Intranasal insulin treatment alleviates methamphetamine induced anxiety-like behavior and neuroinflammation

Beirami, Elmira; Oryan, Shahrbanoo; Tamijani, Seyedeh Masoumeh Seyedhosseini; Ahmadiani, Abolhassan; Dargahi, Leila

doi:10.1016/j.neulet.2017.09.026

Cited by 32 publications

(35 citation statements)

References 71 publications

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“…In accordance with our results, an AD mouse model study showed that spatial learning, memory and cognitive functions were significantly improved after intraperitoneal injection of rosiglitazone (Pedersen et al, 2006). Similarly, a recent study also demonstrated the importance of the protective effects of insulin signal-ing pathways in METH-induced neural damage, showing that insulin effectively relieved METH-induced anxietylike behavior and neuroinflammation in animals (Beirami et al, 2017). These studies suggest that the insulin signaling pathways can be considered useful targets for METHinduced neural damage.…”

Section: Discussionsupporting

confidence: 91%

Methamphetamine exposure upregulates the amyloid precursor protein and hyperphosphorylated tau expression: The roles of insulin signaling in SH-SY5Y cell line

Zhou

Fang

et al. 2019

J. Toxicol. Sci.

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-Methamphetamine (METH) is a potent and highly addictive central nervous system stimulant. The association between METH exposure and Alzheimer's disease (AD) has gained more attention, but, the mechanisms behind METH-induced neuron-related adverse outcomes remain poorly understood. With the western blot assay, our results revealed that METH exposure significantly increased the expression of AD-associated pathological proteins, including the amyloid precursor protein (APP) and the phosphorylated tau protein (p-tau). Meanwhile, the insulin signaling was disturbed after the administration of METH, since the key insulin signaling proteins, such as p-AKT, p-GSK3α, p-GSK3β and pERK , were reduced. Additionally, the linking between the pathological proteins and the insulin signaling mediated by METH in the present work was verified by the treatment with the insulin signaling enhancer rosiglitazone, which was shown to improve the insulin signaling and decrease APP and p-tau expression. Thus, targeting insulin signaling may provide novel insights into potential therapeutic intervention for METHmediated AD-like neurodegeneration.

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Section: Discussionsupporting

confidence: 91%

Methamphetamine exposure upregulates the amyloid precursor protein and hyperphosphorylated tau expression: The roles of insulin signaling in SH-SY5Y cell line

Zhou

Fang

et al. 2019

J. Toxicol. Sci.

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“…Similar findings have been observed in studies of brain stimulation in which nicotine decreases frequency threshold for reinforcement (Bozarth et al 1998a;b;Ivanova and Greenshaw 1997). Alternatively, the reduction in self-administration in the females could instead be interpreted as decreased reinforcement efficacy of methamphetamine, perhaps due to enhanced anxiogenic effects of methamphetamine (Beirami et al 2017;Schutova et al 2009). It will be interesting for future work to replicate and investigate these ideas of altered reinforcing function of methamphetamine.…”

Section: Discussionsupporting

confidence: 57%

Effects of nicotine conditioning history on alcohol and methamphetamine self-administration in rats

Randall

Fortino

Huynh

et al. 2019

Pharmacology Biochemistry and Behavior

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Background.-Smoking constitutes a significant public health risk. Alcohol and methamphetamine use disorders are also highly co-morbid with smoking, further increasing negative health outcomes. An important question in determining the underlying neurobiology of nicotine poly-drug use is understanding whether having a positive history with nicotine effects alters later drug-taking behavior. Methods.-The current experiments sought to elucidate whether having an appetitive nicotine conditioning history would affect later alcohol or methamphetamine self-administration. Adult male and female Long-Evans rats were first trained on a discriminated goal-tracking task in which the interoceptive effects of nicotine predicted sucrose reinforcement. As a control, pseudoconditioned groups were included that had equated nicotine and sucrose experience. Rats were then shifted to either alcohol self-administration or methamphetamine self-administration. Results.-Nicotine conditioning history had no effect on acquisition or maintenance of alcohol self-administration in males or females. In contrast, an appetitive nicotine conditioning history decreased methamphetamine self-administration in female rats, but not males. Conclusions.-In female, but not male rats, an appetitive conditioning history with nicotine decreases methamphetamine, but not alcohol, self-administration. This dissociation suggests that the effects may be due to a specific increase in the reinforcing value of methamphetamine. This Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…In mice exposed to SCI, insulin levels are reduced from 7 to 28 days post-injury (the longest time point studied) (Rouleau et al, 2007). Impairment of insulin signaling, such as by induction Oddo et al, 2008;Yang Y. G. et al, 2009) Risk of hypoglycemia Increased mortality rate van den Berghe et al, 2001;Bilotta et al, 2008;Yang Y. G. et al, 2009a;Vespa et al, 2012Bilotta et al, 2008Oddo et al, 2008;Investigators et al, 2009;Vespa et al, 2012;Hermanides et al, 2018 Increased glucose uptake Improved cognitive function Reduced inflammation Brabazon et al, 2017Brabazon et al, 2017Beirami et al, 2017 Nagamizo et al, 2007;Wu et al, 2007;Yang Y. G. et al, 2009) Wu et al, 2007Yang Y. G. et al, 2009) Wu et al, 2007 Hyperglycemia from exogenous administration causing proinflammatory state Insulin may not produce sufficient response Insulin resistance Prakash and Matta, 2008;Torabi et al, 2018Duckworth et al, 1980Duckworth et al, 1980 N/A N/A Alzheimer's disease Improved memory Craft et al, 1996 Risk of hypoglycemia Insulin resistance Craft et al, 1996Zhong et al, 2012Lutski et al, 2017 Reduced amyloid beta levels, repaired insulin...…”

Section: Insulin In Scimentioning

confidence: 99%

“…Intranasal insulin has been shown to be a promising method for decreasing microglial-induced inflammation in the CNS ( Beirami et al, 2017 ; Brabazon et al, 2017 ). In addition to our work and other work in vitro , mice fed HFDs for 12 weeks demonstrated elevated levels of pro-inflammatory cytokine gene expression the hippocampus that were reduced by hippocampal infusion of insulin (2.64 μL of Humulin insulin per day at 4 mU/μL) ( Gladding et al, 2018 ).…”

Section: Insulin In Tbimentioning

confidence: 99%

Role of Insulin in Neurotrauma and Neurodegeneration: A Review

et al. 2020

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Insulin is a hormone typically associated with pancreatic release and blood sugar regulation. The brain was long thought to be "insulin-independent," but research has shown that insulin receptors (IR) are expressed on neurons, microglia and astrocytes, among other cells. The effects of insulin on cells within the central nervous system are varied, and can include both metabolic and non-metabolic functions. Emerging data suggests that insulin can improve neuronal survival or recovery after trauma or during neurodegenerative diseases. Further, data suggests a strong antiinflammatory component of insulin, which may also play a role in both neurotrauma and neurodegeneration. As a result, administration of exogenous insulin, either via systemic or intranasal routes, is an increasing area of focus in research in neurotrauma and neurodegenerative disorders. This review will explore the literature to date on the role of insulin in neurotrauma and neurodegeneration, with a focus on traumatic brain injury (TBI), spinal cord injury (SCI), Alzheimer's disease (AD) and Parkinson's disease (PD).

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Intranasal insulin treatment alleviates methamphetamine induced anxiety-like behavior and neuroinflammation

Cited by 32 publications

References 71 publications

Methamphetamine exposure upregulates the amyloid precursor protein and hyperphosphorylated tau expression: The roles of insulin signaling in SH-SY5Y cell line

Methamphetamine exposure upregulates the amyloid precursor protein and hyperphosphorylated tau expression: The roles of insulin signaling in SH-SY5Y cell line

Effects of nicotine conditioning history on alcohol and methamphetamine self-administration in rats

Role of Insulin in Neurotrauma and Neurodegeneration: A Review

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