miR-200a-3p modulates gene expression in comorbid pain and depression: Molecular implication for central sensitization

Satyanarayanan, Senthil Kumaran; Shih, Yin-Hwa; Wen, Yeong-Ray; Palani, Mahalakshmi; Lin, Yi‐Wen; Su, Huanxing; Gałecki, Piotr; Su, Kuan‐Pin

doi:10.1016/j.bbi.2019.08.190

Cited by 42 publications

(33 citation statements)

References 101 publications

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“…Understanding and identifying the underlying molecular processes involved in CPDC provides potential therapeutic targets to address the clinical manifestations thereof. To this end, the similarity of symptomatic presentations between chronic pain and depression underline shared biological mechanisms, such as neuroinflammation and central sensitization [ 4 ]. Accordingly, chronic pain states can be observed in a multitude of inflammatory conditions [ 5 ], and the associations of neurobiological conditions pertaining to the development of depression also appear to be triggered or reinforced by these inflammatory processes [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

TRPV1 Responses in the Cerebellum Lobules VI, VII, VIII Using Electroacupuncture Treatment for Chronic Pain and Depression Comorbidity in a Murine Model

Lottering

Lin

2021

IJMS

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Depression is a prominent complex psychiatric disorder, usually complicated through expression of comorbid conditions, with chronic pain being among the most prevalent. This comorbidity is consistently associated with a poor prognosis and has been shown to negatively impact patient outcomes. With a global rise in this condition presenting itself, the importance of discovering long-term, effective, and affordable treatments is crucial. Electroacupuncture has demonstrated renowned success in its use for the treatment of pain and is a widely recognized therapy in clinical practice for the treatment of various psychosomatic disorders, most notably depression. Our study aimed to investigate the effects and mechanisms of Acid-Saline (AS) inducing states of chronic pain and depression comorbidity in the cerebellum, using the ST36 acupoint as the therapeutic intervention. Furthermore, the role of TRPV1 was relatedly explored through the use of TRPV1−/− mice (KO). The results indicated significant differences in the four behavioral tests used to characterize pain and depression states in mice. The AS and AS + SHAM group showed significant differences when compared to the Control and AS + EA groups in the von Frey and Hargreaves’s tests, as well as the Open-Field and Forced Swimming tests. This evidence was further substantiated in the protein levels observed in immunoblotting, with significant differences between the AS and AS + SHAM groups when compared to the AS + EA and AS + KO groups being identified. In addition, immunofluorescence visibly served to corroborate the quantitative outcomes. Conclusively these findings suggest that AS-induced chronic pain and depression comorbidity elicits changes in the cerebellum lobules VI, VII, VIII, which are ameliorated through the use of EA at ST36 via its action on TRPV1 and related molecular pathways. The action of TRPV1 is not singular in CPDC, which would suggest other potential targets such as acid-sensing ion channel subtype 3 (ASIC3) or voltage-gated sodium channels (Navs) that could be explored in future studies.

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Section: Introductionmentioning

confidence: 99%

TRPV1 Responses in the Cerebellum Lobules VI, VII, VIII Using Electroacupuncture Treatment for Chronic Pain and Depression Comorbidity in a Murine Model

Lottering

Lin

2021

IJMS

Self Cite

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“…For example, miR-200a-3p was shown to be down regulated in the PFC of rats exposed to 4 weeks of chronic unpredictable stress in adulthood; a finding similar to our own. In contrast, after 12 weeks of stress exposure this same miRNA was upregulated ( Satyanarayanan et al, 2019 ). We believe that this investigation produced the first known data to examine the global patterns of PFC miRNA expression following adolescent stress.…”

Section: Discussionmentioning

confidence: 99%

Adolescent Stress Reduces Adult Morphine-Induced Behavioral Sensitization in C57BL/6J Mice

Kamens

Miller

Caulfield

et al. 2021

Front. Behav. Neurosci.

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Deaths related to opioid use have skyrocketed in the United States, leading to a public health epidemic. Research has shown that both biological (genes) and environmental (stress) precursors are linked to opioid use. In particular, stress during adolescence–a critical period of frontal lobe development–influences the likelihood of abusing drugs. However, little is known about the biological mechanisms through which adolescent stress leads to long-term risk of opioid use, or whether genetic background moderates this response. Male and female C57BL/6J and BALB/cJ mice were exposed to chronic variable social stress (CVSS) or control conditions throughout adolescence and then tested for morphine locomotor sensitization or morphine consumption in adulthood. To examine possible mechanisms that underlie stress-induced changes in morphine behaviors, we assessed physiological changes in response to acute stress exposure and prefrontal cortex (PFC) miRNA gene expression. Adolescent stress did not influence morphine sensitization or consumption in BALB/cJ animals, and there was limited evidence of stress effects in female C57BL/6J mice. In contrast, male C57BL/6J mice exposed to adolescent CVSS had blunted morphine sensitization compared to control animals; no differences were observed in the acute locomotor response to morphine administration or morphine consumption. Physiologically, C57BL/6J mice exposed to CVSS had an attenuated corticosterone recovery following an acute stressor and downregulation of twelve miRNA in the PFC compared to control mice. The specificity of the effects for C57BL/6J vs. BALB/cJ mice provides evidence of a gene-environment interaction influencing opioid behaviors. However, this conclusion is dampened by limited locomotor sensitization observed in BALB/cJ mice. It remains possible that results may differ to other doses of morphine or other behavioral responses. Long-term differences in stress reactivity or miRNA expression in C57BL/6J mice suggests two possible biological mechanisms to evaluate in future research.

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“…For example, miR-200a-3p was shown to be down regulated in the prefrontal cortex of rats exposed to 4 weeks of chronic unpredictable stress in adulthood; a finding similar to our own. In contrast, after 12 weeks of stress exposure this same miRNA was upregulated (Satyanarayanan et al, 2019). We believe that this investigation produced the first known data to examine the global patterns of prefrontal cortex miRNA expression following adolescent stress.…”

Section: Discussionmentioning

confidence: 99%

Effect of Adolescent Stress on Adult Morphine-Induced Behavioral Sensitization is Dependent Upon Genetic Background

Kamens

Miller

Caulfield

et al. 2021

Preprint

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Deaths related to opioid use have skyrocketed in the United States, leading to a public health epidemic. Research has shown that both biological (genes) and environmental (stress) precursors are linked to opioid use. In particular, stress during adolescence – a critical period of frontal lobe development–influences the likelihood of abusing drugs. However, little is known about the biological mechanisms through which adolescent stress leads to long-term risk of opioid use, or whether genetic background moderates this response. Male and female C57BL/6J and BALB/cJ mice were exposed to chronic variable social stress (CVSS) or control conditions throughout adolescence (postnatal days, PND, 25-59) and then tested for morphine locomotor sensitization or morphine consumption in adulthood. To examine possible mechanisms that underlie stress-induced changes in morphine behaviors, we assessed physiological changes in response to acute stress exposure and miRNA gene expression in the prefrontal cortex. Male C57BL/6J mice exposed to adolescent CVSS had blunted morphine sensitization compared to control animals. No differences were observed in the acute locomotor response to morphine administration or morphine consumption in adult C57BL/6J mice. Stress did not influence morphine behaviors in BALB/cJ animals. C57BL/6J mice exposed to CVSS had a blunted corticosterone recovery following an acute stressor. Twelve miRNA were downregulated in the prefrontal cortex of C57BL/6J mice exposed to CVSS in adolescence, which suggests a biological mechanism through which stress may alter later morphine responses. The specificity of the effects for C57BL/6J versus BALB/cJ mice provides evidence of a gene by environmental interaction influencing opioid behaviors.

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miR-200a-3p modulates gene expression in comorbid pain and depression: Molecular implication for central sensitization

Cited by 42 publications

References 101 publications

TRPV1 Responses in the Cerebellum Lobules VI, VII, VIII Using Electroacupuncture Treatment for Chronic Pain and Depression Comorbidity in a Murine Model

TRPV1 Responses in the Cerebellum Lobules VI, VII, VIII Using Electroacupuncture Treatment for Chronic Pain and Depression Comorbidity in a Murine Model

Adolescent Stress Reduces Adult Morphine-Induced Behavioral Sensitization in C57BL/6J Mice

Effect of Adolescent Stress on Adult Morphine-Induced Behavioral Sensitization is Dependent Upon Genetic Background

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