Glucocorticoid receptor activation is involved in producing abnormal phenotypes of single-prolonged stress rats: A putative post-traumatic stress disorder model

Kohda, Kazuhisa; Harada, Kensuke; Katö, Kunio; Hoshino, Ai; Motohashi, Junko; Yamaji, Takayuki; Morinobu, Shigeru; Matsuoka, Naoki; Kato, Nobuo

doi:10.1016/j.neuroscience.2007.05.041

Cited by 214 publications

(215 citation statements)

References 74 publications

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“…Apparently, this finding is contradictory to the lack of effect on memory reconsolidation of stressed rats after MDZ administration observed in the current research. It is noteworthy that stress experience strengthened fear memory and this influence is revealed by two main effects: (a) enhanced fear retention or fear expression as previously demonstrated using the SPS (Takahashi et al, 2007;Kohda et al, 2007) and/or (b) the impairment of fear extinction or the resistance to extinguish (Rodríguez Manzanares et al, 2005;Akirav and Maroun, 2007;Yamamoto et al, 2008). In contrast, Zhang and Cranney (2008) found no increase of fear expression and no alteration of extinction rate in the rats subjected to modified SPS, despite increased anxiety as evidenced in an elevated plus-maze test.…”

Section: Discussionsupporting

confidence: 62%

“…What is more, under the present experimental protocol, baseline levels of fear averaged 70-80% during reactivation in unstressed rats. Other authors have shown that the exposure to a single-prolonged stress (SPS) protocol resulted in a facilitated contextual fear memory 1 week, but not 1 day after such stressful stimuli (Takahashi et al, 2007;Kohda et al, 2007). Zhang and Cranney (2008) described, using a modified SPS, that MDZ interfered fear memory reconsolidation even in stressed rats.…”

Section: Discussionmentioning

confidence: 99%

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Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Bustos

Giachero

Maldonado

et al. 2009

Neuropsychopharmacol

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It is well known that, under certain boundary conditions, the retrieval of a stable consolidated memory results into a labile one. During this unstable phase, memory can be vulnerable to interference by a number of pharmacological agents, including benzodiazepines. One of the goals of this study was to evaluate the vulnerability to midazolam (MDZ) after reactivation of recent and remote contextual fear memories in animals that experienced a stressful situation before learning. Animals were subjected to a restraint session and trained in a contextual fear paradigm the following day; consolidated memories were reactivated at different times after learning and different MDZ doses (1.5, 3.0 mg/kg) were administered to rats after reactivation. Our results show that MDZ did not affect memory reconsolidation in older-than-one-day memories of stressed animals, even after the administration of a higher MDZ dose and a longer reactivation session (5 min). In contrast, MDZ was effective in blocking reconsolidation at all memory ages in unstressed animals. In addition, the current research investigated whether activating NMDA sites before reactivation promotes the destabilization of resistant memories such as those of stressed animals. We tested the influence of pre-reactivation D-cycloserine (DCS), a partial NMDA agonist, on MDZ's effect on fear memory reconsolidation in stressed animals. Our findings indicate that DCS before reactivation promotes retrieval-induced lability in resistant memory traces, as MDZ-induced memory impairment in stressed rats became evident with pre-reactivation DCS but not after pre-reactivation sterile isotonic saline.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Bustos

Giachero

Maldonado

et al. 2009

Neuropsychopharmacol

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“…It was reported that SPS, a putative PTSD animal model, presents behavioral alterations resembling and shows the most consistent neuroendocrinologic characteristics with PTSD patients (35,36). Rats exposed to SPS exhibited enhanced inhibition of the HPA system and alteration in the glucocorticoid/mineralocorticoid receptor.…”

Section: Discussionmentioning

confidence: 99%

Changes in 5-HT1A receptor in the dorsal raphe nucleus in a rat model of post-traumatic stress disorder

2011

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Abstract. Post-traumatic stress disorder (PTSD) is characterized mainly by symptoms of re-experiencing, avoidance and hyperarousal as a consequence of catastrophic and traumatic events that are distinguished from ordinary stressful life events. Single-prolonged stress (SPS) is an established animal model for post-traumatic stress disorder (PTSD). The dorsal raphe nucleus (DR)-serotonin (5-HT) system is markedly affected by swim stress and has been implicated in affective disorders. The 5-HT1A receptor (5-HT1AR) is critically involved in regulating mood and anxiety levels. In this study, we investigated changes in the expression of 5-HT1AR in the DR of rats after SPS that may reveal part of the pathogenesis of PTSD. 5-HT1AR expression in the DR was examined using immunohistochemistry, Western blotting and reverse transcription polymerase chain reaction. The expression of 5-HT1AR in the DR after SPS exposure was increased when compared to that in the control group (P<0.05). These findings indicate an increase in 5-HT1AR in the DR of SPS rats, which may play important roles in the pathogenesis of PTSD rats.

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“…Furthermore, CORT acts via glucocorticoid receptors to exacerbate pain in mice with a spared nerve injury (SNI) after exposure to restraint stress (25). Kohda K et al (26) conducted a study in rats and reported that SPS exposure inhibited the hypothalamo-pituitary-adrenal (HPA) axis and increased GR expression in the hippocampus. Glucocorticoid receptors are known to also be located in spinal cord dorsal horn neurons, and the activation of GRs regulates pain states and the stress response (27).…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Alleviates Presurgical Anxiety-Induced Persistent Postsurgical Pain via Decreasing the Expression of Glucocorticoid Receptor

Li¹,

Zhang²,

Yin³

et al. 2018

J Anesth Perioper Med

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Background: Preoperative anxiety can worsen postsurgical pain. Glucocorticoids play an important role in psychological anxiety and pain, but the effect of glucocorticoid receptor (GR) on persurgical anxiety-induced persistent postsurgical pain remains unknown. Methods: Adult male Sprague Dawley rats were randomly divided into 10 groups: control group, SPS group, incision group, 'SPS-plus-incision' group, saline group, metyrapone group, Dexmedetomidine group 1 (10 μg/kg), Dexmedetomidine group 2 (20 μg/kg), Dexmedetomidine group 3 (40 μg/kg) and Dexmedetomidine + Corticosterone group. Single-prolonged stress (SPS) was used to induce anxiety behaviors. Intraperitoneal injection of saline and dexmedetomidine was performed at 24 h after SPS and 0.5 h before incision. Intraperitoneal injection of metyrapone (25 mg/kg) was performed at 1h before SPS. Paw withdrawal mechanical threshold (PWMT) was tested at 24 h before SPS and on 1, 4, 7, 14, 21, and 28 days after incision. Corticosterone levels were determined using ELISA. The expression of GR was determined using Western blot. Results: The 'SPS-plus-incision' group decreased PWMT compared with control group and incision group from 1 to 28 days (P<0.05). SPS combined with incision increased plasma corticosterone levels compared with control group (P<0.05). A timedependent increase in GR was also observed in 'SPS-plus-incision' group (P<0.05). Metyrapone significantly blunted the SPS-induced persistent postsurgical pain (P< 0.05). Intraperitoneal administration of dexmedetomidine inhibits SPS-induced persistent pain compared with group saline (P<0.05). The expression of GR decreased after the intraperitoneal administration of dexmedetomidine (P<0.05). Pretreatment with corticosterone blocked this effect. Conclusions: Glucocorticoids contributed to presurgical anxiety-induced persistent postsurgical pain. Dexmedetomidine that decreased the expression of GR alleviated anxiety-induced persistent pain. These results indicated that dexmedetomidine may be an effective agent for preventing presurgical anxiety-induced persistent postoperative pain.

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Glucocorticoid receptor activation is involved in producing abnormal phenotypes of single-prolonged stress rats: A putative post-traumatic stress disorder model

Cited by 214 publications

References 74 publications

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Changes in 5-HT1A receptor in the dorsal raphe nucleus in a rat model of post-traumatic stress disorder

Dexmedetomidine Alleviates Presurgical Anxiety-Induced Persistent Postsurgical Pain via Decreasing the Expression of Glucocorticoid Receptor

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