Treadmill exercise alleviated prenatal buprenorphine exposure-induced depression in rats

Wu, Chih-Cheng; Hung, Chih-Jen; Lin, Shih‐Yi; Wang, Yayu; Chang, Chieh-Ming J.; Chen, Wenying; Liao, Su‐Lan; Raung, Shue-Ling; Yang, Ching-Ping; Chen, Chun-Jung

doi:10.1016/j.neuint.2017.09.012

Cited by 23 publications

(18 citation statements)

References 47 publications

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“…The Morris water maze test is commonly used in behavioral assays for memory and learning. In addition, depression behavior is determined by the FST and TST [ 24 , 29 , 34 , 35 , 36 ]. Herein, data regarding behavioral evaluation have suggested an induction of depression-like and anxiety-like behavior, as well as spatial memory and learning impairment in PCS mice.…”

Section: Discussionmentioning

confidence: 99%

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p-Cresol Sulfate Caused Behavior Disorders and Neurodegeneration in Mice with Unilateral Nephrectomy Involving Oxidative Stress and Neuroinflammation

Sun

Wang

et al. 2020

IJMS

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Protein-bound uremic toxins, such as p-cresol sulfate (PCS), can be accumulated with declined renal function and aging and is closely linked with central nervous system (CNS) diseases. In the periphery, PCS has effects on oxidative stress and inflammation. Since oxidative stress and inflammation have substantial roles in the pathogenesis of neurological disorders, the CNS effects of PCS were investigated in unilateral nephrectomized C57/BL/6 mice. Unlike intact mice, unilateral nephrectomized mice showed increased circulating levels of PCS after exogenous administration. Upon PCS exposure, the unilateral nephrectomized mice developed depression-like, anxiety-like, and cognitive impairment behaviors with brain PCS accumulation in comparison with the nephrectomy-only group. In the prefrontal cortical tissues, neuronal cell survival and neurogenesis were impaired along with increased apoptosis, oxidative stress, and neuroinflammation. Circulating brain-derived neurotrophic factors (BDNF) and serotonin were decreased in association with increased corticosterone and repressor element-1 silencing transcription factor (REST), regulators involved in neurological disorders. On the contrary, these PCS-induced changes were alleviated by uremic toxin absorbent AST-120. Taken together, PCS administration in mice with nephrectomy contributed to neurological disorders with increased oxidative stress and neuroinflammation, which were alleviated by PCS chelation. It is suggested that PCS may be a therapeutic target for chronic kidney disease-associated CNS diseases.

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Section: Discussionmentioning

confidence: 99%

“…The behavioral evaluation was conducted according to our previously reported methods by technicians who were blind to the treatments [ 24 , 29 , 34 , 36 ]. In the open field test, mice were placed on an apparatus 30 cm in length and 30 cm in width.…”

Section: Methodsmentioning

confidence: 99%

p-Cresol Sulfate Caused Behavior Disorders and Neurodegeneration in Mice with Unilateral Nephrectomy Involving Oxidative Stress and Neuroinflammation

Sun

Wang

et al. 2020

IJMS

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“…The opioid of choice in preclinical studies has typical been morphine or methadone likely because of their long history of clinical usage. The growing use of buprenorphine clinically and heroin, oxycodone, and fentanyl recreationally has also translated into their usage in preclinical models (Robinson and Wallace, 2001;Chiang et al, 2010;Davis et al, 2010;Chiang et al, 2014;Devarapalli et al, 2016;Sithisarn et al, 2017;Wu et al, 2017;Griffin et al, 2019;Kvello et al, 2019;Wallin et al, 2019;Alipio et al, 2020). Less commonly used opioids, both clinically and preclinically, include the long acting methadone analogs l-alpha-acetylmethadol and N-desmethyl-l-alpha-noracetylmethadol (Schrott and Sparber, 2004;Hamilton et al, 2005).…”

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confidence: 99%

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

Grecco

Atwood

2020

eNeuro

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The opioid crisis has resulted in an unprecedented number of neonates born with prenatal opioid exposure (POE); however, the long-term effects of POE on offspring behavior and neurodevelopment remain relatively unknown. The advantages and disadvantages of the various preclinical POE models developed over the last several decades are discussed in the context of clinical and translational relevance. Although considerable and important variability exists among preclinical models of POE, the examination of these preclinical models has revealed that opioid exposure during the prenatal period contributes to maladaptive behavioral development as offspring mature including an altered responsiveness to rewarding drugs and increased pain response. The present review summarizes key findings demonstrating the impact of POE on offspring drug selfadministration, drug consumption, the reinforcing properties of drugs, drug tolerance, and other reward-related behaviors such as hypersensitivity to pain. Potential underlying molecular mechanisms which may contribute this enhanced addictive phenotype in POE offspring are further discussed with special attention given to key brain regions associated with reward including the striatum, prefrontal cortex, ventral tegmental area, hippocampus, and amygdala. Improvements in preclinical models and further areas of study are also identified which may advance the translational value of findings and help address the growing problem of POE in clinical populations. Significance Statement As the number of the infants born following prenatal opioid exposure continues to increase, there is a greater need to employ preclinical models to study the potential consequences of POE and brain and behavioral development. A large body of evidence indicates POE is associated with alterations in reward-related behavior and molecular adaptations in reward neurocircuitry. This review seeks to: (1) provide an overview of the various types of preclinical models developed over the last few decades; (2) review the numerous behavioral studies examining drug-reward related behavior in offspring with POE; and (3) discuss potential contributing molecular mechanisms to this enhanced reward phenotype observed in POE offspring.

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“…Preclinical investigations are necessary that examine age differences in sensitivity to adverse effects like respiratory depression. The brain structure (141) and functional abnormalities in rats following relatively low perinatal doses (110,145,150) are concerning and may warrant follow-up (e.g. Diffusion Tensor Imaging to evaluate white matter integrity in buprenorphine exposed nonhuman primates or children).…”

Section: Resultsmentioning

confidence: 99%

“…Prenatal exposure to 1, but not 0.3, mg/kg buprenorphine increased immobility, independent of sex, on the forced swimming and tail suspension tests (110). This profile of behavior was replicated, albeit by the same laboratory, and is interpreted as an increase in depressionlike behavior (142,145). Young-adult rats that had received buprenorphine perinatally (1 mg/kg) showed a pronounced deficit in recognition memory (37).…”

Section: Prenatal Correlates and Consequencesmentioning

confidence: 87%

An Examination of the Complex Pharmacological Properties of the Non-Selective Opioid Receptor Modulator Buprenorphine

Pande¹,

Piper²

2020

Preprint

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Buprenorphine, an analogue of thebaine, is a Schedule III opioid in the United States used for opioid-use disorder and as an analgesic. Research has shown drugs like buprenorphine have a complicated pharmacology with characteristics that challenge traditional definitions of terms like agonist, antagonist, and efficacy. Buprenorphine has a high affinity for the mu (MOR), delta (DOR), kappa (KOR), and intermediate for the nociceptin opioid receptors (NOR). Buprenorphine is generally described as a partial MOR agonist with limited activity and decreased response at the mu-receptor relative to full agonists. In opioid naïve patients, the drug’s analgesic efficacy is equivalent to a full MOR agonist, despite decreased receptor occupancy and the “ceiling effect” produced from larger doses. Some argue buprenorphine’s effects depend on the endpoint measured, as it functions as a partial agonist for respiratory depression, but a full-agonist for pain. Buprenorphine’s active metabolite, norbuprenorphine, attenuates buprenorphine's analgesic effects due to NOR binding and respiratory depressant effects. The method of administration impacts efficacy and tolerance when administered for analgesia. There have been eleven-thousand reports involving buprenorphine and minors (age < 19) to US poison control centers, the preponderance (89.2%) with children. The consequences of prenatal buprenorphine exposure in experimental animals and humans should continue to be carefully evaluated. In conclusion, buprenorphine’s characterization as only a partial mu-agonist is an oversimplification. Contemporary research shows the traditional explanation of the pharmacology of buprenorphine does not take into account changes to receptor theory, pharmacological terminology, route of administration, and biologically active major metabolites.

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Treadmill exercise alleviated prenatal buprenorphine exposure-induced depression in rats

Cited by 23 publications

References 47 publications

p-Cresol Sulfate Caused Behavior Disorders and Neurodegeneration in Mice with Unilateral Nephrectomy Involving Oxidative Stress and Neuroinflammation

p-Cresol Sulfate Caused Behavior Disorders and Neurodegeneration in Mice with Unilateral Nephrectomy Involving Oxidative Stress and Neuroinflammation

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

An Examination of the Complex Pharmacological Properties of the Non-Selective Opioid Receptor Modulator Buprenorphine

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