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PDYN
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Proenkephalin-B precursor (Beta-neoendorphin-dynorphin) (Preprodynorphin) [Contains: Alpha-neoendorphin; Beta-neoendorphin; Big dynorphin (Big Dyn); Dynorphin A(1-17) (Dyn-A17) (Dynorphin A); Dynorphin A(1-13); Dynorphin A(1-8); Leu-enkephalin; Rimorphin (Dynorphin B) (Dyn-B) (Dynorphin B(1-13)); Leumorphin (Dynorphin B-29)] ==Publications== {{medline-entry |title=Influence of age and 17beta-estradiol on kisspeptin, neurokinin B, and prodynorphin gene expression in the arcuate-median eminence of female rhesus macaques. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20519367 |abstract=The neuropeptides kisspeptin, neurokinin B, and dynorphin A (collectively abbreviated as KNDy) are, respectively, encoded by KiSS-1, NKB, and [[PDYN]] and are coexpressed by neurons of the hypothalamic arcuate nucleus ([[ARC]]). Here, using quantitative real-time PCR, we examined age-related changes in the expression of genes encoding KNDy and associated receptors G protein-coupled receptor 54 (encoded by GPR54), neurokinin 3 receptor (encoded by NK3), and kappa-opioid receptor (encoded by KOR), in the female rhesus macaque [[ARC]]-median eminence ([[ARC]]-ME). Expression of KiSS-1 and NKB was highly elevated in old perimenopausal compared with young or middle-aged premenopausal animals. To test whether these age-related changes could be attributed to perimenopausal loss of sex steroids, we then examined KNDy, GPR54, NK3, and KOR expression changes in response to ovariectomy (OVX) and exposure to 17beta-estradiol (E(2)). Short-term (7 months) OVX (with or without 1 month of estrogen replacement) failed to modulate the expression of any of the KNDy-related genes. In contrast, long-term ( approximately 4 yr) OVX significantly increased KiSS-1 and NKB expression, and this was reversed by E(2) administration. Finally, we examined the expression of KNDy-related genes in young adult females during the early follicular, late follicular, or midluteal phases of their menstrual cycle but found no difference. Together, the results suggest that short-term alterations in circulating E(2) levels, such as those occurring during the menstrual cycle, may have little effect on the [[ARC]]-ME expression of KNDy and associated receptors. Nevertheless, they clearly demonstrate that loss of ovarian steroid negative feedback that occurs during perimenopause plays a major role in modulating the activity of KNDy circuits of the aging primate [[ARC]]-ME. |mesh-terms=* Age Factors * Aging * Animals * Arcuate Nucleus of Hypothalamus * Enkephalins * Estradiol * Female * Gene Expression * Genes, Tumor Suppressor * Macaca mulatta * Median Eminence * Neurokinin B * Ovariectomy * Protein Precursors * Receptors, G-Protein-Coupled * Time Factors |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940528 }} {{medline-entry |title=Proenkephalin and prodynorphin mRNA level in brain of rats with absence epilepsy. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/7898641 |abstract=An in situ hybridization method was used to estimate the proenkephalin ([[PENK]]) and prodynorphin ([[PDYN]]) mRNA levels in the brain of epileptic 6-month-old WAG/Rij rats in comparison with non-epileptic: 3-month-old WAG/Rij rats, 3-month-old ACI rats and 6-month-old ACI rats. The epileptic rats had a significantly higher level of [[PENK]] mRNA in the striatum as compared to non-epileptic controls. The [[PDYN]] mRNA level was significantly elevated only in the hippocampus of epileptic rats, whereas age- or strain-related changes in the striatal and cortical [[PDYN]] mRNA levels were found in both epileptic and non-epileptic rats. The changes in the biosynthetic activity of endogenous opioid peptide systems may be important for the occurrence of epileptic discharges in these animals. |mesh-terms=* Aging * Animals * Brain * Cerebral Cortex * Corpus Striatum * Enkephalins * Epilepsy, Absence * Hippocampus * In Situ Hybridization * Male * Protein Precursors * RNA, Messenger * Rats |full-text-url=https://sci-hub.do/10.1016/0143-4179(94)90060-4 }}
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