Chronic minocycline treatment reduces the anxiety-like behaviors induced by repeated restraint stress through modulating neuroinflammation

Liu, Haiyan; Yue, Jiao; Hu, Li‐ning; Cheng, Lifei; Wang, Xin‐shang; Wang, Xiao-Juan; Feng, Bin

doi:10.1016/j.brainresbull.2018.08.015

Cited by 49 publications

(29 citation statements)

References 57 publications

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“…Further evidence in support of an anxiolytic effect of PPARγ signalling comes from recent work by Youssef et al [48], demonstrating that the administration of a PPARγ antagonist blocked the anxiolytic effect of beta-caryophyllene. Additionally, repeated stress decreased PPARγ expression in the amygdala, and treatment with buspirone or minocycline, two drugs having anxiolytic effects, recovered PPARγ expression in the same region [49]. Furthermore, PPARγ blockade or knockout was shown to have anxiogenic effects in mice [12].…”

Section: Discussionmentioning

confidence: 97%

Pharmacological Blockade of PPAR Isoforms Increases Conditioned Fear Responding in the Presence of Nociceptive Tone

et al. 2020

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Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors with three isoforms (PPARα, PPARβ/δ, PPARγ) and can regulate pain, anxiety, and cognition. However, their role in conditioned fear and pain-fear interactions has not yet been investigated. Here, we investigated the effects of systemically administered PPAR antagonists on formalin-evoked nociceptive behaviour, fear-conditioned analgesia (FCA), and conditioned fear in the presence of nociceptive tone in rats. Twenty-three and a half hours following fear conditioning to context, male Sprague-Dawley rats received an intraplantar injection of formalin and intraperitoneal administration of vehicle, PPARα (GW6471), PPARβ/δ (GSK0660) or PPARγ (GW9662) antagonists, and 30 min later were re-exposed to the conditioning arena for 15 min. The PPAR antagonists did not alter nociceptive behaviour or fear-conditioned analgesia. The PPARα and PPARβ/δ antagonists prolonged context-induced freezing in the presence of nociceptive tone without affecting its initial expression. The PPARγ antagonist potentiated freezing over the entire trial. In conclusion, pharmacological blockade of PPARα and PPARβ/δ in the presence of formalin-evoked nociceptive tone, impaired short-term, within-trial fear-extinction in rats without affecting pain response, while blockade of PPARγ potentiated conditioned fear responding. These results suggest that endogenous signalling through these three PPAR isoforms may reduce the expression of conditioned fear in the presence of nociceptive tone.

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Section: Discussionmentioning

confidence: 97%

Pharmacological Blockade of PPAR Isoforms Increases Conditioned Fear Responding in the Presence of Nociceptive Tone

et al. 2020

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“…Our results are in agreement with a growing amount of literature showing that microglia activation is neuroprotective in a variety of contexts, including stroke (Otxoa‐de‐Amezaga et al, ), Alzheimer's disease (Hamelin et al, ), and multiple sclerosis (Napoli & Neumann, ). In contrast, our results differ from studies on anxiety, demonstrating that microglia activation is associated with anxiety‐induced impaired social interaction, which the authors used as one measure of sickness behaviors (Liu et al, ). We observed greatly decreased home cage locomotor activity in animals treated with PLX5622.…”

Section: Discussionmentioning

confidence: 99%

Microglia in the hypothalamus respond to tumor‐derived factors and are protective against cachexia during pancreatic cancer

Burfeind

Zhu

Norgard

et al. 2020

Glia

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Microglia in the mediobasal hypothalamus (MBH) respond to inflammatory stimuli and metabolic perturbations to mediate body composition. This concept is well studied in the context of high fat diet induced obesity (HFDO), yet has not been investigated in the context of cachexia, a devastating metabolic syndrome characterized by anorexia, fatigue, and muscle catabolism. We show that microglia accumulate specifically in the MBH early in pancreatic ductal adenocarcinoma (PDAC)-associated cachexia and assume an activated morphology. Furthermore, we observe astrogliosis in the MBH and hippocampus concurrent with cachexia initiation. We next show that circulating immune cells resembling macrophages infiltrate the MBH. PDAC-derived factors induced microglia to express a transcriptional profile in vitro that was distinct from that induced by lipopolysaccharide (LPS). Microglia depletion through CSF1-R antagonism resulted in accelerated cachexia onset and increased anorexia, fatigue, and muscle catabolism during PDAC. This corresponded with increased hypothalamic-pituitary-adrenal (HPA) axis activation. CSF1-R antagonism had little effect on inflammatory response in the circulation, liver, or tumor. These findings demonstrate that microglia are protective against PDAC cachexia and provide mechanistic insight into this function. K E Y W O R D S brain, cachexia, hypothalamus, microglia, neuroinflammation, pancreatic cancer

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“…As the main immune cells in the central nervous system (CNS), microglia are activated and produce a large amount of pro-inflammatory cytokines including interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, which impact neuronal function and increase cell death in PD (Kannarkat et al, 2013 ; Moehle and West, 2015 ). This suggests that microglia can be a therapeutic target for PD since they can be easily modulated by a series of drugs and compounds such as minocycline, spermidine and TSPO ligand XBD173, among others (Trapani et al, 2013 ; Liu et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Epothilone B Benefits Nigral Dopaminergic Neurons by Attenuating Microglia Activation in the 6-Hydroxydopamine Lesion Mouse Model of Parkinson’s Disease

Yang

et al. 2018

Front. Cell. Neurosci.

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Parkinson’s disease (PD) is characterized by loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc) and a subsequent reduction in striatal DA levels. Recent studies have shown that systemic administration of subtoxic doses of epothilone B (EpoB), a microtubule stabilizing agent, enhances axonal regeneration. However, the underlying alterations in cellular mechanisms remain undetermined. In the present study, we investigated the neuroprotective effects of EpoB on DA neurons in mouse model of PD induced by 6-hydroxyDA (6-OHDA) and in vitro. The results indicated that EpoB improved behavioral deficits, protected the nigrostriatal dopaminergic projections and restored DA level in the striatum of mice exposed to 6-OHDA. Meanwhile, EpoB attenuated microglia activation in the SNc of PD mice. Furthermore, EpoB treatment ameliorated 6-OHDA induced cytotoxicity to MN9D dopaminergic cells in a co-culture transwell system of BV2/MN9D cells, and redistributed the cytoskeleton of microglial BV2 and caused the morphological transition, inhibited the polarization to the M1 phenotype by suppressing expression of pro-inflammatory factors including interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α. Overall, our study suggested that EpoB treatment protects nigral DA neurons and projections through limiting the cytotoxicity of activated microglia in 6-OHDA lesioned mice.

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Chronic minocycline treatment reduces the anxiety-like behaviors induced by repeated restraint stress through modulating neuroinflammation

Cited by 49 publications

References 57 publications

Pharmacological Blockade of PPAR Isoforms Increases Conditioned Fear Responding in the Presence of Nociceptive Tone

Pharmacological Blockade of PPAR Isoforms Increases Conditioned Fear Responding in the Presence of Nociceptive Tone

Microglia in the hypothalamus respond to tumor‐derived factors and are protective against cachexia during pancreatic cancer

Epothilone B Benefits Nigral Dopaminergic Neurons by Attenuating Microglia Activation in the 6-Hydroxydopamine Lesion Mouse Model of Parkinson’s Disease

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