The expression of genes involved in glucose metabolism is affected by N‐methyl‐D‐aspartate receptor antagonism: A putative link between metabolism and an animal model of psychosis

Iasevoli, Felice; Latte, Gianmarco; Avvisati, Livia; Sarappa, Chiara; Aloj, Luigi; Bartolomeis, Andrea de

doi:10.1002/jnr.23071

Cited by 9 publications

(7 citation statements)

References 53 publications

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“…Such antidepressant effects of ketamine were subsequently inhibited by the additional treatment of an ERK1/2 inhibitor. Our results are consistent with previous findings by Lee et al 12 and Iasevoli et al 37 . Immunofluorescent staining further confirmed that astrocytes, but not neurons, exhibited enhanced expression levels of GLUT3 and P-ERK1/2 in the prefrontal cortex.…”

Section: Discussionsupporting

confidence: 94%

“…The results of the present study are consistent with those of Tomioka et al in which they reported the effects of ketamine on glucose uptake by GLUT3 expressed in Xenopus oocytes 36 . In addition, Iasevoli et al found that ketamine increases GLUT3 mRNA expression in rats 37 . However, it is still unclear which signaling pathway may be associated with ketamine-induced increases in GLUT3 levels in astrocytes.…”

Section: Discussionmentioning

confidence: 99%

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Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway

Ouyang

Wang

Luo

et al. 2021

Sci Rep

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To investigate the effects of ketamine on glucose uptake and glucose transporter (GLUT) expression in depressive-like mice. After HA1800 cells were treated with ketamine, 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino]-2-Deoxyglucose (2-NBDG) was added to the cells to test the effects of ketamine on glucose uptake, production of lactate, and expression levels of GLUT, ERK1/2, AKT, and AMPK. Adult female C57BL/6 mice were subjected to chronic unpredictable mild stress (CUMS), 27 CUMS mice were randomly divided into the depression, ketamine (i.p.10 mg/kg), and FR180204 (ERK1/2 inhibitor, i.p.100 mg/kg) + ketamine group. Three mice randomly selected from each group were injected with 18F-FDG at 6 h after treatment. The brain tissue was collected at 6 h after treatment for p-ERK1/2 and GLUTs. Treatment with ketamine significantly increased glucose uptake, extracellular lactic-acid content, expression levels of GLUT3 and p-ERK in astrocytes and glucose uptake in the prefrontal cortex (P < 0.05), and the immobility time was significantly shortened in depressive-like mice (P < 0.01). An ERK1/2 inhibitor significantly inhibited ketamine-induced increases in the glucose uptake in depressive-like mice (P < 0.05), as well as prolonged the immobility time (P < 0.01). The expression levels of p-ERK1/2 and GLUT3 in depressive-like mice were significantly lower than those in normal control mice (P < 0.01). Ketamine treatment in depressive-like mice significantly increased the expression levels of p-ERK1/2 and GLUT3 in the prefrontal cortex (P < 0.01), whereas an ERK1/2 inhibitor significantly inhibited ketamine-induced increases (P < 0.01).Our present findings demonstrate that ketamine mitigated depressive-like behaviors in female mice by activating the ERK/GLUT3 signal pathway, which further increased glucose uptake in the prefrontal cortex.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway

Ouyang

Wang

Luo

et al. 2021

Sci Rep

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“…Animals were sacrificed at 150 minutes after treatment, i.e. in a timerange that is consistent with previously published in situ hybridization studies on brain mRNA expression [19][20][21].…”

Section: Methodsmentioning

confidence: 96%

“…1). Procedures for probe labeling, in situ hybridization, and autoradiography were in agreement with previous published protocols [19,23].…”

Section: Methodsmentioning

confidence: 98%

The Glucocorticoid Analog Dexamethasone Alters the Expression and the Distribution of Dopamine Receptors and Enkephalin within Cortico- Subcortical Regions

Iasevoli¹,

Aloj²,

Latte³

et al. 2014

CMP

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In humans, glucocorticoid excess may cause neuropsychiatric symptoms, including psychosis and cognitive impairment, and glucocorticoid signaling hyperactivation may sensitize to substance of abuse. The aim of this work was to evaluate whether exposure to glucocorticoid excess triggers molecular changes in dopaminergic and opioidergic systems within relevant forebrain areas. We acutely exposed Sprague-Dawley rats to dexamethasone, a glucocorticoid analog, or vehicle and evaluated the mRNA expression of dopamine D1 and D2 receptors and enkephalin within the cortex, the striatum, and the midbrain. Dexamethasone reduced mRNA expression of D1 receptor and enkephalin in the cortex. In the striatum, dexamethasone reduced the expression of D1 receptor mRNA, but not that of D2 receptor and enkephalin. No significant changes in D2 receptor mRNA expression were observed in the midbrain. Basal distribution of D1 and D2 receptor mRNA showed a clear-cut striatal/cortical gradient, while this distribution was less obvious for enkephalin mRNA. Dexamethasone increased the cortico-striatal separation in terms of D1 and D2 receptor mRNA expression. These molecular changes may represent adaptive mechanisms to dexamethasone-induced potentiation of dopaminergic and opioidergic transmission, mostly in cortical areas.

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“…One explanation for the mechanisms of prolonged analgesia exhibited by R5 is that it may induce key changes in early gene expression. It is known that ketamine and other NMDA receptor antagonists cause a variety of changes in expression of a significant number of genes [7, 8]. Therefore, we used mRNA sequencing to quantify gene expression changes induced in four key higher order pain-related regions of the rat brain by a 45 min infusion of ketamine and the related analogues.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional changes in response to ketamine ester-analogs SN 35210 and SN 35563 in the rat brain

et al. 2019

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Background Ketamine ester analogs, SN 35210 and SN 35563, demonstrate different pharmacological profiles to ketamine in animal models. Both confer hypnosis with predictably rapid offset yet, paradoxically, SN35563 induces a prolonged anti-nociceptive state. To explore underlying mechanisms, broad transcriptome changes were measured and compared across four relevant target regions of the rat brain. Results SN 35563 produced large-scale alteration of gene expression in the Basolateral Amygdala (BLA) and Paraventricular Nucleus of the Thalamus (PVT), in excess of 10x that induced by ketamine and SN 35210. A smaller and quantitatively similar number of gene changes were observed in the Insula (INS) and Nucleus Accumbens (ACB) for all three agents. In the BLA and PVT, SN 35563 caused enrichment for gene pathways related to the function and structure of glutamatergic synapses in respect to: release of neurotransmitter, configuration of postsynaptic AMPA receptors, and the underlying cytoskeletal scaffolding and alignment. Conclusion The analgesic ketamine ester analog SN 35563 induces profound large-scale changes in gene expression in key pain-related brain regions reflecting its unique prolonged pharmacodynamic profile. Electronic supplementary material The online version of this article (10.1186/s12864-019-5649-6) contains supplementary material, which is available to authorized users.

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The expression of genes involved in glucose metabolism is affected by N‐methyl‐D‐aspartate receptor antagonism: A putative link between metabolism and an animal model of psychosis

Cited by 9 publications

References 53 publications

Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway

Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway

The Glucocorticoid Analog Dexamethasone Alters the Expression and the Distribution of Dopamine Receptors and Enkephalin within Cortico- Subcortical Regions

Transcriptional changes in response to ketamine ester-analogs SN 35210 and SN 35563 in the rat brain

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