Abstract: |
In contrast to the pharmacological studies implicating δ-opioid receptor subtypes, cloning studies have identified only a single cDNA encoding a δ receptor, DOR-1. Antisense studies have established the importance of DOR-1 in δ analgesia in mice. Antisense mapping extends this approach to include oligodeoxynucleotides which are targeted against each of the exons of the gene. Five different antisense oligodeoxynucleotides based upon the three DOR-1 exons all block both spinal and supraspinal analgesic actions of the δ2 ligand [D-Ala2,Glu4]deltorphin, consistent with the suggestion that DOR-1 encodes the δ2 receptor. At the spinal level, [D-Pen2,D-Pen5]enkephalin (DPDPE) also acts through δ2 receptors and all the antisense probes block spinal DPDPE analgesia. However, supraspinally only the two antisense probes targeting exon 3 block DPDPE analgesia. The remaining three antisense probes based upon exons 1 and 2 are inactive. Thus, the δ receptors responsible for spinal and supraspinal DPDPE analgesia can be discriminated at the molecular level by antisense mapping. |
Keywords: |
exons; nonhuman; mouse; animals; mice; animal experiment; dna, antisense; mice, inbred strains; cloning, molecular; gene mapping; nucleotide sequence; oligopeptides; analgesia; antisense mapping; opiate receptor; oligonucleotides, antisense; peptide mapping; deltorphin; receptors, opioid, delta; antisense oligonucleotide; male; priority journal; article; enkephalin derivative; enkephalins; enkephalin, d-penicillamine (2,5)-; δ receptor; δ1; δ2; dor-1
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