Stress-induced hyperthermia and anxiety: pharmacological validation

Olivier, Berend; Zethof, T. J. J.; Pattij, Tommy; Boogaert, Meg van; Oorschot, Ruud van; Leahy, Christina; Oosting, Ronald S.; Bouwknecht, Arjan; Veening, Jan G.; Gugten, Jan van der; Groenink, Lucianne

doi:10.1016/s0014-2999(03)01326-8

Cited by 187 publications

(146 citation statements)

References 65 publications

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“…Body temperature was reported to increase in response to anxiogenic or stress-inducing stimuli and injury (surgery and trauma) for the activation of the endogenous mechanisms related to inflammation (Takakazu et al, 2001;Olivier et al, 2003;Roth et al, 2009). Inflammatory mediators such as TNF-α and IL-1β are considered the main endogenous pyrogens (Roth et al, 2009) and they were observed to increase in piglets 3 h after castration (Moya et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Can novel methods be useful for pain assessment of castrated piglets?

Lonardi

Scollo

Normando

et al. 2015

Animal

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Given that surgical castration is a painful practice performed on millions of pigs every year, a need to identify novel reliable pain assessment tools exists in order to test anaesthetic and analgesic protocols that may reduce related pain. Two treatments were considered: handling (H) and surgical castration (C). Physiological (cortisol, lactate, glycaemia, rectal and eye temperature) and behavioural variables (latency to move after treatment and alterations in posture and walking) were analysed. Cortisol showed the greatest level in C piglets within 20 min after the surgical procedure and a positive correlation with glucose concentration. Eye temperature was higher in C piglets, and the same difference was detected for rectal temperature 3 h after castration. Behavioural parameters revealed that C piglets had longer latency to move and a higher percentage of them showed alterations in posture and walking. Results of this study showed that, in castrated piglets behavioural and physiological alterations occur mainly in the first 3 h from treatment. Latency to move, alterations in posture and walking, and eye temperature appear to give additional and useful information in piglet pain assessment. However, differently from the behavioural parameters considered, eye temperature involves several manipulations of the animals and a long process to acquire the data.

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Section: Discussionmentioning

confidence: 99%

Can novel methods be useful for pain assessment of castrated piglets?

Lonardi

Scollo

Normando

et al. 2015

Animal

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“…Using immobilization bags may increase the risk for contact with urine and feces and may also affect thermoregulation due to the restrictive nature and materials of the bag. Maintaining thermoregulatory control is important because body temperature increases in response to a variety of stressors, causing a stress-induced hyperthermia (Marazziti et al, 1992;Olivier et al, 2003). Moreover, the duration that body temperature remains elevated after termination of stress depends on the severity of the stressor (Bhatnagar et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

The effects of chronic stress on hippocampal morphology and function: An evaluation of chronic restraint paradigms

et al. 2007

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Chronic restraint stress for 6h/21d causes hippocampal CA3 apical dendritic retraction, which parallels spatial memory impairments in male rats. Recent research suggests that chronic immobilization stress for 2h/10d induces CA3 dendritic retraction (Vyas et al., 2002) and questions whether CA3 dendritic retraction and spatial memory deficits can be produced sooner than found following 6h/21d of restraint stress. Therefore, this study investigated the effects of four different durations of chronic restraint stress (varied by hours/day and total number of days) and the subsequent effects on hippocampal CA3 morphology and spatial memory in the same male Sprague-Dawley rats. The results showed that only rats exposed to the 6h/21d restraint paradigm exhibited CA3 apical dendritic retraction, consistent spatial memory deficits, and decreased body weight gain compared to experimental counterparts and controls. While chronically stressing a rat with wire mesh restraint has a physical component, it acts primarily as a psychological stressor, and these findings support the interpretation that chronic psychological stress produces hippocampal-dependent cognitive deficits that are consistent with hippocampal structural changes. Differences in stress effects observed across different studies may be due to rat strain, type of stressor, and housing conditions; however, the current findings support the use of chronic restraint stress, with wire mesh, for 6h/21d as a reliable and efficient method to produce psychological stress and to cause CA3 dendritic retraction and spatial memory deficits in male Sprague-Dawley rats.

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“…For example, stress-induced hyperthermia, but not infection-induced fever, is attenuated by anxiolytic drugs, such as diazepam (Fig. 8B) (76,122,178,193), whereas cyclooxygenase inhibitors block infection-induced fever, but not stress-induced hyperthermia (76,155,178,182,188). Furthermore, EP3 receptor-deficient mice can exhibit intact stressinduced hyperthermia, but fail to exhibit LPS-induced fever (119).…”

Section: Psychological Stress-induced Hyperthermiamentioning

confidence: 99%

Central circuitries for body temperature regulation and fever

Nakamura

2011

American Journal of Physiology-Regulatory, Integrative and Comp

432

394

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Nakamura K. Central circuitries for body temperature regulation and fever. Am J Physiol Regul Integr Comp Physiol 301: R1207-R1228, 2011. First published September 7, 2011 doi:10.1152/ajpregu.00109.2011.-Body temperature regulation is a fundamental homeostatic function that is governed by the central nervous system in homeothermic animals, including humans. The central thermoregulatory system also functions for host defense from invading pathogens by elevating body core temperature, a response known as fever. Thermoregulation and fever involve a variety of involuntary effector responses, and this review summarizes the current understandings of the central circuitry mechanisms that underlie nonshivering thermogenesis in brown adipose tissue, shivering thermogenesis in skeletal muscles, thermoregulatory cardiac regulation, heat-loss regulation through cutaneous vasomotion, and ACTH release. To defend thermal homeostasis from environmental thermal challenges, feedforward thermosensory information on environmental temperature sensed by skin thermoreceptors ascends through the spinal cord and lateral parabrachial nucleus to the preoptic area (POA). The POA also receives feedback signals from local thermosensitive neurons, as well as pyrogenic signals of prostaglandin E 2 produced in response to infection. These afferent signals are integrated and affect the activity of GABAergic inhibitory projection neurons descending from the POA to the dorsomedial hypothalamus (DMH) or to the rostral medullary raphe region (rMR). Attenuation of the descending inhibition by cooling or pyrogenic signals leads to disinhibition of thermogenic neurons in the DMH and sympathetic and somatic premotor neurons in the rMR, which then drive spinal motor output mechanisms to elicit thermogenesis, tachycardia, and cutaneous vasoconstriction. Warming signals enhance the descending inhibition from the POA to inhibit the motor outputs, resulting in cutaneous vasodilation and inhibited thermogenesis. This central thermoregulatory mechanism also functions for metabolic regulation and stress-induced hyperthermia.

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Stress-induced hyperthermia and anxiety: pharmacological validation

Cited by 187 publications

References 65 publications

Can novel methods be useful for pain assessment of castrated piglets?

Can novel methods be useful for pain assessment of castrated piglets?

The effects of chronic stress on hippocampal morphology and function: An evaluation of chronic restraint paradigms

Central circuitries for body temperature regulation and fever

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