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Prednisone and ketamine



  Ketamine, synthesized as a phenylcyclidine PCP derivative over 50 years ago, has long been used as general anesthetic acting primarily through blockade of NMDA receptors in the brain Li and Vlisides, ❿  


Prednisone and ketamine



  A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Sprague-Dawley male and female rats between the ages of 8—10 weeks old were obtained from Charles River Wilmington, MA. Recapitulation and reversal of a persistent depression-like syndrome in rodents.     ❾-50%}

 

Prednisone and ketamine



    Body weight was recorded on a weekly basis, and overnight fluid consumption was monitored twice per week.

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Recent research into the rapid antidepressant effect of subanesthetic doses of ketamine have identified a series of relevant protein cascades activated within hours of administration. Prior to, or concurrent with, these activation cascades, ketamine treatment generates dissociative and psychotomimetic side effects along with an increase in circulating glucocorticoids. Hippocampal tissue from ketamine, but not HNK, injected animals displayed a significant increase in the expression of sgk1a downstream effector of glucocorticoid receptor signaling.

Under anesthesia, ketamine failed to increase circulating corticosterone levels relative to saline controls. Concurrent with its antidepressant effects, ketamine generates a release of glucocorticoids potentially linked to disturbing cognitive side effects and the activation of distinct molecular pathways which should be considered when attempting to delineate the molecular mechanisms of its antidepressant function.

Ketamine, synthesized as a phenylcyclidine PCP derivative over 50 years ago, has long been used as general anesthetic acting primarily through blockade of NMDA receptors in the brain Li and Vlisides, Ketamine, at subanesthetic 0.

Even at subanesthetic doses, ketamine produces psychotomimetic and dissociative effects within minutes of administration, increasing the potential for abuse, largely restricting administration to a clinical setting. After administration ketamine is metabolized to a series of structurally distinct metabolites, with the potential to activate unique pathways.

Intense research into the RAAD effect of subanesthetic doses of ketamine have identified a series of protein cascades and transcriptional programs activated within an hour of administration and associated with increased neuronal connectivity and excitability Zanos and Gould Recent evidence in rodents highlights the potential contributions of a ketamine metabolite 2R, 6R -hydroxynorketamine HNKindicating HNK is sufficient to reproduce the antidepressant effects seen with ketamine, including increased neuroexcitability and synaptic strengthening Zanos et al.

There has also been an effort to uncouple its antidepressant mechanisms from its psychotropic effects which would allow more flexibility in clinical use. We sought to compare the downstream molecular pathways of ketamine and HNK administration, note any differences, and begin to identify pathways unique to the dissociative effects of ketamine. Our results did reveal molecular differences on an unexpected platform, namely activation of the hypothalamic-pituitary-adrenal HPA axis.

HPA axis hyperactivity, along with the generation of glucocorticoid resistance, has repeatedly been linked to the manifestation of MDD making effects of ketamine on this pathway of particular interest when parsing out its RAAD mechanisms Pariante This report will further characterize this phenomenon of ketamine administration versus HNK, including gender differences, and begin to address the mechanisms of its generation.

Sprague-Dawley male and female rats between the ages of 8—10 weeks old were obtained from Charles River Wilmington, MA. Male and female rat cohorts were done separately. Food and water were administered ad libitum. Body weight was recorded on a weekly basis, and overnight fluid consumption was monitored twice per week. The pH was adjusted to between 7. Corticosterone was administered to the rats through their drinking water according to Gourley et al.

Gourley, Wu et al. A freshly prepared solution was provided every 3 days. Daily dosages of corticosterone were calculated using overnight water consumption values and body weight. The rats were returned to regular drinking water for 3—7 days to wash out exogenous corticosterone before injection and sacrifice Figure 1A. Schematic representation of the timeline for oral corticosterone exposure, drug administration, and tissue collection.

The rats were returned to regular drinking water for 3—7 days to wash out exogenous corticosterone before injection and sacrifice. Measurement of corticosterone levels in serum and brain tissue in male and female rats 1-h post injection. B Circulating corticosterone levels in male rats. C Cortical brain levels of corticosterone in male rats. D Circulating corticosterone levels in female rats. E Cortical brain levels of corticosterone in female rats. Animals were euthanized by decapitation 1-h after receiving an intraperitoneal i.

Each treatment group contained five to six animals. Two male cohorts and one female cohort were used. Treatment groups were staggered throughout the day to avoid natural oscillations in circadian pathways from affecting any one treatment group. Trunk blood was collected in serum collection tubes BD Bioscience and allowed to clot 15—30 min before centrifugation. After initial sedation, the animals were maintained under anesthesia at 1. A heating pad was used to maintain body temperature.

Hind limbs were shaved and treated with a chemical depilatory to allow visualization of the saphenous vein. After the initial blood collection, an i. The animals remained under anesthesia for 60 min after the injection when blood was collected again through the saphenous vein.

Animals were allowed to recover and returned to their cages. For the cortical tissue, a separate steroid ethyl acetate extraction procedure was required before corticosterone measurement. Samples were compared to a standard curve using a 4-parameter logistical regression model.

Two-way ANOVA was performed to compare the effects of gender and treatment condition on corticosterone levels. Tukey multiple comparison tests were conducted to examine significant effects between treatment groups.

Eta-squared was used to calculate all effect sizes. Graphpad Prism was used to perform all statistical analyses. The experimental timeline, which includes a weaning process to facilitate the recovery of endogenous corticosterone production, is shown in Figure 1A.

This protocol is effective in inducing pro-depressive like behaviors including anhedonia, anxiety, and helplessness Gourley et al. We chose this timepoint because protein cascades initiated within the first hour of ketamine or HNK administration are critical to its antidepressant effect Li et al.

TABLE 1. Increased levels of circulating corticosterone in the blood correlates with increased concentrations found in tissue from the cerebral cortex. Females exhibited the same pattern as the males in response to ketamine treatment, however their corticosterone response exceeded that of the males. These surges in serum corticosterone seen in both male and female rats were well above the daily rise in corticosterone levels seen due to normal circadian oscillations. Male animals were given an i.

Next we examined corticosterone levels in cortical brain tissue collected at the 1-h post-injection timepoint. Corticosterone, as a steroid hormone, can readily pass through the blood-brain barrier and cell membranes, therefore analysis of a single brain region should be representative of all regions de Kloet et al.

We chose the cerebral cortex to illustrate corticosterone levels throughout the CNS, thereby preserving the nuclei more relevant to depression and anxiety for a more detailed molecular analysis. Glucocorticoids bind to intracellular receptors which lead to the modification of various transcriptional programs Madalena and Lerch Serum glucocorticoid kinase 1 sgk1 is a well-documented downstream effector of glucocorticoid signaling involved in regulating ion channel activity and neuronal excitability Lang et al.

We examined sgk1 expression as a gauge of increased glucocorticoid signaling within the hippocampus. Both male and female 1-h treatment groups and the male h treatment groups were also examined for differences in FKBP5 expression, another glucocorticoid receptor downstream target, however there was no change in expression at either the 1- or h timepoints for any of the groups data not shown.

All values are presented as a fold change from stress control animals injected with saline. Within minutes of administration of subanesthetic doses of ketamine, freely mobile conscious rats begin to exhibit locomotor deficits including ataxia and stereotypic behavior Danysz et al. This is embodied by a staggered gait, weaving and falling over.

The severity of the locomotor effect has a positive correlation with increasing ketamine dosages Imre et al. We hypothesized this behavior is an outward manifestation of the dissociative effects described by human subjects in response to subanesthetic ketamine administration. We reasoned this novel experience could generate confusion and anxiety in the animal resulting in activation of the HPA axis. Isoflurane was chosen based on research showing it to have minimal effect on circulating corticosterone levels in male rats Wu et al.

Importantly, isoflurane also appears to leave the HPA axis intact as repeated blood draws under anesthesia increase circulating corticosteroids in humans, rodents and rabbits Vachon and Moreau ; Nishiyama et al. Our experimental design is depicted in Figure 3A. There was no statistical difference between anesthetized saline and ketamine groups in pre-injection corticosterone levels There was a modest upwards trend in the ketamine pre versus post corticosterone levels Mean of Diff Importantly, the fold changes seen in the ketamine group did not approach the levels seen in conscious animals Figure 3C.

Circulating corticosterone levels of male rats under isoflurane anesthesia before and after saline or ketamine injection. A Timeline showing the experimental design. Blood collection and injection timepoints are noted with black arrows. C Fold increases between pre and post corticosterone levels after injection. Cortisol, corticosterone in rodents, is released from the adrenal cortex in response to pathways initiated in the hypothalamus and pituitary gland.

Research has shown that depression and the HPA axis are intimately intertwined Pariante and Miller, In fact, several studies document an increase in volume in both the pituitary and adrenal glands in patients with MDD Pariante, Glucocorticoid signaling in acute bouts, has physiological properties and contributes to learning and coping skills Cattaneo and Riva, However, when the signaling persists, due to prolonged stress or when coping is not accomplished, the effects of glucocorticoids become pathological Raison and Miller, Because of the pathological effects of continued exposure to glucocorticoids, prolonged treatment with corticosterone has been utilized as a model for stress-induced depressive behaviors in rodents.

In this vein, we used a chronic oral corticosterone treatment protocol preceding experimental or saline injections to identify differences between ketamine and HNK treatment.

Following the wash-out period of the chemically-induced stress protocol, the HPA axis activity returns to baseline. Corticosterone measurements from serum and brain tissue presented here represent the endogenous levels as exogenously administered corticosterone has been cleared out of the body system.

We observed that ketamine generated an acute, robust, several-fold increase in serum corticosterone versus controls, however there was no such effect in animals treated with HNK or saline. Gender played a role in the effect of ketamine administration on circulating corticosterone, with females displaying significantly increased levels compared to males.

This difference is not unprecedented with females showing increased HPA activation in response to novel and acute stressors Lesniewska et al. Additionally, female rats have been shown to display a larger motor disruption than age matched males, which could also account for the increased stress response McDougall et al. However another independent study reported no gender difference on locomotor activity in rodents Zanos et al.

The release is transient, with levels returning to baseline within a couple hours of treatment completion, in both rodents and humans Krystal et al.

As a consequence of its global permeation, local responses to glucocorticoids in the CNS depend on the differential expression of intracellular receptors, namely the mineralocorticoid and glucocorticoid receptors, with the hippocampus CA1 region having the highest concentration of glucocorticoid receptors GR within the CNS Pariante and Miller, ; Madalena and Lerch, ; Joels, By analyzing levels of sgk1 mRNA, a GRE containing gene, in hippocampal tissue from our animals, we were able to confirm that the GR pathway is active in a nucleus shown to be intimately involved in the manifestation of depression and anxiety.

Clinical and postmortem studies of MDD patients show the hippocampus, part of the limbic system and the primary stress response circuit, has evidence of atrophy, reduced neurogenesis and an overall reduction in volume Duric and Duman ; Cattaneo and Riva ; Boku et al.

medications are known to interact with ketamine. Includes gabapentin, tramadol, trazodone. Concurrent with its antidepressant effects, ketamine generates a release of glucocorticoids potentially linked to disturbing cognitive side. Drug interactions are reported among people who take Prednisone and Ketamine hydrochloride. Common interactions include diarrhoea among females and. Some medications used to treat depression, bipolar disorder and other conditions may affect how ketamine therapy works for mood disorder and chronic pain. Recent research into the rapid antidepressant effect of subanesthetic doses of ketamine have identified a series of relevant protein cascades. Bekhbat, M. Intense research into the RAAD effect of subanesthetic doses of ketamine have identified a series of protein cascades and transcriptional programs activated within an hour of administration and associated with increased neuronal connectivity and excitability Zanos and Gould Recent research into the rapid antidepressant effect of subanesthetic doses of ketamine have identified a series of relevant protein cascades activated within hours of administration. We chose this timepoint because protein cascades initiated within the first hour of ketamine or HNK administration are critical to its antidepressant effect Li et al.

Drug interactions are reported among people who take Prednisone and Ketamine hydrochloride. Common interactions include diarrhoea among females and peripheral motor neuropathy among males. The phase IV clinical study analyzes what interactions people who take Prednisone and Ketamine hydrochloride have. It is created by eHealthMe based on reports of 12 people who take Prednisone and Ketamine hydrochloride from the FDA, and is updated regularly. You can use the study as a second opinion to make health care decisions.

With medical big data and AI algorithms, eHealthMe enables everyone to run phase IV clinical trial to detect adverse drug outcomes and monitor effectiveness. Prednisone has active ingredients of prednisone. It is often used in rheumatoid arthritis. Ketamine hydrochloride has active ingredients of ketamine hydrochloride.

You can discuss the study with your doctor, to ensure that all drug risks and benefits are fully discussed and understood. The study uses data from the FDA. It is based on prednisone and ketamine hydrochloride the active ingredients of Prednisone and Ketamine hydrochloride, respectively , and Prednisone and Ketamine hydrochloride the brand names. Other drugs that have the same active ingredients e. Dosage of drugs is not considered in the study.

With medical big data and proven AI algorithms, eHealthMe provides a platform for everyone to run phase IV clinical trials. We study millions of patients and 5, more each day. Our analysis results are available to researchers, health care professionals, patients testimonials , and software developers open API. All information is observation-only. Our phase IV clinical studies alone cannot establish cause-effect relationship. Different individuals may respond to medication in different ways.

Every effort has been made to ensure that all information is accurate, up-to-date, and complete, but no guarantee is made to that effect. The use of the eHealthMe site and its content is at your own risk. If you use this eHealthMe study on publication, please acknowledge it with a citation: study title, URL, accessed date.

All rights reserved. Use of this site constitutes acceptance of eHealthMe. Toggle navigation eHealth Me. Home Analysis Prednisone Ketamine-hydrochloride. Prednisone and Ketamine hydrochloride drug interactions - a phase IV clinical study of FDA data Summary: Drug interactions are reported among people who take Prednisone and Ketamine hydrochloride.

What is Prednisone? What is Ketamine hydrochloride? Some reports may have incomplete information. Who is eHealthMe?



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