Effect of paroxetine on enhanced contextual fear induced by single prolonged stress in rats

Takahashi, Terumichi; Morinobu, Shigeru; Iwamoto, Yasuyuki; Yamawaki, Shigeto

doi:10.1007/s00213-006-0545-6

Cited by 130 publications

(98 citation statements)

References 43 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: 66%

“…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: 66%

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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“…SPS rats underwent the SPS procedure on the first day. The SPS protocol was based on a combined plural stress paradigm (7,20): immobilization (compression with plastic bags) for 2 h, forced swimming for 20 min (24±1˚C), rest for 15 min, followed by drying and ether anesthesia (until consciousness was lost).…”

Section: Methodsmentioning

confidence: 99%

“…These neuroendocrine findings specific to PTSD have served as the basis for animal models that are useful for elucidating the pathophysiology of PTSD. Singleprolonged stress (SPS) is a reliable animal model of PTSD based on the time-dependent dysregulation of the HPA axis and has been developed and employed for PTSD research (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Xiao

Han²,

Shi³

2009

Int J Mol Med

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Abstract. Single-prolonged stress (SPS) is an established animal model for post-traumatic stress disorder (PTSD). The calcium (Ca 2+ )-calmodulin (CaM)-CaM kinase (K)II· signal passage plays an important role in the plasticity of central nervous, learning and memory, mind and behavior and other types of cognitive activities. The amygdala is known to play an important role in fear, rage and emotional memory. In this study, we investigated changes in Ca 2+ -CaM-CaMKII· in the basolateral amygdala of rats after SPS which may reveal part of the pathogenesis of PTSD. The intracellular free calcium level in the basolateral amygdala was examined by fluorescence spectrophotometry. CaM and CaMKII· expression in basolateral amygdala was examined using immunohistochemistry, western blotting and reverse transcriptionpolymerase chain reaction. The intracellular free calcium level in the basolateral amygdala was increased when compared to that in the control group 1 day after SPS exposure (P<0.05). CaM expression significantly increased, and CaMKII· expression significantly decreased (P<0.05) in the basolateral amygdala after SPS. These findings suggest dysfunction of Ca 2+ -CaM-CaMKII· in the basolateral amygdala of SPS rats, which may play important roles in the pathogenesis of PTSD rats.

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“…Thus, in the present study, a rat model of PTSD was built following the previously established SPS protocol (17,18), and immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting analysis approaches were used to identify the expression of VDR in the rat hippocampal cells. In addition, the expression of LVSCC-A1C protein and mRNA was examined, as well as the Ca 2+ levels.…”

Section: Introductionmentioning

confidence: 99%

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

Tong

Peng

et al. 2014

Molecular Medicine Reports

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Abstract. Vitamin D signaling not only controls calcium (Ca 2+ ) and phosphorus uptake and transport, but also correlates with neurocognitive decline and neurodegenerative diseases. Almost all actions of Vitamin D are mediated by the transcription factor, vitamin D receptor (VDR), which has been widely identified in the central nervous system. Although previous studies have substantially advanced the understanding of the action of VDR in the brain, much remains unknown concerning how VDR relates to stress. Multiple lines of evidence indicate that the downregulation of L-type voltage-sensitive Ca 2+ -channels α-1C (LVSCC-A1C) by vitamin D in hippocampal neurons is able to reduce the influx and excitotoxic effects of Ca 2+ to neurons. Along these lines, the purpose of the present study was to analyze the relative expression of VDR in the hippocampus of rats exposed to single prolonged stress (SPS) as a putative animal model for human post-traumatic stress disorder (PTSD). Furthermore, changes in the levels of expression of LVSCC-A1C and Ca 2+ (neurotransmitter content) were examined during the onset periods of PTSD. The results revealed an increase in the expression of VDR at 1, 3 and 7 days post-stress compared with the control group. The intracellular free Ca 2+ levels in the hippocampus increased 1 day after SPS exposure, and then decreased gradually to the normal level at 14 days, consistent with the expression pattern of LVSCC-A1C. These results indicated that VDR may be involved in the pathogenesis of SPS rats, thereby providing an alternative preparation to search for optimal therapeutic strategies for PTSD. IntroductionPost-traumatic stress disorder (PTSD) is a severe anxiety disorder that may develop following exposure to any threat or injury that results in psychological trauma. Diagnostic symptoms for PTSD include re-experiencing the original trauma through flashbacks or nightmares, avoidance of stimuli associated with the trauma and increased arousal. Single-prolonged stress (SPS), an animal model of PTSD, has been extensively developed and employed in the investigation of PTSD (1-3). The three areas of the brain whose function may be altered in PTSD have been identified as the prefrontal cortex, the amygdala and the hippocampus, among which, the hippocampus is a key organ of the limbic system involved in learning and memory, as well as being a regulatory center for the stress response (4).Alterations in brain neurochemistry have been linked with neuropsychiatric disorders, including schizophrenia, Alzheimer's disease, depression and cognitive decline. Previous studies have identified a positive association between vitamin D signaling and cognitive function (5). Vitamin D may regulate neurotransmission, neuroprotection and neuroimmunomodulation as a neurosteroid hormone (5,6), in addition to its critical role in calcium (Ca 2+ ) and phosphorous regulation and skeletal mineralization (7). Hypovitaminosis D is associated with several neuropsychiatric disorders, including dementia, Parkinson's d...

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Effect of paroxetine on enhanced contextual fear induced by single prolonged stress in rats

Abstract: Our results suggest that SPS can reproduce behavioral alteration similar to that observed in patients with PTSD, and this elevated fear response can be alleviated by the chronic administration of PRX at doses producing clinically relevant serum concentrations.

Cited by 130 publications

References 43 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

Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

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