Escitalopram reversed the traumatic stress-induced depressed and anxiety-like symptoms but not the deficits of fear memory

Lin, Chen-Cheng; Tung, Che‐Se; Liu, Yia-Ping

doi:10.1007/s00213-015-4194-5

Cited by 57 publications

(42 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several previous studies have observed behavioral effects of SPS that persist for several weeks. Increased anxiodepressive behavior is seen shortly after SPS and persists for at least 2-3 weeks (Ji et al, 2014;Khan & Liberzon, 2004;Lin, Tung, & Liu, 2016;Miao et al, 2014;Patki et al, 2014;Peng et al, 2010;Takahashi, Morinobu, Iwamoto, & Yamawaki, 2006), consistent with the increase in anxietylike behavioral changes observed here 1-2 weeks after stress. We found that elevated plus maze behavior and NSF returned to normal within 5 weeks of SPS in normal (wild type) rats.…”

Section: Long-term Effects Of Acute Stresssupporting

confidence: 85%

New neurons restore structural and behavioral abnormalities in a rat model of PTSD

et al. 2019

View full text Add to dashboard Cite

Post-traumatic stress disorder (PTSD) has been associated with anxiety, memory impairments, enhanced fear, and hippocampal volume loss, although the relationship between these changes remain unknown. Single-prolonged stress (SPS) is a model for PTSD combining three forms of stress (restraint, swim, and anesthesia) in a single session that results in prolonged behavioral effects. Using pharmacogenetic ablation of adult neurogenesis in rats, we investigated the role of new neurons in the hippocampus in the long-lasting structural and behavioral effects of SPS. Two weeks after SPS, stressed rats displayed increased anxiety-like behavior and decreased preference for objects in novel locations regardless of the presence or absence of new neurons. Chronic stress produced by daily restraint for 2 or 6 hours produced similar behavioral effects that were also independent of ongoing neurogenesis. At a longer recovery time point, one month after SPS, rats with intact neurogenesis had normalized, showing control levels of anxiety-like behavior. However, GFAP-TK rats, which lacked new neurons, continued to show elevated anxiety-like behavior and enhanced serum corticosterone response to anxiogenic experience. Volume loss in ventral CA1 paralleled increases in anxiety-like behavior, occurring in all rats exposed to SPS at the early time point and only rats lacking adult neurogenesis at the later time point. In chronic stress experiments, volume loss occurred broadly throughout the dentate gyrus and CA1 after 6-hour daily stress but was not apparent in any hippocampal subregion after 2-hr daily stress. No effect of SPS was seen on cell proliferation in the dentate gyrus, but the survival of young neurons born a week after stress was decreased. Together, these data suggest that new neurons are functionally important for recovery of normal behavior and hippocampal structure following a strong acute stress and point to the ventral CA1 region as a potential key mediator of stress-induced anxiety-like behavior.

show abstract

Section: Long-term Effects Of Acute Stresssupporting

confidence: 85%

New neurons restore structural and behavioral abnormalities in a rat model of PTSD

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Defective DA signaling has been implicated in PTSD, including deficits in the reward and reinforcement circuits, decreased reward anticipation and reduced hedonic responses, reduced DA metabolites in cerebral spinal fluid following traumatic reminders, altered expression of striatal DA transporter, and polymorphisms in genes encoding DAT and DA receptors in PTSD patients (40). A reduced basal spiking rate of VTA DA neurons (55) and altered DA level (56) were reported in PTSD models. We have provided clear evidence of impaired fear suppression and the absence of potentiated activation of VTA DA neurons after SL, while DA-dmPFC connections appear to be largely intact.…”

Section: Discussionmentioning

confidence: 99%

Elevated dopamine signaling from ventral tegmental area to prefrontal cortical parvalbumin neurons drives conditioned inhibition

Yan

Wang

Zhou

2019

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Conditioned inhibition is an important process to suppress learned responses for optimal adaptation, but its underlying biological mechanism is poorly understood. Here we used safety learning (SL)/fear discrimination after fear conditioning as a conditioned inhibition model because it demonstrates the essential properties of summation and retardation. Activity of the dorsomedial prefrontal cortex (dmPFC) parvalbumin (PV) neurons bidirectionally regulates spiking levels of dmPFC excitatory neurons and fear states. Responses to safety cues are increased in dopaminergic (DA) neurons in the ventral tegmental area (VTA) and in PV neurons in dmPFC after SL. Plasticity in the VTA is implicated, since SL requires activation of N-methyl-D-aspartate receptors. Furthermore, in a posttraumatic stress disorder model, impaired SL is associated with impaired potentiation of VTA DA neuron activity. Our results demonstrate a DA-dependent learning process that targets prefrontal inhibitory neurons for suppression of learned responses, and have implications for the pathogenesis and treatment of various psychiatric diseases. dopamine | prefrontal cortex | ventral tegmental area | parvalbumin neurons | safety learning

show abstract

“…We have shown that PTSD animals treated with OLE had significant increases in 5-HT levels in the hippocampus and that this may have inhibited the pathophysiology of PTSD. The effects of OLE can be reversed by 5-HT manipulation (Lin et al 2016 ). Thus, the present findings indicate that OLE, like FLX, attenuates the behavior and neurochemical responses associated with anxiety by modulating NPY expression and the serotonergic system in the brain (Aykaç et al 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Oleuropein reduces anxiety-like responses by activating of serotonergic and neuropeptide Y (NPY)-ergic systems in a rat model of post-traumatic stress disorder

Lee

Shim

Lee

et al. 2018

Animal Cells and Systems

View full text Add to dashboard Cite

Post-traumatic stress disorder (PTSD) is a stress-related mental disorder caused by traumatic experiences. This psychopathological response to traumatic stressors induces anxiety in rats. Oleuropein (OLE), a major compound in olive leaves, reportedly possesses several pharmacological properties, including anti-cancer, anti-diabetic, and anti-atherosclerotic and neuropsychiatric activities. However, the anxiolytic-like effects of OLE and its mechanism of action in PTSD are unclear. The present study used several behavioral tests to examine the effects of OLE on symptoms of anxiety in rats after a single prolonged stress (SPS) exposure by inhibiting the hypothalamic-pituitary-adrenal axis. Male Sprague Dawley rats received OLE (10, 50 and 70 mg/kg, i.p., once daily) for 14 days after SPS exposure. Daily OLE (70 mg/kg) administration significantly increased the number and duration of open arm visits in the elevated plus maze (EPM) test, reduced the anxiety index and grooming behavior in the EPM test, and increased the time spent and number of central zone crossings in the open field test. OLE also blocked the SPS-induced decrease in hippocampal serotonin and neuropeptide Y expression in hippocampus. These findings suggest that OLE has anxiolytic-like effects on behavioral and biochemical symptoms similar to those observed in patients with PTSD.

show abstract

Escitalopram reversed the traumatic stress-induced depressed and anxiety-like symptoms but not the deficits of fear memory

Abstract: PTSD-induced mood dysfunction is psychopathologically different from PTSD-induced fear disruption in terms of disequilibrium of monoamines within the fear circuit areas.

Cited by 57 publications

References 67 publications

New neurons restore structural and behavioral abnormalities in a rat model of PTSD

New neurons restore structural and behavioral abnormalities in a rat model of PTSD

Elevated dopamine signaling from ventral tegmental area to prefrontal cortical parvalbumin neurons drives conditioned inhibition

Oleuropein reduces anxiety-like responses by activating of serotonergic and neuropeptide Y (NPY)-ergic systems in a rat model of post-traumatic stress disorder

Contact Info

Product

Resources

About