Engaging endogenous opioid circuits in pain affective processes

Kimmey, Blake A.; McCall, Nora M.; Wooldridge, Lisa M.; Satterthwaite, Theodore D.; Corder, Gregory

doi:10.1002/jnr.24762

Cited by 18 publications

(21 citation statements)

References 327 publications

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“…Such differences may be due to both heritable factors and environmental influences that interact with the genome through epigenetic or transcription mechanisms to produce long-term alterations in the endogenous opioid system [252]. Endogenous opioid peptides are found throughout the peripheral and central nervous systems, where they play a role in many different types of functions, including nociception and analgesia, stress responses, physiological functions, social behavior, mood, and reinforcement [127,[253][254][255][256][257]. Normally, this system is activated by acute stress, leading to the release of endogenous opioids at multiple sites in the brain.…”

Section: Effects Of Els On Endogenous Opioid Functionmentioning

confidence: 99%

“…ous systems, where they play a role in many different types of functions, including nociception and analgesia, stress responses, physiological functions, social behavior, mood, and reinforcement [127,[253][254][255][256][257]. Normally, this system is activated by acute stress, leading to the release of endogenous opioids at multiple sites in the brain.…”

Section: Effects Of Els On Endogenous Opioid Functionmentioning

confidence: 99%

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Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Oswald

Dunn

Seminowicz

et al. 2021

JPM

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A robust body of research has shown that traumatic experiences occurring during critical developmental periods of childhood when neuronal plasticity is high increase risks for a spectrum of physical and mental health problems in adulthood, including substance use disorders. However, until recently, relatively few studies had specifically examined the relationships between early life stress (ELS) and opioid use disorder (OUD). Associations with opioid use initiation, injection drug use, overdose, and poor treatment outcome have now been demonstrated. In rodents, ELS has also been shown to increase the euphoric and decrease antinociceptive effects of opioids, but little is known about these processes in humans or about the neurobiological mechanisms that may underlie these relationships. This review aims to establish a theoretical model that highlights the mechanisms by which ELS may alter opioid sensitivity, thereby contributing to future risks for OUD. Alterations induced by ELS in mesocorticolimbic brain circuits, and endogenous opioid and dopamine neurotransmitter systems are described. The limited but provocative evidence linking these alterations with opioid sensitivity and risks for OUD is presented. Overall, the findings suggest that better understanding of these mechanisms holds promise for reducing vulnerability, improving prevention strategies, and prescribing guidelines for high-risk individuals.

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Section: Effects Of Els On Endogenous Opioid Functionmentioning

confidence: 99%

Section: Effects Of Els On Endogenous Opioid Functionmentioning

confidence: 99%

Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Oswald

Dunn

Seminowicz

et al. 2021

JPM

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“…Opioid receptors, including mu, delta, and kappa receptors, are expressed throughout the brain, especially in areas associated with pain and reward processing (12). These receptors are the active sites of endogenous opioid peptides and exogenous painkillers such as morphine (13,14). Among opioid receptors, the mu-opioid receptors are mainly expressed in mesocorticolimbic areas (15).…”

Section: Introductionmentioning

confidence: 99%

Region Specificity in Endogenous Opioid Peptides and Mu-opioid Receptor Gene Expression in Rat Brain Areas Involved in Addiction After Frequent Morphine Treatment

Ahmadi

Masoudi

Talvar

et al. 2022

Jentashapir J Cell Mol Biol

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Backgrounds: Molecular mechanisms involved in adverse effects of morphine, including tolerance and dependence, have remained elusive. We examined possible alterations in the gene expression of proenkephalin (Penk), prodynorphin (Pdyn), and mu-opioid receptor (Oprm1) in reward brain areas following frequent morphine treatment. Methods: Two groups of male Wistar rats were used. The groups received either saline (1 mL/kg) or morphine (10 mg/kg) twice daily for eight days. On day 8, rats were decapitated, brain areas involved in addiction were dissected, including the midbrain, striatum, prefrontal cortex (PFC), hippocampus, and hypothalamus, and gene expression was evaluated with real-time PCR. Results: Prolonged morphine treatment decreased Penk, Pdyn, and Oprm1 gene expressions in the midbrain but upregulated them in the striatum compared to the control group treated with saline. Significant increases in Pdyn and Oprm1 gene expressions were detected in the PFC, but there was no significant difference in Penk gene expression between the two groups. Besides, Pdyn gene expression was decreased in the hippocampus and hypothalamus; however, no significant differences in Penk and Oprm1 gene expressions were detected between the groups in these areas. Conclusions: The expression of endogenous opioid peptides and receptors after frequent use of morphine follows a region specificity in brain areas involved in addiction. These alterations may result in new physiological setpoints outside the normal range, which need to be considered when using morphine in medicine.

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“…The endogenous opioid system (EOS) is a critical neurotransmitter system regulating the presentation and processing of emotions and pain [54]. This system includes three opioid receptor types, µ-(MOR), δ-(DOR), and κ-(KOR), which are preferentially activated by β-endorphin, enkephalins, and dynorphins, respectively.…”

Section: Lateralization Of Neurotransmitter Systems Involved In Pain Processing Asymmetric Lateralization Of Opioid Receptors In Areas Inmentioning

confidence: 99%

Asymmetric Lateralization during Pain Processing

Roza

Martinez-Padilla

2021

Symmetry

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Pain is defined as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage”. This complex perception arises from the coordinated activity of several brain areas processing either sensory–discriminative or affective–motivational components. Functional studies performed in healthy volunteers revealed that affective–emotional components of pain are processed bilaterally but present a clear lateralization towards the right hemisphere, regardless of the site of stimulation. Studies at the cellular level performed in experimental animal models of pain have shown that neuronal activity in the right amygdala is clearly pronociceptive, whilst activation of neurons in the left amygdala might even exert antinociceptive effects. A shift in lateralization becomes evident during the development of chronic pain; thus, in patients with neuropathic pain symptoms, there is increased activity in ipsilateral brain areas related with pain. These observations extend the asymmetrical left–right lateralization within the nervous system and provide a new hypothesis for the pathophysiology of chronic forms of pain. In this article, we will review experimental data from preclinical and human studies on functional lateralization in the brain during pain processing, which will help to explain the affective disorders associated with persistent, chronic pain.

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Engaging endogenous opioid circuits in pain affective processes

Cited by 18 publications

References 327 publications

Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Region Specificity in Endogenous Opioid Peptides and Mu-opioid Receptor Gene Expression in Rat Brain Areas Involved in Addiction After Frequent Morphine Treatment

Asymmetric Lateralization during Pain Processing

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