Ketamine, but not fluoxetine, rapidly rescues corticosterone-induced impairments on glucocorticoid receptor and dendritic branching in the hippocampus of mice

Fraga, Daiane B.; Camargo, Anderson; Padilha, Dayane Azevedo; Mina, Francielle; Budni, Josiane; Brocardo, Patrícia S.; Rodrigues, Ana Lúcia S.

doi:10.1007/s11011-021-00743-2

Cited by 15 publications

(7 citation statements)

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“…Another clinical paper showed that among persons with stress-related mood and anxiety disorders, SV2A expression in the dlPFC was negatively associated with measures of worry and tension/anxiety ( 168 ). These data are aligned with other findings showing that excess glucocorticoids/stress negatively impacts spine density, which can be reversed by ketamine ( 41 , 56 , 92 , 94 , 95 , 130 , 169 ) and LSD ( 147 ). Interestingly, across several studies in which stress exposure did not lead to changes in synaptic markers, ketamine did not influence synaptic markers either ( 51 , 88 – 90 , 93 , 126 , 135 , 140 , 136 ).…”

Section: Discussionsupporting

confidence: 90%

“…Two studies did not find ketamine post-treatment (0.1-1 mg/kg) to effect PSD-95 or synapsin-1 in the hippocampus and PFC of rodents treated chronically with corticosterone (89, 126). By contrast, four studies found that ketamine (1-5 mg/kg) pre-and/or post-treatment ameliorated corticosterone-reduced dendritic arborization, PSD-95, and/or synapsin-1 in the hippocampus (92,94,95,127).…”

Section: Ketamine Effects In Animal Models Of Stress In Vivomentioning

confidence: 89%

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Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review

et al. 2023

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BackgroundKetamine and psychedelics have abuse liability. They can also induce “transformative experiences” where individuals experience enhanced states of awareness. This enhanced awareness can lead to changes in preexisting behavioral patterns which could be beneficial in the treatment of substance use disorders (SUDs). Preclinical and clinical studies suggest that ketamine and psychedelics may alter markers associated with synaptic density, and that these changes may underlie effects such as sensitization, conditioned place preference, drug self-administration, and verbal memory performance. In this scoping review, we examined studies that measured synaptic markers in animals and humans after exposure to ketamine and/or psychedelics.MethodsA systematic search was conducted following PRISMA guidelines, through PubMed, EBSCO, Scopus, and Web of Science, based on a published protocol (Open Science Framework, DOI: 10.17605/OSF.IO/43FQ9). Both in vivo and in vitro studies were included. Studies on the following synaptic markers were included: dendritic structural changes, PSD-95, synapsin-1, synaptophysin-1, synaptotagmin-1, and SV2A.ResultsEighty-four studies were included in the final analyses. Seventy-one studies examined synaptic markers following ketamine treatment, nine examined psychedelics, and four examined both. Psychedelics included psilocybin/psilocin, lysergic acid diethylamide, N,N-dimethyltryptamine, 2,5-dimethoxy-4-iodoamphetamine, and ibogaine/noribogaine. Mixed findings regarding synaptic changes in the hippocampus and prefrontal cortex (PFC) have been reported when ketamine was administered in a single dose under basal conditions. Similar mixed findings were seen under basal conditions in studies that used repeated administration of ketamine. However, studies that examined animals during stressful conditions found that a single dose of ketamine counteracted stress-related reductions in synaptic markers in the hippocampus and PFC. Repeated administration of ketamine also counteracted stress effects in the hippocampus. Psychedelics generally increased synaptic markers, but results were more consistently positive for certain agents.ConclusionKetamine and psychedelics can increase synaptic markers under certain conditions. Heterogeneous findings may relate to methodological differences, agents administered (or different formulations of the same agent), sex, and type of markers. Future studies could address seemingly mixed results by using meta-analytical approaches or study designs that more fully consider individual differences.

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Section: Discussionsupporting

confidence: 90%

Section: Ketamine Effects In Animal Models Of Stress In Vivomentioning

confidence: 89%

Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review

et al. 2023

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“…Interestingly, ketamine failed to reverse swim stress-induced decrease of digging; however, this could be due to a compounding effect as a single injection of ketamine has been shown to increase corticosterone in rats following chronic corticosterone administration (Wegman-Points et al, 2020). However, there are plenty of studies demonstrating ketamine’s ability to reverse corticosterone-induced depression of behavior and cellular signaling (Fraga et al, 2021; Sowa et al, 2019; Wang et al, 2019). The lack of ketamine effect in following swim stress could be due to several variables including, but not limited to, dose tested, pretreatment time on test days, and/or dosing regimen.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of repeated fluoxetine and ketamine administration on behavioral and pharmacological stressor-induced depression of digging behavior in mice.

Partridge,

Hillhouse

2024

Experimental and Clinical Psychopharmacology

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Major depressive disorder is a multifactorial disorder that originates from a complex web of variables and overlaps with similar disorders (e.g., depression and anxiety). As such, animal models should account for the considerable symptom overlap between psychiatric disorders. We sought to extend the findings of behavioral assays that encompass both anxiety and stress/depression components. To do so, we have focused on digging behavior, a compulsive-like behavior displayed in mice, in which we employed behavioral and pharmacological stressors to reduce digging behaviors, producing a depression-like state. Locomotor activity was assessed during each test session. We found that digging behavior remains consistent, but locomotor activity decreased when exposed to multiple test sessions over 4 weeks and no sex differences were observed. A time-course study showed a single swim stress significantly reduced digging behavior for at least 3 days but rebounded to baseline levels by Day 7. Repeated treatment of 10 mg/kg/day fluoxetine, but not ketamine, partially reversed swim stress-induced depression of digging behavior on Days 3 and 7. The pharmacological stressor yohimbine (1.0-5.0 mg/kg) dose-dependently decreased digging behavior. Repeated treatment of 10 mg/kg/day ketamine, but not fluoxetine, reversed yohimbineinduced depression of digging behavior on Days 3 and 7. These data suggest that digging behavior is a stable and consistent behavior displayed by all mice. We were able to depress digging behavior with both behavioral and pharmacological stress. However, the reversal of stress-induced depression of digging behavior was stimulus-(e.g., behavioral vs. pharmacological) and drug-dependent and will require further investigation. Public Health SignificanceResearchers have argued that psychiatric disorders should be viewed on a spectrum to account for overlap between disorders. As such, animal models should account for the considerable symptom overlap between psychiatric disorders. This study indicates that behavioral and pharmacological stressors can be added to the assay of compulsive digging to depress digging behavior in mice (moving toward an animal model with an anxiety/compulsive and depression component), which can be reversed by clinically approved antidepressant drugs.

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“…These effects may be related to their rapid antidepressant response. 135 In addition, a single dose of S-ketamine, instead of R-ketamine, can cause the loss of paralbumin (PV)-positive cells in the medial prefrontal cortex and the anterior DG area. 136 Moreover, anxiety disorders, currently the most prevalent psychiatric disorder, cause a high social impact and economic burden.…”

Section: The Effects Of Ketamine In Improving Perioperative Sleep Qualitymentioning

confidence: 99%

A Novel Application of Ketamine for Improving Perioperative Sleep Disturbances

Song¹,

Zhu²

2021

NSS

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Perioperative sleep disturbances are commonly observed before, during, and after surgery and can be caused by several factors, such as preoperative negative moods, general anesthetics, surgery trauma, and pain. Over the past decade, the fast-acting antidepressant effects of the N-methyl-D-aspartate (NMDA) receptor antagonist ketamine represent one of the most attractive discoveries in the field of psychiatry, such as antidepressant and anxiolytic effects. It is also widely used as a short-acting anesthetic and analgesic. Recent research has revealed new possible applications for ketamine, such as for perioperative sleep disorders and circadian rhythm disorders. Here, we summarize the risk factors for perioperative sleep disturbances, outcomes of perioperative sleep disturbances, and mechanism of action of ketamine in improving perioperative sleep quality.

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Ketamine, but not fluoxetine, rapidly rescues corticosterone-induced impairments on glucocorticoid receptor and dendritic branching in the hippocampus of mice

Cited by 15 publications

References 61 publications

Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review

Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review

Differential effects of repeated fluoxetine and ketamine administration on behavioral and pharmacological stressor-induced depression of digging behavior in mice.

A Novel Application of Ketamine for Improving Perioperative Sleep Disturbances

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