Fine Topography of Brain Areas Activated by Cold Stress

Abstract

Neuronal activity in response to acute cold exposure was mapped in the central nervous system of adult rats using Fos immunostaining. A single, 3-hour exposure to cold elicited strong Fos-like immunoreactivity in the medial preoptic nucleus that is known as the thermoregulatory center of the brain. By this technique, pontine and medullary thermosensitive areas have been first localized and outlined anatomically. The medullary thermosensitive neurons occupy well-demarcated areas immediately ventral and dorsal to the spinal trigeminal nucleus, termed peritrigeminal and paratrigeminal nuclei, respectively. Cold-sensitive neurons were present in the dorsal part of the pontine reticular formation. Topographically, this area corresponds to the ‘pontine thermoregulatory area’, named on the basis of neurophysiological observations. In addition, thermosensitive neurons were found in the rostral thalamus and zona incerta. Several cell groups that showed strong Fos-like immunoreactivity in our previous pain-related stress experiments were also activated by cold exposure. The midline thalamic, hypothalamic dorsomedial, supramamillary and lateral parabrachial nuclei were targets of cold stress-induced noxious stimuli. Fos-positive neurons established specific topographical patterns in the paraventricular, arcuate, central amygdaloid nuclei, and the nucleus of the solitary tract. The possible involvement of central noradrenergic neurons in stress response to acute cold exposure was investigated by double immunostaining for tyrosine hydroxylase (TH) and Fos. None of the tyrosine hydroxylase positive neurons in the brain stem established Fos-like immunoreactivity, suggesting that the central noradrenergic system may have a minor, if any, role in cold-induced stress responses. Based on the topographical distribution of Fos-activated neurons, this study suggests that in addition to the hypothalamo-pituitary-adrenal axis, some other stress effector systems may play an important role in the maintenance of homeostasis during cold stress.

Stressor-specific alterations in corticosterone and immune responses in mice

“…Low Temperature: (n=9) Mice were separated into individual polycarbonate cages and placed into a ventilated cold chamber (4º C) for 2 h. The cages were cleaned each day and empty cages remained in the cold chamber overnight (Baffi and Palkovits, 2000;Miyata et al, 1995;Zoeller et al, 1990).…”

“…Mice were subjected to restraint, a largely psychological stressor (Dayas et al, 2001;Madrigal et al, 2003;Schmitz et al, 2002), as well as other commonly used laboratory stressors, including: low temperature, a physical and metabolic (energetic) stressor (Baffi and Palkovits, 2000;Miyata et al, 1995;Zoeller et al, 1990); isolation, a social stressor (Bartolomucci et al, 2003;Palanza, 2001); and forced swim, a psychological, physical and metabolic stressor (Dayas et al, 2001;Leitner, 1989;Rauch and Lieberman, 1990). We also included a group of mice that were handled each day to control for any potential influences of daily manipulation (Balcombe et al, 2004;Neigh et al, 2004).…”

Arousal from hibernation and BAT thermogenesis against cold: central mechanism and molecular basis

“…Other brainstem regions including peritrigeminal, paratrigeminal, supramamillary, lateral parabrachial nuclei, the dorsal part of the pontine reticular formation, nucleus of the solitary tract have also been demonstrated to be responsive to acute 3 hr cold exposure in rats (Baffi and Palkovits, 2000), of these regions the parabrachial nucleui (PBN) in pontine region could be involved in the regulation of NST.…”

The effect of vasopressin 1b receptors (V1bRs) blockade on the HPA axis activity in rats exposed to acute heat stress

“…Previous results have revealed that thermal stressors, such as low or high ambient temperature, classified as physical stressors (Kvetnansky et al, 2009), elicit an abundance of neuroendocrine responses including activation of the hypothalamo-pituitary-adrenal (HPA) axis and arginine vasopressin (AVP) release (Aguilera, 1994;Featherby and Lawrence, 2004;Jasnic et al, 2010;Koko et al, 2006;Perčinić-Popovska et al, 2011). It was shown that several brain nuclei are involved in the integration and triggering of this response, with hypothalamic centers playing the pivotal role (Baffi and Palkovits, 2000;Dayas et al, 2001;Herman et al, 2005). The beginning of the cascade of events, leading to HPA axis activation, may lie in the brainstem catecholaminergic nuclei or limbic brain structures, depending on the nature of the stressor (Herman and Cullinan, 1997).…”