Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

Amri, Jamal; Sadegh, Mehdi; Moulaei, Neda; Palizvan, Mohammad Reza

doi:10.1080/00952990.2017.1348509

Cited by 17 publications

(8 citation statements)

References 58 publications

(71 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This suggests that the actions of TNF-α and IL-1β are interconnected; however, little is known about the role TNF-α plays in opioid use and withdrawal, as well as the development of hyperarousal states of PTSD. TNF-α has been shown to be upregulated following opioid use [26] and during withdrawal [27]. Likewise, translational evidence from both rodent and clinical studies has implicated TNF-α in stressrelated disorders, such as PTSD [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Parekh

Paniccia²,

Adams³

et al. 2021

Mol Neurobiol

View full text Add to dashboard Cite

There is significant comorbidity of opioid use disorder (OUD) and post-traumatic stress disorder (PTSD) in clinical populations. However, the neurobiological mechanisms underlying the relationship between chronic opioid use and withdrawal and development of PTSD are poorly understood. Our previous work identified that chronic escalating heroin administration and withdrawal can produce enhanced fear learning, an animal model of hyperarousal, and is associated with an increase in dorsal hippocampal (DH) interleukin-1β (IL-1β). However, other cytokines, such as TNF-α, work synergistically with IL-1β and may have a role in the development of enhanced fear learning. Based on both translational rodent and clinical studies, TNF-α has been implicated in hyperarousal states of PTSD, and has an established role in hippocampal-dependent learning and memory. The first set of experiments tested the hypothesis that chronic heroin administration followed by withdrawal is capable of inducing alterations in DH TNF-α expression. The second set of experiments examined whether DH TNF-α expression is functionally relevant to the development of enhanced fear learning. We identified an increase of TNF-α immunoreactivity and positive cells at 0, 24, and 48 h into withdrawal in the dentate gyrus DH subregion. Interestingly, intra-DH infusions of etanercept (TNF-α inhibitor) 0, 24, and 48 h into heroin withdrawal prevented the development of enhanced fear learning and mitigated withdrawal-induced weight loss. Overall, these findings provide insight into the role of TNF-α in opioid withdrawal and the development of anxiety disorders such as PTSD.

show abstract

Section: Introductionmentioning

confidence: 99%

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Parekh

Paniccia²,

Adams³

et al. 2021

Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…Morphine exposure enhances the production of TNF-α by mesangial cells in response to lipopolysaccharide (Kapasi, Gibbons, Mattana, & Singhal, 2000). Amri, Sadegh, Moulaei and Palizvan (2018) showed that morphine administration to rats, even before mating and pregnancy, increased the TNF-α level in the neonatal hippocampus (Amri et al 2018). In the current study, morphine administration increased TNF-α and CRP levels in brain tissue compared to other groups after HI brain injury.…”

Section: Discussionmentioning

confidence: 99%

Morphine consumption during pregnancy exacerbates neonatal hypoxia‐ischemia injury in rats

Bornavard

Fanaei

Mirshekar

et al. 2020

Intl J of Devlp Neuroscience

View full text Add to dashboard Cite

Objective Hypoxia‐Ischemia (HI) is the most common cause of death and disability in human infants. The use of opiate in pregnant women affects their children. The aim of this study was to evaluate the effect of morphine consumption during pregnancy and lactation on vulnerability to neonatal HI in rats. Materials and methods Female Wistar rats were randomly assigned into two groups: Group 1‐Rats that did not receive any treatment during pregnancy and lactation and Group 2‐Rats that received morphine during pregnancy and lactation. After delivery, male offspring were divided into four groups including: (a) SHAM, (b) SHAM/Morphine (SHAM/MO), (c) HI, (d) HI/Morphine (HI/MO). Seven days after HI induction, neurobehavioral tests were performed, and then, brain tissue was taken from the skull to measure cerebral edema, infarct volume, inflammatory factors, oxidative stress, and brain‐derived neurotrophic factor (BDNF). Results Total antioxidant capacity (TAC) and BDNF levels in the HI/MO group were significantly lower than HI and SHAM groups. TNF‐α, C‐reactive protein and total oxidant capacity levels in the HI/MO group were significantly higher than HI and SHAM groups. Cerebral edema and infarct volume in the HI/MO group were significantly higher than the HI group. Conclusion Based on the results, morphine consumption during pregnancy and lactation enhanced the deleterious effects of HI injury in pups.

show abstract

“…S100β, another astrocytic marker, plays a key role in neuroinflammation by activating signaling cascades that lead to the production and secretion of inflammatory cytokines. Its levels increase in hippocampal tissue, cerebrospinal fluid and serum during anoxic brain damage and pathophysiological situations, acting as a neuroapoptotic factor [153,154]. Serum S100β levels increased in pediatric patients following general anesthesia by a combination of fentanyl with non-opioid drugs; only the total dose of fentanyl was significantly correlated with the difference between post-exposure and baseline S100β levels [154].…”

Section: Repeated Exposure To Tramadol and Tapentadol Alters The Exprmentioning

confidence: 99%

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

et al. 2021

View full text Add to dashboard Cite

Tramadol and tapentadol, two structurally related synthetic opioid analgesics, are widely prescribed due to the enhanced therapeutic profiles resulting from the synergistic combination between μ-opioid receptor (MOR) activation and monoamine reuptake inhibition. However, the number of adverse reactions has been growing along with their increasing use and misuse. The potential toxicological mechanisms for these drugs are not completely understood, especially for tapentadol, owing to its shorter market history. Therefore, in the present study, we aimed to comparatively assess the putative lung, cardiac, and brain cortex toxicological damage elicited by the repeated exposure to therapeutic doses of both prescription opioids. To this purpose, male Wistar rats were intraperitoneally injected with single daily doses of 10, 25, and 50 mg/kg tramadol or tapentadol, corresponding to a standard analgesic dose, an intermediate dose, and the maximum recommended daily dose, respectively, for 14 consecutive days. Such treatment was found to lead mainly to lipid peroxidation and inflammation in lung and brain cortex tissues, as shown through augmented thiobarbituric acid reactive substances (TBARS), as well as to increased serum inflammation biomarkers, such as C reactive protein (CRP) and tumor necrosis factor-α (TNF-α). Cardiomyocyte integrity was also shown to be affected, since both opioids incremented serum lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) activities, while tapentadol was associated with increased serum creatine kinase muscle brain (CK-MB) isoform activity. In turn, the analysis of metabolic parameters in brain cortex tissue revealed increased lactate concentration upon exposure to both drugs, as well as augmented LDH and creatine kinase (CK) activities following tapentadol treatment. In addition, pneumo- and cardiotoxicity biomarkers were quantified at the gene level, while neurotoxicity biomarkers were quantified both at the gene and protein levels; changes in their expression correlate with the oxidative stress, inflammatory, metabolic, and histopathological changes that were detected. Hematoxylin and eosin (H & E) staining revealed several histopathological alterations, including alveolar collapse and destruction in lung sections, inflammatory infiltrates, altered cardiomyocytes and loss of striation in heart sections, degenerated neurons, and accumulation of glial and microglial cells in brain cortex sections. In turn, Masson’s trichrome staining confirmed fibrous tissue deposition in cardiac tissue. Taken as a whole, these results show that the repeated administration of both prescription opioids extends the dose range for which toxicological injury is observed to lower therapeutic doses. They also reinforce previous assumptions that tramadol and tapentadol are not devoid of toxicological risk even at clinical doses.

show abstract

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

Cited by 17 publications

References 58 publications

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Morphine consumption during pregnancy exacerbates neonatal hypoxia‐ischemia injury in rats

Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats

Contact Info

Product

Resources

About