Sex specific effects of buprenorphine on behavior, astrocytic opioid receptor expression and neuroinflammation after pediatric traumatic brain injury in mice

Hamood, Yesmine; Abdullah, Mauda; Ghoul, Hassan El; Saad, Nazeh; Dysko, Robert C.; Zhi, Zhang

doi:10.1016/j.bbih.2022.100469

Cited by 6 publications

(20 citation statements)

References 104 publications

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“…Other studies investigating the effects of Bup on rodent models have also found varying impacts on weight. One study found weight loss to be more severe following Bup-SR-Lab treatment compared to saline controls [ 41 ], while another found that weight loss was slightly reduced following Bup treatment [ 42 ]. There have also been studies that, like the current study, found no weight-related differences in rats treated with Bup-SR compared to controls [ 17 , 18 ], demonstrating the variation in weight-related results.…”

Section: Discussionmentioning

confidence: 99%

“…Prenatal exposure to Bup resulted in higher GFAP levels specifically within the hippocampus [ 64 ]. Another group found a slight reduction in the percentage of GFAP+ area covered in the corpus callosum of mice days following Bup administration [ 42 ]. These regional Bup-associated differences could be associated with differences in expression of opioid receptors in the cortex compared to the thalamus.…”

Section: Discussionmentioning

confidence: 99%

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Post-Injury Buprenorphine Administration Is Associated with Long-Term Region-Specific Glial Alterations in Rats

et al. 2022

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Traumatic brain injury (TBI) is a major leading cause of death and disability. While previous studies regarding focal pathologies following TBI have been done, there is a lack of information concerning the role of analgesics and their influences on injury pathology. Buprenorphine (Bup), an opioid analgesic, is a commonly used analgesic in experimental TBI models. Our previous studies investigated the acute effects of Buprenorphine-sustained release-Lab (Bup-SR-Lab) on diffuse neuronal/glial pathology, neuroinflammation, cell damage, and systemic physiology. The current study investigated the longer-term chronic outcomes of Bup-SR-Lab treatment at 4 weeks following TBI utilizing a central fluid percussion injury (cFPI) model in adult male rats. Histological assessments of physiological changes, neuronal damage, cortical and thalamic cytokine expression, microglial and astrocyte morphological changes, and myelin alterations were done, as we had done in our acute study. In the current study the Whisker Nuisance Task (WNT) was also performed pre- and 4w post-injury to assess changes in somatosensory sensitivity following saline or Bup-SR-Lab treatment. Bup-SR-Lab treatment had no impact on overall physiology or neuronal damage at 4w post-injury regardless of region or injury, nor did it have any significant effects on somatosensory sensitivity. However, greater IL-4 cytokine expression with Bup-SR-Lab treatment was observed compared to saline treated animals. Microglia and astrocytes also demonstrated region-specific morphological alterations associated with Bup-SR-Lab treatment, in which cortical microglia and thalamic astrocytes were particularly vulnerable to Bup-mediated changes. There were discernable injury-specific and region-specific differences regarding myelin integrity and changes in specific myelin basic protein (MBP) isoform expression following Bup-SR-Lab treatment. This study indicates that use of Bup-SR-Lab could impact TBI-induced glial alterations in a region-specific manner 4w following diffuse brain injury.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Post-Injury Buprenorphine Administration Is Associated with Long-Term Region-Specific Glial Alterations in Rats

et al. 2022

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“…Two groups of mice, the acute and chronic phases, were used in this study. In accordance with the literature, 24th hour after TBI was considered as acute phase, and the 28th to 30th days after TBI was considered as chronic phase [12,19]. The acute phase group was sacrificed by cervical dislocation 24 h after mTBI, as it is widely accepted as the acute phase for mice.…”

Section: Transferring Mimic-mir-126-3p Into Mouse Embryos By Microinj...mentioning

confidence: 99%

Alterations in Serum miR-126-3p Levels over Time: A Marker of Pituitary Insufficiency following Head Trauma

Tufan,

Taheri,

Karaca

et al. 2023

Neuroendocrinology

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TBI is a condition caused by a head injury that poses a high risk of developing pituitary insufficiency in patients. We have previously reported alterations in miR-126-3p levels in sera from patients with TBI-induced pituitary deficiency. To investigate why TBI-induced pituitary deficiency develops in only some patients and to reveal the relationship of miR-126-3p with the hormone axes, we used mice epigenetically modified with miR-126-3p at the embryonic stage in this study. These modified mice were subjected to mild-TBI(mTBI) according to the Marmarou-weight-drop model. The alterations of miR-126-3p levels after mTBI of both wild-type and modified-miR-126-3p* lines of mice validated our human results. In addition, the hypothalamus, pituitary, and adrenal tissues were analyzed for the related transcripts and serum hormone levels. We report that mir-126-3p directly affects the upregulation of the Hypothamus-Pituitary-Adrenal (HPA) axis and ACTH secretion in the acute phase after mTBI. We have also demonstrated that miR-126-3p suppresses Gnrh transcripts in the hypothalamus and pituitary, but this is not reflected in FSH/LH serum levels. The increase in ACTH levels in the acute phase may indicate that the up-regulation of miR-126-3p has a protective effect on the HPA axis after TBI. Notably, the most prominent transcript response is found in the adrenals, highlighting their role in the pathophysiology of TBI. Our study revealed the role of miR-126-3p in TBI and pituitary deficiency developing after TBI, and the data obtained will significantly contribute to unraveling the mechanism of pituitary deficiency developing after TBI and developing new diagnostic and treatment strategies.

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“…Therefore, using astrocytic activation markers other than GFAP alone should help to define astrocyte reactivity. Increased mRNA expression of cytokines (IL-1β, IL-6, TNF-α, TGF-1β) has been described up to 7 days after juvenile brain trauma (PND20–21) ( Hamood et al, 2022 ). Associated with astrocyte changes, microglia cells and macrophages are recruited in the neonatal brain ( Kempuraj et al, 2017 ; Tong et al, 2002 ) with increased microglial cells observed one month after injury in a model of juvenile (PND 28) CCI ( Smith et al, 2019 ).…”

Section: Do Astrocytes Play An Immune Role In Pediatric Traumatic Bra...mentioning

confidence: 99%

Do astrocytes act as immune cells after pediatric TBI?

Panchenko,

Hippauf,

Konsman

et al. 2023

Neurobiology of Disease

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Sex specific effects of buprenorphine on behavior, astrocytic opioid receptor expression and neuroinflammation after pediatric traumatic brain injury in mice

Cited by 6 publications

References 104 publications

Post-Injury Buprenorphine Administration Is Associated with Long-Term Region-Specific Glial Alterations in Rats

Post-Injury Buprenorphine Administration Is Associated with Long-Term Region-Specific Glial Alterations in Rats

Alterations in Serum miR-126-3p Levels over Time: A Marker of Pituitary Insufficiency following Head Trauma

Do astrocytes act as immune cells after pediatric TBI?

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