Long-lasting effects of chronic stress on DOI-induced hyperthermia in male rats

Matuszewich, Leslie; Yamamoto, Bryan K.

doi:10.1007/s00213-003-1498-7

Cited by 41 publications

(28 citation statements)

References 60 publications

(88 reference statements)

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“…Unpredictable stress exposure did not result in similar structural or immediate behavioral changes, which may suggest that different neural substrates mediate the increase in anxiety behaviors following predictable compared to unpredictable stress [57,58]. We have previously found that CUS alters serotonin receptor mediated responses for several months following termination of the last stressor [34]. The increase in anxiety responses following unpredictable stress exposure may be related to alterations in the serotonin receptor system, although glutamatergic alterations have also been reported [27,28].…”

Section: Discussionmentioning

confidence: 87%

The delayed effects of chronic unpredictable stress on anxiety measures

Matuszewich

Karney

Carter

et al. 2007

Physiology & Behavior

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Previous research has found that exposure to unpredictable stress can augment anxiety in humans and animals. The appearance of anxiety symptoms in humans frequently develop after stress exposure has terminated, but few rodent studies have systematically examined the delayed anxiogenic effects of unpredictable stress. Therefore, the current study investigated whether anxiety-like behaviors in rats would increase at several time intervals following exposure to chronic unpredictable stress (CUS). Unconditioned and conditioned response tasks were used to assess anxiety in male rats 1, 7 or 14 days following exposure to 10 days of a variety of stressors. Rats exposed to CUS showed increased burying behaviors and immobility during the defensive burying test, a conditioned anxiety test. The effects on burying behavior were apparent 7 and 14 days after the termination of the unpredictable stress procedure, but not when tested 1 day after CUS. Total time immobile in the defensive burying test also increased 14 days after termination of the last stressor. In contrast, there were no significant effects of CUS on behavioral measures in the unconditioned response tasks, the elevated plus-maze or light-dark box, at any time point following exposure to CUS. The current findings suggest that CUS may be a useful model of human conditioned anxiety that develops subsequent to chronic stress exposure.

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Section: Discussionmentioning

confidence: 87%

The delayed effects of chronic unpredictable stress on anxiety measures

Matuszewich

Karney

Carter

et al. 2007

Physiology & Behavior

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“…It has also been well established that central dopaminergic and serotoninergic pathways originating from the VTA and DRN are activated by a variety of physical and psychological stressors, including conditioned fear (Inoue et al, 1994;Beck and Fibiger, 1995;Yoshioka et al, 1995Yoshioka et al, , 1996Morrow et al, 1999). Furthermore, evidence shows that prior exposure to acute or chronic stressors can result in behavioral and pharmacological sensitization effects caused by changes dopaminergic (Pani et al, 2000;de Jong et al, 2005) and serotonergic tone (Adell et al, 1988;Chung et al, 2000;Matuszewich and Yamamoto, 2003). In support of this view, Watkins and Maier have shown that the habenula is essential for the normal sensitization of DRN neurons after uncontrollable stress (Maier et al, 1995;Maswood et al, 1998;Grahn et al, 1999;Amat et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

Heldt

Ressler

2006

Brain Research

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The habenula complex modulates the a ctivity of dopamine and serotonin systems in the brain. An important question remains whether there is a link between habenula dysfunction and monoaminerelated disorders, such as schizophrenia. In this study, we describe an interaction between habenula lesions and stress that produces long-lasting effects on behavior. Mice received control lesions or bilateral electrolytic lesions of the habenula and were tested for fear-potentiated startle and freezing measures of conditioned fear. They w ere also tested for prepulse inhibition (PPI) and locomotor activity in the presence or absence of a dopaminergic agonist (apomorphine) or an atypical antipsychotic with mixed dopamine/serotonin antagonist properties (clozapine). There were no detectable effects of habenula lesions on fear conditioning and no effects on PPI in the absence o f stress. However, following conditioned fear stress, habenula-lesioned animals showed decreased PPI which normalized with clozapine. Lesioned animals also showed diminished activity at baseline, with hyperlocomotion following apomorphine. These data support the hypothesis that the habenula may be normally involved in stress-dependent regulation of monoamine systems.

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“…In any event it is unlikely that corticosterone is the only factor mediating the changes documented in this study. While long-term glucocorticoid treatment sensitizes DOI-induced wet-dog shakes and desensitizes 8-OH-DPAT-mediated hypothermia, no changes in the lethality of DOI have ever been documented following this treatment Matuszewich and Yamamoto, 2003 ;Takao et al, 1997). However, it should be noted that 10-d treatment with corticosterone has been documented to enhance the induction of 5-HT syndrome in response to carbidopa and 5-hydroxytryptophan, demonstrating that glucocorticoids do possess the ability to sensitize the induction of 5-HT syndrome (Young et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Altered responsiveness of serotonin receptor subtypes following long-term cannabinoid treatment

Hill¹,

Sun²,

Tse³

et al. 2005

Int. J. Neuropsychopharm.

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This study examined the effects of long-term cannabinoid administration on the responsivity of 5-HT 1A and 5-HT 2A receptors, which have been implicated in depression. Animals received 12 d administration of the potent cannabinoid receptor agonist HU-210 (100 mg/kg), following which they were monitored on their behavioural, physiological and hormonal responses to a single challenge of a 5-HT 1A and 5-HT 2A receptor agonist, 8-OH-DPAT (0.3 mg/kg) and DOI (1 mg/kg) respectively. Chronic HU-210 treatment lead to a significant enhancement of DOI-induced wet-dog shakes, but a reduction of DOI-induced back muscle contractions. DOI-induced corticosterone release was unaffected by HU-210 treatment. The hyperthermic response to DOI appeared to be potentiated by long-term HU-210 treatment, as 50 % of these subjects died from an apparent serotonin syndrome with core temperatures exceeding 43 xC. The 8-OH-DPAT-induced hypothermic response and elevation of corticosterone were both significantly attenuated by long-term HU-210 treatment. These data imply that chronic cannabinoid treatment may up-regulate 5-HT 2A receptor activity while concurrently down-regulating 5-HT 1A receptor activity, a finding similar to that sometimes observed in depression. This may partially explain the association between excessive cannabis consumption and the induction of affective disease.

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Long-lasting effects of chronic stress on DOI-induced hyperthermia in male rats

Abstract: The enhancement of 5-HT receptor function by chronic stress persists even after the environmental stressor is removed. This lasting increase in 5-HT receptor function may have implications for clinical disorders associated with stress, such as depression or post-traumatic stress disorder.

Cited by 41 publications

References 60 publications

The delayed effects of chronic unpredictable stress on anxiety measures

The delayed effects of chronic unpredictable stress on anxiety measures

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

Altered responsiveness of serotonin receptor subtypes following long-term cannabinoid treatment

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