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1 f the proNKB neurons were immunoreactive for prodynorphin.
2 evated GluR2 was accompanied by decreases in prodynorphin.
3 as c-fos, fos-related antigen-2 (fra-2), and prodynorphin.
4 s the opioid neuropeptide precursor protein, prodynorphin.
5 icotropin-releasing hormone, vasopressin, or prodynorphin.
6 in neural and cardiac tissues and represses prodynorphin and c-fos gene expression by binding to DNA
11 intake of the CHO diet resulted in levels of proDynorphin and Dynorphin A1-17 that were similar in th
15 duced phospho-ERK primarily colocalized with prodynorphin and NK-1 in superficial dorsal horn neurons
17 ding to DNA to activate the transcription of prodynorphin and other downstream genes in pain control.
19 ofluorescence to explore the distribution of prodynorphin and proNKB immunoreactivity in the rat hypo
20 alamic projections of fibers expressing both prodynorphin and proNKB provide evidence that these neur
21 othalamus where neuronal somata coexpressing prodynorphin and proNKB-immunoreactivity were identified
23 localized in some puncta and fibers, but the prodynorphin antibody additionally labeled cell bodies.
24 n volunteers bearing the (T) allele of PDYN (prodynorphin) at rs1997794 showed reduced fear extinctio
25 date genes revealed by our screening, namely prodynorphin, BDNF, and MHC class I molecules, to the fa
27 o study the basal and evoked release of this prodynorphin derived peptide in the spinal cord of ureth
28 NL induced a sustained release of endogenous prodynorphin-derived opioid peptides that activated an a
30 igators to contain perikarya that synthesize prodynorphin-derived peptides, except the pedunculoponti
31 LID, including overexpression of DeltaFosB, prodynorphin, dynorphin A, cyclin-dependent kinase 5, an
33 3 (SCA23) is caused by missense mutations in prodynorphin, encoding the precursor protein for the opi
34 s in the brain associated with inhibition of prodynorphin-expressing (Pdyn-expressing) and of proenke
36 onsistent with this result, mice lacking the prodynorphin gene did not show a stress-induced potentia
37 s have demonstrated that stress may increase prodynorphin gene expression, and kappa opioid agonists
38 esis, transgenic mice possessing a disrupted prodynorphin gene showed no increase in immobility or st
42 ts with an ShA history showed an increase in prodynorphin immunoreactivity in both the nucleus accumb
44 calized with and decreased the expression of prodynorphin in nucleus accumbens medium spiny neurons,
45 al increases expression of pCREB, c-Fos, and prodynorphin in the superficial dorsal horn, changes tha
46 dditionally, we investigated whether arcuate prodynorphin-ir (immunoreactive) neurons expressed the n
54 o true: 96% of neurons in the LHA containing prodynorphin mRNA also expressed prepro-orexin mRNA.
55 loss of the orexin neurons completely lacked prodynorphin mRNA in this area, further confirming that
57 O, ad libitum intake of Fat/Sucrose elevated proDynorphin mRNA levels in the arcuate and Dynorphin A1
58 real-time PCR was used to show that KOR and prodynorphin mRNA levels were decreased in the NAc, wher
59 ce and orexin knock-out mice showed abundant prodynorphin mRNA-expressing neurons in the LHA, but ore
62 in neurons are activated by fasting and that prodynorphin neurons restrain food intake during schedul
67 id were also examined on mRNA expression for prodynorphin (PDYN) and kappa-opioid receptors (KORs) in
71 the relationship of genetic variants of the prodynorphin (PDYN) gene, which is enriched in the stria
73 strated significant increases in whole brain prodynorphin (Pdyn) mRNA in WSP mice only during EtOH wi
76 alized with a subset of preproenkephalin and prodynorphin positive spiny neurons within the dorsomedi
80 ad libitum intake resulted in mRNA levels of proDynorphin, proEnkephalin and POMC, and Dynorphin A1-1
81 on of the same diet decreases mRNA levels of proDynorphin, proEnkephalin and POMC, as well as levels
82 f neuropeptides including those derived from prodynorphin, proenkephalin, proSAAS, and amyloid precur
85 and proopiomelanocortin, proenkephalin, and prodynorphin transcript levels in cortex, hippocampus, a
87 ere was some colocalization of dynorphin and prodynorphin with CGRP and substance P, but not with iso
88 here was no co-localization of dynorphin (or prodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin
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