Effects of ceftriaxone on hydrocodone seeking behavior and glial glutamate transporters in P rats

Alshehri, Fahad S.; Hakami, Alqassem Y.; Althobaiti, Yusuf S.; Sari, Youssef

doi:10.1016/j.bbr.2018.03.043

Cited by 32 publications

(35 citation statements)

References 106 publications

(130 reference statements)

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“…Animal brains were collected on day 16, immediately frozen, and stored at −80 • C. The NAc was collected as pooled tissue containing NAc (core and shell) and isolated using a cryostat machine (Leica Biosystems). The NAc region (1.2-3.7 mm from bregma) was identified using the Brain Rat Atlas (Paxinos and Watson, 2006) and as performed previously in Alshehri et al (2018) and Hammad et al (2017).…”

Section: Brain Tissue Collectionmentioning

confidence: 99%

“…Therefore, several studies have evaluated the contribution of the NAc in drug-related behaviors. For instance, opioid reinforcing and seeking effects are mediated through the dopaminergic and glutamatergic neurotransmission in the NAc (LaLumiere and Kalivas, 2008 ; Alshehri et al, 2018 ; Corre et al, 2018 ). Moreover, it has been found that morphine injection in the ventral tegmental area showed an augmented increase of the dopamine level in NAc (Leone et al, 1991 ).…”

Section: Introductionmentioning

confidence: 99%

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Melatonin Blocks Morphine-Induced Place Preference: Involvement of GLT-1, NF-κB, BDNF, and CREB in the Nucleus Accumbens

Alghamdi

Alshehri

2021

Front. Behav. Neurosci.

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Opioid addiction remains a widespread issue despite continuous attempts by the FDA to help maintain abstinence. Melatonin is a neurohormone considered to be involved only in the neuroendocrine and reproductive systems; however, recent reports have demonstrated its potential to attenuate drug addiction and dependence. Cumulative studies have suggested that melatonin can attenuate the rewarding effects of several drugs of abuse, including opioids. This study aimed to investigate the effect of melatonin (50 mg/kg) on morphine (5 mg/kg) to produce place preference. We also investigated the effect of melatonin and morphine on the expression of GLT-1, BDNF, NF-κB, and CREB within the nucleus accumbens. Male Wistar rats were divided into control, morphine, melatonin, and the morphine + melatonin groups. The study involved a two-phase habituation phase from day 1 to day 3 and an acquisition phase from day 5 to day 14. The conditioned place preference (CPP) score, distance traveled, resting time, ambulatory count, and total activity count were measured for all animals. Rats that received morphine showed a significant increase in CPP score compared to those in the control group. Morphine treatment reduced the mRNA expression of GLT-1, BDNF, and CREB and increased that of NF-κB. However, melatonin treatment administered 30 min before morphine treatment attenuated morphine place preference and reversed GLT-1, BDNF, NF-κB, and CREB expression levels. In conclusion, the study results indicate, for the first time, the new potential targets of melatonin in modulating morphine-induced CPP.

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Section: Brain Tissue Collectionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Melatonin Blocks Morphine-Induced Place Preference: Involvement of GLT-1, NF-κB, BDNF, and CREB in the Nucleus Accumbens

Alghamdi

Alshehri

2021

Front. Behav. Neurosci.

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“…Since then, ceftriaxone has been the most commonly used β-lactam to increase GLT-1 levels, which was subsequently found to also promote the expression of xCT and increase system Xc − activity [155]. Ceftriaxone has been shown to reduce the reinstatement of drug paired behavior and seeking of cocaine [156], amphetamine [157], ethanol (including direct inhibition of consumption) [158][159][160], opioids [161], and nicotine [162], showing the broad-spectrum of the recovering of glutamate homeostasis in the treatment of drug addiction. Methamphetamine self-administration also reduced extracellular glutamate levels in the NAcc and prefrontal cortex of rats after an extinction period [149].…”

Section: The Recovery Of Glt-1 and System XC − Activities Inhibits Drmentioning

confidence: 99%

Oxidative Stress and Neuroinflammation as a Pivot in Drug Abuse. A Focus on the Therapeutic Potential of Antioxidant and Anti-Inflammatory Agents and Biomolecules

et al. 2020

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Drug abuse is a major global health and economic problem. However, there are no pharmacological treatments to effectively reduce the compulsive use of most drugs of abuse. Despite exerting different mechanisms of action, all drugs of abuse promote the activation of the brain reward system, with lasting neurobiological consequences that potentiate subsequent consumption. Recent evidence shows that the brain displays marked oxidative stress and neuroinflammation following chronic drug consumption. Brain oxidative stress and neuroinflammation disrupt glutamate homeostasis by impairing synaptic and extra-synaptic glutamate transport, reducing GLT-1, and system Xc− activities respectively, which increases glutamatergic neurotransmission. This effect consolidates the relapse-promoting effect of drug-related cues, thus sustaining drug craving and subsequent drug consumption. Recently, promising results as experimental treatments to reduce drug consumption and relapse have been shown by (i) antioxidant and anti-inflammatory synthetic molecules whose effects reach the brain; (ii) natural biomolecules secreted by mesenchymal stem cells that excel in antioxidant and anti-inflammatory properties, delivered via non-invasive intranasal administration to animal models of drug abuse and (iii) potent anti-inflammatory microRNAs and anti-miRNAs which target the microglia and reduce neuroinflammation and drug craving. In this review, we address the neurobiological consequences of brain oxidative stress and neuroinflammation that follow the chronic consumption of most drugs of abuse, and the current and potential therapeutic effects of antioxidants and anti-inflammatory agents and biomolecules to reduce these drug-induced alterations and to prevent relapse.

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“…These studies suggest that chronic e-cig exposure alters glutamate homeostasis. It is noteworthy that chronic exposure to drugs of abuse (e.g., nicotine, ethanol, methamphetamine, hydrocodone and cocaine) was associated with downregulation of GLT-1 [ 21 , 22 , 23 , 24 ] and xCT protein expression [ 23 , 24 , 25 ] in key reward brain regions in P rats. In these studies, β lactams, known to upregulate GLT-1 and xCT expression, were tested and showed attenuating effects on drug-seeking behaviors.…”

Section: Introductionmentioning

confidence: 99%

Effects of 3-Month Exposure to E-Cigarette Aerosols on Glutamatergic Receptors and Transporters in Mesolimbic Brain Regions of Female C57BL/6 Mice

Alhaddad

Wong

Sari

et al. 2020

Toxics

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Electronic cigarettes (e-cigs) use has been dramatically increased recently, especially among youths. Previous studies from our laboratory showed that chronic exposure to e-cigs, containing 24 mg/mL nicotine, was associated with dysregulation of glutamate transporters and neurotransmitter levels in the brain of a mouse model. In this study, we evaluated the effect of three months’ continuous exposure to e-cig vapor (JUUL pods), containing a high nicotine concentration, on the expression of glutamate receptors and transporters in drug reward brain regions such as the nucleus accumbens (NAc) core (NAc-core), NAc shell (NAc-shell) and hippocampus (HIP) in female C57BL/6 mice. Three months’ exposure to mint- or mango-flavored JUUL (containing 5% nicotine, 59 mg/mL) induced upregulation of metabotropic glutamate receptor 1 (mGluR1) and postsynaptic density protein 95 (phosphorylated and total PSD95) expression, and downregulation of mGluR5 and glutamate transporter 1 (GLT-1) in the NAc-shell. In addition, three months’ exposure to JUUL was associated with upregulation of mGluR5 and GLT-1 expression in the HIP. These findings demonstrated that three-month exposure to e-cig vapor containing high nicotine concentrations induced differential effects on the glutamatergic system in the NAc and HIP, suggesting dysregulation of glutamatergic system activity in mesolimbic brain regions.

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Effects of ceftriaxone on hydrocodone seeking behavior and glial glutamate transporters in P rats

Cited by 32 publications

References 106 publications

Melatonin Blocks Morphine-Induced Place Preference: Involvement of GLT-1, NF-κB, BDNF, and CREB in the Nucleus Accumbens

Melatonin Blocks Morphine-Induced Place Preference: Involvement of GLT-1, NF-κB, BDNF, and CREB in the Nucleus Accumbens

Oxidative Stress and Neuroinflammation as a Pivot in Drug Abuse. A Focus on the Therapeutic Potential of Antioxidant and Anti-Inflammatory Agents and Biomolecules

Effects of 3-Month Exposure to E-Cigarette Aerosols on Glutamatergic Receptors and Transporters in Mesolimbic Brain Regions of Female C57BL/6 Mice

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