RPEP-00020 · 1984Two versions of somatostatin-28 were isolated from anglerfish tissue. Both came from the same gene, but one had a modified amino acid: 5-hydroxylysine at position 23.
Mass spectrometry confirmed the two forms had molecular weights of 3,220 (hydroxylated) and 3,204 (non-hydroxylated). The 16-unit difference matches exactly what adding one oxygen atom would do.
This was the first documented case of a hydroxylated peptide hormone. Before this, hydroxylysine was known almost exclusively from collagen (the protein that gives skin and bones their structure).
Andrews, P C; Hawke, D; Shively, J E; Dixon, J E · In Vitro
RPEP-00026 · 1985The paper argued that certain molecules made by immune cells can send signals directly to the brain. The authors named these 'immunotransmitters,' a new term for molecules that carry information from the immune system to the central nervous system (CNS).
Examples include thymosin alpha 1 and thymosin beta 4 (peptides from the thymus gland), as well as ACTH (a stress hormone), TSH (thyroid hormone), and beta-endorphin (a natural painkiller) produced by lymphocytes (white blood cells).
The review presented evidence that thymosin peptides can alter the hypothalamic-pituitary-adrenal (HPA) axis, which is the brain's master hormone control system. They also appeared to affect the gonadal (reproductive hormone) axis.
Hall, N R; McGillis, J P; Spangelo, B L; Goldstein, A L · Review
RPEP-00045 · 1987A single injection of kainic acid (1 microgram) into rat brains caused seizures lasting 3 to 6 hours. During seizures, hippocampal met-enkephalin dropped 31% and dynorphin A dropped 63%, suggesting these opioid peptides were being released.
By 24 hours, levels returned to normal. By 48 hours, met-enkephalin surged to 270% of normal and dynorphin to 150%. The brain had ramped up production to replace what was used.
The biosynthetic machinery confirmed this: mRNA for preproenkephalin (the genetic template for making enkephalin) jumped to 400% of control at 6 hours. The actual precursor protein followed at 24 hours, reaching 300% of control.
The seizure-induced shaking behavior (wet-dog shakes) was directly linked to enkephalin. Naloxone (an opioid blocker) reduced the shaking. Anti-enkephalin antibodies also reduced it. Injecting enkephalin peptides into the hippocampus mimicked the shaking.
Hong, J S; Grimes, L; Kanamatsu, T; McGinty, J F · Animal Study
RPEP-00050 · 1987Rats drinking 2% salt solution showed progressive increases in three neuropeptide mRNAs in the hypothalamus (a brain region controlling hormones):
Vasopressin, oxytocin, and dynorphin mRNAs all increased in the magnocellular neurons of the supraoptic and paraventricular nuclei. These are the brain cells that make these peptide hormones.
Enkephalin mRNA was not detectable in these brain areas under normal conditions. It only appeared after 12 days of salt loading or after the acute stress of a salt injection into the abdomen.
Lactating mother rats (10 days postpartum) showed a very large increase in oxytocin mRNA, with smaller increases in vasopressin and dynorphin. No enkephalin or CRF (corticotrophin-releasing factor) changes were seen in lactating rats.
Lightman, S L; Young, W S · Animal Study
RPEP-00055 · 1987Delta sleep-inducing peptide (DSIP) administered intravenously at 25 nmol/kg over four nights showed some improvements in sleep metrics in chronic insomniacs — including reduced awakenings, decreased waking time, and increased total sleep time — but these changes were not statistically significant compared to placebo. The only significant increases were in NREM sleep time and stage 2 sleep, but these differences already existed at baseline, undermining the finding. The authors concluded that DSIP's sleep-improving effects are of little clinical significance.
Monti, J M; Debellis, J; Alterwain, P; Pellejero, T; Monti, D · Randomized Controlled Trial
RPEP-00066 · 1988Enterochromaffin (EC) cells are the most abundant hormone-producing cells in the gut. They were known to make serotonin. Whether they also make peptides was debated for years.
Using antibodies against all three families of opioid peptide precursors, researchers tested gut tissue from dogs, guinea pigs, and humans. EC cells contained pro-dynorphin-derived peptides: dynorphin A and alpha-neo-endorphin.
They did not contain pro-opiomelanocortin derivatives (like endorphin) or pro-enkephalin derivatives. Previous reports of enkephalin in EC cells were likely due to antibody cross-reactivity.
The number and staining characteristics of opioid-positive EC cells varied considerably between species and between different segments of the gut, suggesting species-specific processing of the dynorphin precursor.
Cetin, Y · In Vitro
RPEP-00079 · 1988Endogenous opioid peptides inhibit the release of both vasopressin and oxytocin from the posterior pituitary. They also affect anterior pituitary hormones through the hypothalamic portal blood system.
Dynorphin mRNA co-exists in the same neurons as vasopressin. Stimuli that increase vasopressin secretion (like salt loading) also increase dynorphin mRNA accumulation. This parallel regulation strongly suggests dynorphin has a genuine role alongside vasopressin.
Pro-enkephalin A mRNA co-exists with CRF in a different group of hypothalamic cells. Stresses that increase CRF mRNA also increase pro-enkephalin mRNA in the same area.
The co-existence of opioid peptides with established hormones in the same cells, combined with their coordinated regulation, provides powerful evidence that opioids are genuine neuroendocrine regulators, not incidental bystanders.
Lightman, S L · Review
RPEP-00083 · 1988Alpha-helical CRF9-41 (a CRF receptor blocker) applied to hypothalamic slices in vitro caused beta-endorphin and met-enkephalin to drop significantly within 10 minutes. At the same time, LHRH (luteinizing hormone-releasing hormone) rose significantly.
Dynorphin also decreased but the change was not statistically significant.
When the antagonist was removed, the pattern reversed within 10 minutes: beta-endorphin, met-enkephalin, and dynorphin rose back up while LHRH fell back down.
The same results were obtained in vivo using push-pull perfusion of the arcuate-median eminence region in anesthetized rats. This confirmed the in vitro findings in living animals.
Nikolarakis, K E; Almeida, O F; Sirinathsinghji, D J; Herz, A · Animal Study
RPEP-00084 · 1988GABA at concentrations from 10^-8 to 10^-4 M caused a dose-dependent increase in GnRH release from rat hypothalamic slices. The GABA-A receptor agonist isoguvacine replicated this, while the GABA-B agonist baclofen had no effect. The GABA-A antagonist SR95103 blocked the GABA effect.
Blockade of nerve conduction with tetrodotoxin abolished GABA's stimulatory effect, meaning it works through neural circuits, not directly on GnRH cells.
Naloxone (opioid blocker) prevented GABA-induced GnRH release. The CRF antagonist also blocked it. CRF itself decreased GnRH release, and GABA could not reverse this.
GABA stimulated the release of beta-endorphin, dynorphin, and met-enkephalin from the same tissue, connecting opioid peptide release to the control of reproduction.
Nikolarakis, K E; Loeffler, J P; Almeida, O F; Herz, A · In Vitro
RPEP-00088 · 1988Regardless of which nerve was cut (right or left sciatic, both sciatic, right brachial plexus, saphenous, or sural), the same brain-wide pattern emerged.
Beta-endorphin decreased significantly in all brain areas except the striatum. Met-enkephalin increased in all brain areas and in the affected spinal cord segments. Substance P, somatostatin, and dynorphin were unaffected.
The changes appeared within 24 hours of surgery and persisted for at least 4 months, indicating a long-lasting reorganization of the opioid system.
There was no lateralization: unilateral nerve cuts produced bilateral brain changes. This means local nerve damage triggers a global brain response.
Serotonergic drugs normalized beta-endorphin levels, suggesting the serotonin system mediates the opioid changes after nerve injury.
Panerai, A E; Sacerdote, P; Brini, A; Bianchi, M; Mantegazza, P · Animal Study
RPEP-00090 · 1988Intrathecal (spinal cord) met-enkephalin at low doses markedly reduced the aversive behavior caused by intrathecal substance P. At these same low doses, met-enkephalin produced no measurable analgesia in the tail-flick pain test.
Met-enkephalin needed much higher doses to produce general analgesia.
Beta-endorphin and dynorphin-(1-17) were different. They blocked substance P-induced behavior and produced general analgesia at roughly the same doses. There was no separation between the two effects.
This suggests met-enkephalin has a specific, preferential interaction with substance P-mediated pain signaling in the spinal cord, separate from its general painkilling effects.
Sakurada, T; Takahashi, K; Sakurada, S; Kisara, K; Folkesson, R; Terenius, L · Animal Study
RPEP-00093 · 1988Three opioid peptide families showed distinct, non-overlapping distributions in the preoptic brain region.
Beta-endorphin fibers were mainly in the periventricular nucleus. Dynorphin B fibers were more uniformly distributed with few cell bodies. Enkephalin (peptide E) had hundreds of cell bodies, concentrated in specific nuclei.
The key sexual dimorphism: male rats had significantly more enkephalin cells in the anteroventral periventricular nucleus (AVPv) than females. This was despite the AVPv being physically larger in female rats.
This sex difference was at least partially dependent on perinatal gonadal steroids. Early hormone exposure during the critical developmental window permanently organized the number of enkephalin cells, a process called organizational hormone effects.
No sex difference was found in enkephalin cells in the anterodorsal preoptic nucleus, showing the dimorphism was region-specific, not a general property of enkephalin neurons.
Simerly, R B; McCall, L D; Watson, S J · Animal Study
RPEP-00098 · 1988Local neurons within the ganglion contribute more peptide-containing nerve fibers than researchers previously believed. Different peptide types follow distinct pathways.
Webber, R H; Heym, C · Animal Study
RPEP-00103 · 1989Prostatic opioid innervation comes exclusively from proenkephalin-derived peptides. No prodynorphin or pro-opiomelanocortin products were detected in either species.
Aumüller, G; Jungblut, T; Malek, B; Konrad, S; Weihe, E · Cross Sectional
RPEP-00107 · 1989The rat anterior pituitary contains at least six distinct high-molecular-weight intermediates of prodynorphin, and similar forms exist in spinal cord and hypothalamus.
Day, R; Akil, H · Animal Study
RPEP-00108 · 1989AtT-20 pituitary cells contain all the enzymes needed to process prodynorphin correctly, including at rare monobasic cleavage sites. The processed peptides were released in response to CRF stimulation.
Devi, L; Gupta, P; Douglass, J · In Vitro
RPEP-00109 · 1989Holostean fish have enkephalin peptides with a 3:1 met-to-leu ratio and a novel modified met-enkephalin form, but no detectable prodynorphin-derived peptides.
Dores, R M; McDonald, L K; Crim, J W · Animal Study
RPEP-00111 · 1989Prodynorphin and proenkephalin peptides in the superior cervical ganglion respond differently to drugs and denervation, confirming they operate as separate systems with different origins.
Folan, J C; Heym, C · Animal Study
RPEP-00113 · 1989Brain alanyl aminopeptidase's efficiency drops dramatically with opioid peptide chain length. Dynorphin(1-17) acts as a competitive inhibitor rather than a substrate.
Gibson, A M; McDermott, J R; Lauffart, B; Mantle, D · In Vitro
RPEP-00118 · 1989Proenkephalin-derived peptide nerve fibers in human prostate were concentrated in the dorsolateral stroma and decreased in density with age. No prodynorphin or POMC-derived peptides were detected.
Jungblut, T; Aumüller, G; Malek, B; Melchior, H · Cross Sectional
RPEP-00125 · 198942% of enkephalin terminal targets in the blood pressure control region were catecholamine neurons. Some neurons co-contained both enkephalin and tyrosine hydroxylase.
Milner, T A; Pickel, V M; Reis, D J · Animal Study
RPEP-00126 · 1989Three opioid peptides from different families all inhibited TRH release from rat stomach in a dose-dependent manner, reversible by naloxone.
Mitsuma, T; Hirooka, Y; Nakada, K; Nomura, A; Nogimori, T · In Vitro
RPEP-00127 · 1989All three families of opioid peptides inhibited TRH release from rat cecum tissue in a dose-dependent, naloxone-reversible manner.
Mitsuma, T; Hirooka, Y; Nakata, K; Nogimori, T · In Vitro
RPEP-00129 · 1989Prodynorphin peptide distribution differs substantially between hamster and rat in reproduction and emotion-related brain regions, and hamsters may process the precursor protein differently.
Neal, C R; Newman, S W · Animal Study
RPEP-00130 · 1989Endogenous opioid peptide release from hippocampal slices was demonstrated by competitive radioligand displacement. The strongest release occurred in stratum lacunosum moleculare of CA3.
Neumaier, J F; Chavkin, C · In Vitro
RPEP-00133 · 1989Alpha-neoendorphin is the major prodynorphin end product in Xenopus brain. Leu-enkephalin is produced from prodynorphin processing, not from proenkephalin, in this species.
Sei, C A; Richard, R; Dores, R M · Animal Study
RPEP-00135 · 1989A novel endoprotease with high specificity for dynorphin B (Km = 11 µM) was identified in bovine spinal cord. It does not act on other prodynorphin-derived peptides.
Silberring, J; Nyberg, F · In Vitro
RPEP-00136 · 1989Subchronic cocaine selectively increased striatonigral dynorphin through a dopaminergic mechanism requiring both D1 and D2 receptors. Enkephalin and substance P were unaffected.
Sivam, S P · Animal Study
RPEP-00139 · 1989Dynorphin B mossy fiber terminal fields in the hippocampus vary by mouse genotype, with C57BL/6 mice having larger intra- and infrapyramidal projections than DBA/2 mice.
van Daal, J H; Zanderink, H E; Jenks, B G; van Abeelen, J H · Animal Study
RPEP-00145 · 1990Opioid peptides have differential effects on neonatal cerebral vasculature: enkephalins dilate, beta-endorphin constricts, and dynorphin switches depending on blood pressure status. All effects are prostaglandin-dependent.
Armstead, W M; Mirro, R; Busija, D W; Leffler, C W · Animal Study
RPEP-00146 · 1990Full-length dynorphin A (1-17 or 1-13), leumorphin, and alpha-neo-endorphin induced rapid feeding in pigs. Shorter fragments were ineffective. Naloxone blocked all feeding effects.
Baldwin, B A; de la Riva, C; Ebenezer, I S · Animal Study
RPEP-00147 · 1990Aminopeptidase M in human CSF degrades opioid peptides at rates inversely proportional to chain length. Met-enkephalin is degraded ~13x faster than dynorphin A.
Benter, I F; Hirsh, E M; Tuchman, A J; Ward, P E · In Vitro
RPEP-00149 · 1990All three opioid peptide families are present in the guinea pig endocrine pancreas but in different cell types, with processing pathways distinct from other organs.
Cetin, Y · Animal Study
RPEP-00152 · 1990Prodynorphin and proenkephalin genes are expressed in 16-day embryonic rat brain cultures, earlier than previously known. This is the first evidence of early opioid gene expression in the developing nervous system.
Di Scala-Guenot, D; Strosser, M T; Felix, J M; Richard, P · In Vitro
RPEP-00153 · 1990Dynorphin A(1-8) is extensively converted to leu-enkephalin by metalloendopeptidase EC 3.4.24.15 across all brain regions, effectively switching opioid signaling from kappa to delta receptors.
Dixon, D M; Traynor, J R · In Vitro
RPEP-00157 · 1990Endogenous opioid peptides tonically inhibit dopamine release from both pituitary regions. Opioid peptides show differential potency between the two regions, suggesting different receptor distributions.
Garris, P A; Ben-Jonathan, N · In Vitro
RPEP-00159 · 1990Enkephalin, beta-endorphin, and dynorphin are not growth factors for ventral spinal cord neurons. They did not affect neurite extension or glial cell proliferation in embryonic cultures.
Iwasaki, Y; Kinoshita, M; Ikeda, K; Shiojima, T · In Vitro
RPEP-00160 · 1990Opioid peptides selectively inhibit non-cholinergic excitatory neurotransmission in airways via prejunctional receptors, with dynorphin being the most potent endogenous peptide.
Kamikawa, Y; Shimo, Y · In Vitro
RPEP-00168 · 1990Prodynorphin processing matures much faster in the substantia nigra (day 7) than the pituitary (day 21). Late-developing conversion of dynorphin products to leu-enkephalin changes the enkephalin ratio in adults.
Sei, C A; Dores, R M · Animal Study
RPEP-00169 · 1990The marginal division of the striatum has higher densities of zinc, dynorphin B-immunoreactive terminals, and substance P-immunoreactive terminals compared to the rest of the striatum.
Shu, S Y; McGinty, J F; Peterson, G M · Animal Study
RPEP-00170 · 1990Mu and delta opioids increase, while kappa opioids decrease, dopamine release in the nucleus accumbens. This differential modulation explains their opposing motivational effects.
Spanagel, R; Herz, A; Shippenberg, T S · Animal Study
RPEP-00171 · 1990All submucous neurons in guinea pig ileum are immunoreactive for prodynorphin peptides. Multiple distinct populations of opioid neurons with different neurochemical codes project to secretory pathways.
Steele, P A; Costa, M · Animal Study
RPEP-00174 · 1990Spinal dynorphin A raises blood pressure through kappa opioid receptors independently from vasopressin. Chain length of at least 13 amino acids is required for the cardiovascular effect.
Thornhill, J A; Pittman, Q J · Animal Study
RPEP-00175 · 1990Both amphetamine (dopamine agonist) and haloperidol (dopamine antagonist) significantly altered levels of prodynorphin peptides in the striatum, substantia nigra, and hippocampus.
Trujillo, K A; Day, R; Akil, H · Animal Study
RPEP-00177 · 1990Physiological-like high-frequency stimulation of opioid-containing pathways releases detectable amounts of endogenous opioids in hippocampal slices. The release is pathway-specific and frequency-dependent.
Wagner, J J; Caudle, R M; Neumaier, J F; Chavkin, C · In Vitro
RPEP-00178 · 1990Glucocorticoids regulate hypothalamic VIP expression and prolactin secretion but do not affect beta-endorphin, dynorphin A, or met-enkephalin immunostaining in the hypothalamus.
Watanobe, H · Animal Study
RPEP-00179 · 1990Apocarboxypeptidase B-Sepharose selectively adsorbs opioid peptides with C-terminal basic residues, providing a novel separation tool for peptide processing research.
Yasuhara, T; Ohashi, A · In Vitro
RPEP-00180 · 1991Acute central opioid pretreatment produces rapid sensitization to naltrexone, predominantly through mu receptors. This represents an early stage of physical dependence occurring within hours.
Adams, J U; Holtzman, S G · Animal Study
RPEP-00182 · 1991Hemorrhagic hypotension raised brain fluid opioid levels and caused pial artery dilation in newborn pigs. Blood pressure dropped from 63 to 33 mmHg.
Armstead, W M; Mirro, R; Busija, D W; Desiderio, D M; Leffler, C W · Animal Study
RPEP-00184 · 1991Cerebrospinal fluid MERGL levels were significantly low in Parkinson's patients after overnight medication withdrawal. Steady-state levodopa infusion did not restore them.
Baronti, F; Conant, K E; Giuffra, M; Davis, T L; Brughitta, G; Iadarola, M J; Berrettini, W H; Chase, T N; Mouradian, M M · Cross Sectional