and WKY were acclimated at a thermoneutral air temperature (35 degrees C) and then exposed to successive decreases in ambient temperature (30.5 degrees C, 26.5 degrees C, 23 degrees C, and 17 degrees C) while thermal and metabolic measures were recorded. Although both strains increased BAT thermogenesis and oxygen consumption in response to cold exposure, SHR cooled more than WKY and exhibited lower levels of oxygen consumption at the lowest air temperatures. Experiment 2 was identical to experiment 1 except that cardiac rate was also measured. Again, SHR exhibited substantial thermoregulatory deficits compared with WKY; in addition, they were less able than WKY to maintain cardiac rate at the 2 lowest air temperatures tested. Finally, in experiment 3, infant SHR exhibited diminished BAT thermogenesis in response to a range of doses of a selective beta3-adrenoceptor agonist. We hypothesize that long-term thermoregulatory deficits during the early postnatal period influence cardiovascular function and contribute to the development of hypertension in SHR.

Acclimatization↗

Geotaxis in 2-week-old Norway rats (Rattus norvegicus): A reevaluation.

In 1926, Crozier and Pincus first reported that 2-week-old rats placed head-down on an inclined plane orient in a head-up direction; this response is called negative geotaxis. In Experiment 1, we replicated this finding by testing 12- to 14-day-old rats on an inclined plane covered with wire mesh. Pups oriented in a head-up direction and avoided the head-down direction at inclines of 45 degrees but not 30 degrees. Because pups in Experiment 1 appeared to grasp the wire mesh with their claws, pups in Experiment 2 were now tested on a smooth but high-friction substrate. At inclines of 30 degrees, 35 degrees, and 40 degrees, pups did not exhibit significant tendencies to orient in a head-up direction or avoid a head-down direction. Finally, in Experiment 3, the effect of substrate on geotaxis was tested further by comparing pups' behaviors at 40 degrees with the inclined plane covered with either wire mesh or the high-friction substrate. Pups' orientation behaviors differed on the two substrates. Taken together, these data suggest that testing substrate affects the orientation behaviors of young rats and raise questions about the plausibility of applying the concept of geotaxis to young mammals, at least when tested on an inclined plane.

Animals↗

Thermoregulatory competence and behavioral expression in the young of altricial species--revisited.

The behavioral and physiological thermoregulatory capabilities of newborn and infant mammals have been studied for over half a century. Psychobiologists have noted that the infants of altricial species (e.g., rats) have physical and physiological limitations such that heat loss overwhelms heat production, thus forcing a reliance on behavioral thermoregulation for the maintenance of body temperature. Recent evidence, however, suggests that a modification of this view is justified. Specifically, throughout a range of moderately cold air temperatures, nonshivering thermogenesis by brown adipose tissue contributes significantly to the infant rat's behavioral and physiological adaptations to cold challenge. Given the prominent use of altricial species for the study of infant behavior, increased understanding of the infant's physiological responses to cold and the effect of thermal factors on behavior is warranted.

Adaptation, Physiological↗

Active sleep in cold-exposed infant Norway rats and Syrian golden hamsters: the role of brown adipose tissue thermogenesis.

It was previously hypothesized that brown adipose tissue (BAT) thermogenesis helps to maintain high rates of myoclonic twitching during cold exposure in infant rats (M. S. Blumberg & M. A. Stolba, 1996). To test this hypothesis, the sensitivity of twitching to various levels of cold exposure was assessed in week-old rats that were untreated or whose BAT thermogenesis was inhibited using a ganglionic blocker. Because week-old golden hamsters do not exhibit BAT thermogenesis, their sleep behaviors during cold exposure also were examined. Additional investigations in infant rats were conducted in which supplemental heat was provided to the interscapular region using a thermode and in which BAT was activated pharmacologically in ganglionically blocked pups. The results support the hypothesis that myoclonic twitching is sensitive to the prevailing air temperature and the activation of BAT thermogenesis.

Adipose Tissue, Brown↗

Further evidence that BAT thermogenesis modulates cardiac rate in infant rats.

Previous research in infant rats suggested that brown adipose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a ganglionic blocker), and then BAT thermogenesis was stimulated by injection with the beta3-agonist CL-316243. In experiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments, cardiac rate, oxygen consumption, and physiological temperatures were monitored. Activation of BAT thermogenesis substantially increased cardiac rate in saline- and chlorisondamine-treated pups, and focal cooling of the interscapular region was sufficient to lower cardiac rate. The results of these studies support the hypothesis that BAT thermogenesis contributes directly to the modulation of cardiac rate.

Adipose Tissue, Brown↗

Maintenance of arterial pressure in infant rats during moderate and extreme thermal challenge.

It has recently been demonstrated in week-old rats that extreme cold challenges that lead to significant bodily cooling result in decreased cardiac rate. To determine whether pups are able to maintain arterial pressure in the face of decreasing cardiac rate in extreme cold, we measured blood pressure in unanesthetized week-old rats. Instrumented pups were thermally challenged and thermoregulatory and cardiovascular responses were monitored. Despite pronounced decreases in cardiac rate in the cold, pups were able to maintain mean arterial pressure (MAP), presumably by increasing peripheral resistance. At the lowest air temperature (17 degrees C) pups emitted ultrasonic vocalizations, and these emissions were accompanied by pulsatile increases in intraabdominal pressure (IAP) and MAP. We hypothesize that these pulsatile increases in IAP during extreme cooling reflect the use of the abdominal compression reaction to increase venous return during periods of diminished cardiac output.

Abdomen↗

Thermogenic, respiratory, and ultrasonic responses of week-old rats across the transition from moderate to extreme cold exposure.

Previously, it was reported that week-old rats exposed to air temperatures that elicited submaximal levels of heat production (designated moderate cold exposure) remained asleep and did not vocalize (Blumberg & Stolba, 1996). In contrast, pups exposed to air temperatures that elicited maximal levels of heat production (designated extreme cold exposure) woke up and emitted ultrasonic vocalizations. We now report on the physiological and behavioral responses of pups in the transitional region between moderate and extreme air temperatures. Small decreases in air temperature across the transition resulted in pronounced decreases in physiological temperature and concomitant increases in ultrasound production. In a second experiment, it was shown that during moderate cold exposure respiratory frequency increased as air temperature decreased but, as extreme air temperatures were reached, respiratory frequency was maximized as ultrasound production began. The results from these two experiments illustrate how air temperatures that differ by as little as 2 degrees C can differentially modify the physiological and behavioral responses of neonates.

Animals↗