Effect of δ-Opioid Receptor Activation on BDNF-TrkB vs. TNF-α in the Mouse Cortex Exposed to Prolonged Hypoxia

Tian, Xue; Fang, Hua; Sandhu, Harleen K.; Chao, Dongman; Balboni, Gianfranco; Salvadori, Severo; He, Xiaozhou; Xia, Ying

doi:10.3390/ijms140815959

Cited by 36 publications

(32 citation statements)

References 46 publications

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“…Triple-labeled confocal images also showed that BDNF and DOR/MAP-2 protein were co-localized in the neuronal-like cells in the frontoparietal cortex (Fig. 2B, C) [107]. …”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

“…Note that MCAO significantly reduced the expression of 140 KDa TrkB in the cortex, while DOR activation with TAN67 largely reversed such ischemic reduction. Cited from Tian et al [107]. …”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

“…In another study [107], we further investigated if DOR modulates the BDNF-TrkB pathway in cerebral ischemia.…”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

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Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

Sheng¹,

Huang²,

Ren³

et al. 2018

Cell Physiol Biochem

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The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR’s role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain, we clarified DOR’s specific role in the brain against hypoxic/ischemic injury and reconciled previous controversies in this aspect. Our serial studies have strongly demonstrated that DOR is a unique neuroprotector against hypoxic/ischemic injury in the brain, which has been well confirmed in current research. Moreover, mechanistic studies have shown that during acute phases of hypoxic/ischemic stress, DOR protects the neurons mainly by the stabilization of ionic homeostasis, inhibition of excitatory transmitter release, and attenuation of disrupted neuronal transmission. During prolonged hypoxia/ischemia, however, DOR neuroprotection involves a variety of signaling pathways. More recently, our data suggest that DOR may display its neuroprotective role via the BDNF-TrkB pathway. This review concisely summarizes the progress in this field.

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“…Triple-labeled confocal images also showed that BDNF and DOR/MAP-2 protein were co-localized in the neuronal-like cells in the frontoparietal cortex (Fig. 2B, C) [107]. …”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

“…Note that MCAO significantly reduced the expression of 140 KDa TrkB in the cortex, while DOR activation with TAN67 largely reversed such ischemic reduction. Cited from Tian et al [107]. …”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

See 1 more Smart Citation

Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

Sheng¹,

Huang²,

Ren³

et al. 2018

Cell Physiol Biochem

Self Cite

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“…An increased level of TNF-α has been reported in disorders such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis (24,25). Morphine binds to μ-opioid receptors in microglia and increases the secretion of inflammatory factors such as TNF-α (26,27). Moreover, TNF-α and S100B exist in different regions of the hippocampus and are involved in hippocampal physiology and pathophysiology (28,29).…”

Section: Introductionmentioning

confidence: 99%

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

Amri

Sadegh

Moulaei

et al. 2017

The American Journal of Drug and Alcohol Abuse

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“…The effects of recurrent moderate hypoglycemia are not known. Other conditions that perturb energy metabolism in the postnatal period, such as recurrent hypoxia, are associated with suppressed BDNF expression in the PFC [21,22]. …”

Section: Introductionmentioning

confidence: 99%

Recurrent Moderate Hypoglycemia Suppresses Brain-Derived Neurotrophic Factor Expression in the Prefrontal Cortex and Impairs Sensorimotor Gating in the Posthypoglycemic Period in Young Rats

Rao

Ennis

Mitchell³

et al. 2016

Dev Neurosci

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Recurrent hypoglycemia is common in infants and children. In developing rat models, recurrent moderate hypoglycemia leads to neuronal injury in the medial prefrontal cortex. To understand the effects beyond neuronal injury, 3-week-old male rats were subjected to 5 episodes of moderate hypoglycemia (blood glucose concentration, approx. 30 mg/dl for 90 min) once daily from postnatal day 24 to 28. Neuronal injury was determined using Fluoro-Jade B histochemistry on postnatal day 29. The effects on brain-derived neurotrophic factor (BDNF) and its cognate receptor, tyrosine kinase receptor B (TrkB) expression, which is critical for prefrontal cortex development, were determined on postnatal day 29 and at adulthood. The effects on prefrontal cortex-mediated function were determined by assessing the prepulse inhibition of the acoustic startle reflex on postnatal day 29 and 2 weeks later, and by testing for fear-potentiated startle at adulthood. Recurrent hypoglycemia led to neuronal injury confined primarily to the medial prefrontal cortex. BDNF/TrkB expression in the prefrontal cortex was suppressed on postnatal day 29 and was accompanied by lower prepulse inhibition, suggesting impaired sensorimotor gating. Following the cessation of recurrent hypoglycemia, the prepulse inhibition had recovered at 2 weeks. BDNF/TrkB expression in the prefrontal cortex had normalized and fear-potentiated startle was intact at adulthood. Recurrent moderate hypoglycemia during development has significant adverse effects on the prefrontal cortex in the posthypoglycemic period.

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Effect of δ-Opioid Receptor Activation on BDNF-TrkB vs. TNF-α in the Mouse Cortex Exposed to Prolonged Hypoxia

Cited by 36 publications

References 46 publications

Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

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

Recurrent Moderate Hypoglycemia Suppresses Brain-Derived Neurotrophic Factor Expression in the Prefrontal Cortex and Impairs Sensorimotor Gating in the Posthypoglycemic Period in Young Rats

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