Disease relevance of Oprd1

• Whereas an AS ODN probe directed against the KOR3/ORL-1 clone produced small (36%), but significant reductions in 2DG-induced hyperphagia, an AS ODN probe directed against the DOR-1 clone was ineffective [1].
• In contrast to HPC-induced increase in DADLE binding density, prolonged hypoxia caused severe neuronal injury with a significant decrease in DADLE binding density and DOR mRNA level [2].
• Long-term treatment with ethanol increases delta-opioid receptor (DOR) expression in the NG108-15 neuroblastoma x glioma hybrid cell line [3].
• The specific role of the Delta opioid receptor (DOR), in opioid-induced respiratory depression in the ventral respiratory group (VRG) is largely unknown [4].
• These results indicate that DOR in the MPO, particularly in the MPNm, plays an important role in the regulation of lordosis [5].

High impact information on Oprd1

• There is also synergy between DOR or CB1 with ethanol, another addicting agent [6].
• Here we determine the role of dopamine D2 receptors (D2) in PKA signaling responses to delta-opioid (DOR) and cannabinoid (CB1) receptors [6].
• Thirty-five percent of DOR labeling was observed within dendrites and dendritic spines [7].
• In axons and terminals, DOR labeling was distributed along plasma and vesicular membranes [7].
• The shell compartment of the nucleus accumbens (AcbSh) is prominently involved in the rewarding aspects of delta-opioid receptor (DOR) agonists, including one of its putative endogenous ligands, Met5-enkephalin (Enk) [7].

Chemical compound and disease context of Oprd1

• In comparison with delta-opioid receptor (DOR)-induced protection in DIV20 neurons exposed to 72 h of hypoxia, glycine-induced protection was weaker than that of DOR but stronger than that of GABA and taurine [8].
• In this study we examined the effects of the DOR agonist, (+)-4-[(alpha R)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethyl-benzamide (SNC80), on behavioral seizures and hippocampal histopathology in the pilocarpine model of temporal lobe epilepsy [9].
• [D-Pen(2), D-Pen(5)]-enkephalin (DPDPE), a DOR agonist, microinfused into the MPO, 52-54h after EB-priming, inhibited lordosis when compared with the aCSF (vehicle) control (P <== 0.05) [5].

Biological context of Oprd1

• In VGLUT1-positive pyramidal cells, weak DOR but no MOR gene expression was detected [10].
• The deduced amino acid sequence (372 aa) closely resembles the murine delta-opioid receptor, DOR-1 [11].
• In contrast, CAR induced a distinct downregulation in DOR- and KOR-LIs [12].
• After induction of unilateral paw inflammation, mRNA content for DOR remained unchanged, but a bi-phasic upregulation for MOR mRNA with an early peak at 1-2 h and a late increase at 96 h was found in ipsilateral DRG [13].
• The ODN targeting the DOR nucleotide sequence 280 - 299 (aODN280 - 299, exon 2), decreased brain delta-opioid receptor density significantly more than aODNs targeting exon 1 (aODN239 - 258), exon 2 (aODN361 - 380), or exon 3 (aODN741 - 760) (to 52% vs 79, 72, and 68%) [14].

Anatomical context of Oprd1

• More than 90% of the parvalbumin-positive neurons in the hippocampal formation strongly expressed the DOR gene [10].
• Immunohistochemistry for delta-opioid receptor (DOR) was performed on the rat cranial sensory ganglia [15].
• Amplification of RNAs from rat cerebral cortex (positive control) and rat cochlea with MOR, DOR and KOR primers resulted in products of the predicted lengths, 564, 356 and 276 bp, respectively [16].
• The aim of the present study was therefore to identify and localize the mu (MOR), delta (DOR) and kappa (KOR) opioid receptor subtypes within the rat cochlea [16].
• DOR and KOR immunoreactivity was found in inner and outer hair cells, bipolar cells of the spiral ganglion and interdental cells of the limbus [16].

Associations of Oprd1 with chemical compounds

• Expression of high DOR mRNA levels was restricted to GAD-positive neurons in the principal cell layers, oriens layer and hilus [10].
• This was carried out by combining immunocytochemical staining for MOR1, DOR1, and serotonin with fluorescent retrograde tract-tracing [17].
• No changes in the levels of mRNA for DOR were detected after exposure to cocaine in the brain regions examined [18].
• Following microinjection of DAMGO into the PAG, either the highly selective DOR antagonist TIPP[psi] or the DOR2 antagonist naltriben (NTB) was microinjected into the RVM [19].
• Although SH caused a decrease in DOR expression and neuronal injury, HPC induced an increase in DOR mRNA and protein levels and reversed the reduction in levels of the endogenous DOR peptide, leucine enkephalin, normally seen during SH, thus protecting the neurons from SH insult [20].

Regulatory relationships of Oprd1

• The proportion of DRG cell profiles expressing DOR1 mRNA was significantly higher than that expressing MOR1 mRNA (P < 0.0001, chi-square test) [21].

Other interactions of Oprd1

• DOR1 immunostaining patterns revealed primarily a postsynaptic localization of the receptor in pallidal cell bodies adjacent to enkephalin- or synaptophysin-positive fiber terminals [22].
• To examine whether this increase is related to transcription, the mRNA of Delta- (DOR) and mu-opioid receptor (MOR) in lumbar DRG was quantified by real time Light Cycler polymerase chain reaction (LC-PCR), and correlated to ligand binding in DRG and sciatic nerve [13].

Analytical, diagnostic and therapeutic context of Oprd1

• Protein and mRNA levels of DOR were detected by receptor binding and RT-PCR, respectively [2].
• In the present study, we examined the expression of DOR1 and MOR1 mRNAs in PAG neurons projecting to RVM using quantitative in situ hybridization and retrograde tract-tracing [23].
• To specifically address the relative pre- and postsynaptic contribution to spinal opioid analgesia, we have quantitatively assessed the pre- vs. postsynaptic distribution of the mu-opioid (MOR-1, MOP(1)) and delta-opioid receptors (DOR-1, DOP(1)) [24].
• Two immunoreactive bands were seen on Western blots of brainstem lysates for both MOR (50 and 70 kDa) and DOR (30 and 60 kDa) [25].
• We confirmed the changes in expression for the genes encoding the nuclear protein prothymosin(alpha) and the delta-1 opioid receptor (DOR1) by Northern blotting or in situ hybridization [26].

References