Stress-induced hyperthermia as a putative anxiety model

Zethof, T. J. J.; Heyden, J.A.M. van der; Tolboom, Jeroen; Olivier, Berend

doi:10.1016/0014-2999(95)00520-x

Cited by 106 publications

(62 citation statements)

References 29 publications

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“…The anxiolytic diazepam blocked the stress-induced hyperthermia at the highest dose (4.0 mg/kg) in line with earlier reports (Groenink et al 1996;Van der Heyden et al 1997;Zethof et al 1995;Olivier et al 2001) in both WT and KO mice. Stress-induced tachycardia was not affected by diazepam in either genotype, as also reported before in rats (Tornatzky and Miczek 1995).…”

Section: Discussionsupporting

confidence: 90%

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Pattij

Groenink

Hijzen

et al. 2002

Neuropsychopharmacology

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Section: Discussionsupporting

confidence: 90%

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Pattij

Groenink

Hijzen

et al. 2002

Neuropsychopharmacology

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“…Two methods were used. First, mice were injected with DOI (1 mg/kg i.p., four times, 2-h interval between injections), a 5-hydroxytryptamine (serotonin) 2A (5-HT 2A ) receptor agonist that also causes hyperthermia (Zethof et al, 1995). Second, a heating blanket was wrapped around a small shoe box cage containing five mice, and a heat lamp was placed above the cage to increase body temperature to 40°C.…”

Section: Methodsmentioning

confidence: 99%

Methamphetamine Neurotoxicity in Dopamine Nerve Endings of the Striatum Is Associated with Microglial Activation

Thomas

Walker²,

Benjamins³

et al. 2004

J Pharmacol Exp Ther

282

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Methamphetamine intoxication causes long-lasting damage to dopamine nerve endings in the striatum. The mechanisms underlying this neurotoxicity are not known but oxidative stress has been implicated. Microglia are the major antigen-presenting cells in brain and when activated, they secrete an array of factors that cause neuronal damage. Surprisingly, very little work has been directed at the study of microglial activation as part of the methamphetamine neurotoxic cascade. We report here that methamphetamine activates microglia in a dose-related manner and along a time course that is coincident with dopamine nerve ending damage. Prevention of methamphetamine toxicity by maintaining treated mice at low ambient temperature prevents drug-induced microglial activation. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which damages dopamine nerve endings and cell bodies, causes extensive microglial activation in striatum as well as in the substantia nigra. In contrast, methamphetamine causes neither microglial activation in the substantia nigra nor dopamine cell body damage. Dopamine transporter antagonists (cocaine, WIN 35,428 [(Ϫ)-2-␤-carbomethoxy-3-␤-(4-fluorophenyl)tropane 1,5-naphthalenedisulfonate], and nomifensine), selective D1 (SKF 82958 [(Ϯ)-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide]), D2 (quinpirole), or mixed D1/D2 receptor agonists (apomorphine) do not mimic the effect of methamphetamine on microglia. Hyperthermia, a prominent and dangerous clinical response to methamphetamine intoxication, was also ruled out as the cause of microglial activation. Together, these data suggest that microglial activation represents an early step in methamphetamine-induced neurotoxicity. Other neurochemical effects resulting from methamphetamine-induced overflow of DA into the synapse, but which are not neurotoxic, do not play a role in this response.

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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

440

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 as a putative anxiety model

Cited by 106 publications

References 29 publications

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Methamphetamine Neurotoxicity in Dopamine Nerve Endings of the Striatum Is Associated with Microglial Activation

Central circuitries for body temperature regulation and fever

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