Lesions of the anteroventral third ventricle region (AV3V) disrupt cardiovascular responses to an elevation in core temperature

Abstract

Blood flow is redistributed from the viscera to the periphery during periods of heat stress to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by nonthermal inputs such as hydration status. At present, little is known about where thermal and nonthermal information is integrated to generate an appropriate effector response. Recently, the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in unanesthetized, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of approximately 0.03 degrees C/min in sham- and AV3V-lesion rats using an infrared heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes, and heat-induced salivation was estimated using the spit-print technique. The rise in mean arterial pressure (MAP), heart rate (HR), and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3V-lesion rats; however, hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR, and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment.

Lesions of the anteroventral third ventricle region exaggerate neuroendocrine and thermogenic but not behavioral responses to a novel environment

“…More recently, Romanovsky et al (26) found that electrolytic lesions of this region resulted in a prolonged hyperthermia that lasted upward of 3 wk. In contrast to both of these lesion studies, we have previously reported that AV3V-lesion animals produce an exaggerated stress-induced fever in response to gentle handling (35,37).…”

“…In the current study (protocol 1), we used a radiotelemetry system, as opposed to a colonic probe, to monitor T C , allowing the animal to remain undisturbed until the cage switch occurred. Given that AV3V-lesion rats develop an exaggerated stress-induced fever and do not appear to habituate to a given stressor, even after extensive handling (35,37), this may be a critical factor for the study of thermoregulation in this model.…”

“…Recent work by Yoshida et al (38) has shown that many MnPO neurons activated by heat stress synapse in the rostral periaqueductal gray, an area crucial for tail dilation (39). Ablation of the AV3V region results in an inability to appropriately redistribute blood flow or salivate in response to high environmental temperatures and consequently produces a reduced thermal tolerance (36,37). This loss of the ability to fine-tune cutaneous vascular tone could by itself result in the observed overheating and delayed rectification; however, evidence also exists to suggest that neurons within the MnPO also inhibit nonshivering thermogenesis (24), thereby providing a secondary drive that could push T C higher.…”

“…More recently, Romanovsky et al (26) found that electrolytic lesions of this region resulted in a prolonged hyperthermia that lasted upward of 3 wk. In contrast to both of these lesion studies, we have previously reported that AV3V-lesion animals produce an exaggerated stress-induced fever in response to gentle handling (35,37).Therefore, the purpose of the current study was to directly examine stress-induced fever in the AV3V-lesion rat model. Given that stress-induced fever is just one component of a complex array of physiological and behavioral outputs elicited in response to a perceived threat, we also determined whether there were changes in the activation of the hypothalamopituitary-adrenocortical (HPA) axis as well as stress-related behaviors.…”

“…The animals with AV3V ablations, which typically destroy the organum vasculosum of the lamina terminalis, ventral MnPO, rostral periventricular tissue, and the medial portion of the medial preoptic nucleus (1,35,37), showed an immediate cessation of water intake in the 24 h immediately after surgery (water intake, AV3V 8.8 Ϯ 2.19 ml to sham 26.5 Ϯ 3.05 ml, t 66 ϭ 4.69, P Ͻ 0.001).…”