Related Experiment Video
Updated: May 18, 2026

The Analysis of Neurovascular Remodeling in Entorhino-hippocampal Organotypic Slice Cultures
Published on: October 23, 2014
Neuroprotection against hypoxia/ischemia: δ-opioid receptor-mediated cellular/molecular events
Xiaozhou He1, Harleen K Sandhu, Yilin Yang
1The Third Clinical College of Suzhou University, Changzhou, Jiangsu, China.
Abstract:
Hypoxic/ischemic injury remains the most dreaded cause of neurological disability and mortality. Despite the humbling experiences due to lack of promising therapy, our understanding of the complex cascades underlying the neuronal insult has led to advances in basic science research. One of the most noteworthy has been the effect of opioid receptors, especially the delta-opioid receptor (DOR), on hypoxic/ischemic neurons. Our recent studies, and those of others worldwide, present strong evidence that sheds light on DOR-mediated neuroprotection in the brain, especially in the cortex. The mechanisms of DOR neuroprotection are broadly categorized as: (1) stabilization of the ionic homeostasis, (2) inhibition of excitatory transmitter release, (3) attenuation of disrupted neuronal transmission, (4) increase in antioxidant capacity, (5) regulation of intracellular pathways-inhibition of apoptotic signals and activation of pro-survival signaling, (6) regulation of specific gene and protein expression, and (7) up-regulation of endogenous opioid release and/or DOR expression. Depending upon the severity and duration of hypoxic/ischemic insult, the release of endogenous opioids and DOR expression are regulated in response to the stress, and DOR signaling acts at multiple levels to confer neuronal tolerance to harmful insult. The phenomenon of DOR neuroprotection offers a potential clue for a promising target that may have significant clinical implications in our quest for neurotherapeutics.
Insights
Delta-opioid receptors (DOR) show neuroprotective effects against hypoxic/ischemic brain injury. Targeting DOR offers a promising therapeutic strategy for neurological conditions.
Area of Science:
- Neuroscience
- Cellular Biology
- Pharmacology
Background:
- Hypoxic/ischemic (HI) injury is a major cause of neurological disability and mortality.
- Current therapeutic options for HI injury are limited, highlighting the need for novel treatments.
- Advances in understanding neuronal insult mechanisms have identified opioid receptors, particularly delta-opioid receptors (DOR), as key players.
Purpose of the Study:
- To investigate the neuroprotective mechanisms of DOR in the context of hypoxic/ischemic brain injury.
- To explore the potential of DOR as a therapeutic target for neurological disorders.
Main Methods:
- Review of recent studies on DOR-mediated neuroprotection.
- Analysis of DOR's role in stabilizing ionic homeostasis, regulating neurotransmitter release, and modulating neuronal signaling.
- Examination of DOR's impact on antioxidant capacity, apoptosis, and pro-survival pathways.
- Investigation of DOR's influence on gene/protein expression and endogenous opioid systems.
Main Results:
- DOR activation confers neuroprotection against HI insults, particularly in the cerebral cortex.
- Mechanisms include maintaining ionic balance, reducing excitotoxicity, and enhancing cellular defense.
- DOR signaling modulates apoptotic and pro-survival pathways, regulates gene expression, and influences endogenous opioid release.
- DOR expression and endogenous opioid release are dynamically regulated by the severity and duration of HI insult.
Conclusions:
- DOR-mediated neuroprotection is a significant finding with potential clinical applications.
- Targeting DOR presents a promising therapeutic avenue for treating neurological damage caused by HI injury.
- Further research into DOR signaling could lead to novel neuroprotective strategies.
Related Concept Videos
Opioid Receptors: Overview
Analgesia and Pain Management
Regulation of Angiogenesis and Blood Supply
Cellular Injury I: Introduction
Cellular Injury IV: Necrosis
Ischemic Stroke ll: Pathophysiology
