RPEP-00073 · 1988In rabbit ear and saphenous (leg) arteries, both delta-selective opioid agonists (leu-enkephalin and met-enkephalin) and kappa-selective agonists (dynorphin-(1-13) and ethylketocyclazocine) inhibited nerve-stimulation-evoked contractions.
Delta agonists showed a vessel-specific difference: their maximum inhibitory effect was significantly less in the saphenous artery than in the ear artery. Kappa agonists worked similarly in both vessels.
Yohimbine (an alpha-2 adrenergic blocker) did not enhance opioid inhibitory effects at any stimulation frequency in either vessel. This disproved the hypothesis that opioid receptors work by boosting alpha-2 receptor inhibition of noradrenaline release.
Gan, E A; Duckles, S P · In Vitro
RPEP-00074 · 1988The mu-selective opioid agonist DAGO (Tyr-D-Ala-Gly-(Me)Phe-Gly-ol) increased food intake when injected into the central nucleus of the amygdala at doses of 1 and 3 nanomoles.
Neither DSLET (a delta-selective agonist) nor dynorphin A (a kappa-selective agonist) affected food intake at the same location, even at the highest dose of 3 nanomoles.
Dynorphin A did increase food intake when injected into the medial hypothalamus at 2 nanomoles. This shows that different brain regions use different opioid receptor types to control eating.
Bilateral injections of DAGO were no more effective than unilateral injections. Naloxone and the long-acting antagonist beta-chlornaltrexamine both blocked DAGO's feeding effect, confirming opioid receptor involvement.
Gosnell, B A · Animal Study
RPEP-00075 · 1988Six opioid-related substances were tested on isolated rat adipocytes (fat cells):
- Beta-endorphin, dynorphin, met-enkephalin, leu-enkephalin, and morphine (agonists)
- Naloxone (antagonist)
None altered insulin binding to fat cells. None changed 2-deoxy-glucose uptake (a measure of sugar absorption). None affected glucose incorporation into lipids (fat production). None showed lipolytic (fat-breaking) activity.
The conclusion: endogenous opioids do not directly affect fat cell metabolism. The glucose problems seen with opioid drugs must happen through other mechanisms, likely in the brain, liver, or pancreas.
Hauner, H; Glatting, G; Ditschuneit, H H; Pfeiffer, E F · In Vitro
RPEP-00076 · 1988After seizures (from electroshock, kainic acid, or kindling), both dynorphin and enkephalin initially decrease in the hippocampus, indicating release. But their recovery patterns differ dramatically.
Enkephalin shows a rapid, sustained rebound above normal levels after all three seizure types. Dynorphin shows a large, sustained decrease after electroshock and kindling, with slow recovery.
Mu-opioid receptor antagonists shortened the kindling process (where repeated mild stimulation eventually produces seizures). This strongly suggests brain opioid peptides are involved in how seizure susceptibility develops.
Enkephalin in the hippocampus appears to mediate wet-dog shakes (a specific seizure behavior seen in rodents), connecting it to the opioid withdrawal syndrome.
Hong, J S; McGinty, J F; Grimes, L; Kanamatsu, T; Obie, J; Mitchell, C L · Review
RPEP-00077 · 1988Cortisol at 25 mg/kg given 24 hours before testing decreased prolactin release triggered by all four opioid peptides (dynorphin, beta-endorphin, met-enkephalin, D-Met-Pro-enkephalinamide) injected into the brain.
Actinomycin D pretreatment blocked cortisol's inhibitory effect. This means cortisol works by triggering new protein synthesis, not by directly blocking opioid receptors.
In adrenalectomized (no adrenal glands) rats, cortisol's inhibitory effect was even stronger. Maximum inhibition was reached at only 5 mg/kg, lower than the 25 mg/kg used in intact rats.
Cortisol did not affect opioid-induced corticosterone release. This selectivity means cortisol specifically targets the prolactin pathway, not all opioid effects.
Kiem, D T; Kanyicska, B; Stark, E; Fekete, M I · Animal Study
RPEP-00078 · 1988A commercially purchased synthetic dynorphin A-(1-13) raised cytosolic calcium in rat pituitary cells. However, this effect was NOT caused by dynorphin itself.
When the same preparation was purified by HPLC, the calcium-raising effect disappeared. HPLC combined with LHRH radioimmunoassay revealed contamination with a LHRH-like compound (luteinizing hormone-releasing hormone).
The LHRH antagonist blocked the calcium effect, confirming the contamination. Pure dynorphin A-(1-13), dynorphin A-(2-13), leu-enkephalin, beta-endorphin, morphine, and U50,488H all had zero effect on pituitary calcium.
LHRH itself raised calcium by about 50 nM, which was blocked by the LHRH antagonist.
Knepel, W; Schöfl, C; Wesemeyer, G; Götz, D M · 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-00080 · 1988GHK-Cu stimulated collagen synthesis in fibroblast cell cultures. The effect began at concentrations between 10 picomolar (10^-12 M) and 100 picomolar (10^-11 M), an extraordinarily low threshold.
The stimulation maximized at 1 nanomolar (10^-9 M). Above this concentration, the effect plateaued.
The collagen increase was independent of cell number changes. GHK-Cu was not simply making more cells; it was making existing cells produce more collagen.
A GHK tripeptide sequence (glycine-histidine-lysine) exists naturally within the alpha 2(I) chain of type I collagen. The authors proposed that when wounds break down collagen, proteases could release GHK fragments. These fragments would then bind copper and stimulate new collagen production at the wound site, creating a self-healing feedback loop.
Maquart, F X; Pickart, L; Laurent, M; Gillery, P; Monboisse, J C; Borel, J P · In Vitro
RPEP-00081 · 1988Within 24 hours of inflammation, dynorphin increased specifically in the ipsilateral (same-side) dorsal horn of the spinal cord. Met-enkephalin, leu-enkephalin, and opioid receptor densities did not change.
The inflamed paw showed pronounced supersensitivity to morphine's painkilling effect against pressure pain, starting at 24 hours and increasing at 1 week.
Opioid antagonists (naloxone and the kappa-preferring MR 2266) made the pain worse, suggesting endogenous opioids were already partially controlling the pain.
By 3-5 weeks, inflammation had spread to the opposite paw. Dynorphin was now elevated bilaterally and in the cervico-thoracic cord. Met-enkephalin and leu-enkephalin also rose bilaterally. Adrenal glands were enlarged and plasma beta-endorphin was elevated, signs of chronic stress.
No changes in mu, delta, or kappa receptor density were found at any time point.
Millan, M J; Członkowski, A; Morris, B; Stein, C; Arendt, R; Huber, A; Höllt, V; Herz, A · Animal Study
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-00085 · 1988DADLE (D-Ala2-D-Leu5 enkephalin), a delta-opioid receptor agonist, at 1.50 mg/kg/day induced summer hibernation comparable to that caused by natural Hibernation Induction Trigger (HIT).
Morphine (1.50 mg/kg/day), morphiceptin (0.82 mg/kg/day), and dynorphin A (0.82 mg/kg/day) did not induce hibernation.
Strikingly, morphine, morphiceptin, and dynorphin A actually antagonized HIT-induced hibernation. They blocked the natural hibernation signal.
This suggests delta-opioid receptors promote hibernation while mu and kappa opioid receptors promote the arousal (waking) state. Natural hibernation may involve a shift in the balance between these receptor systems.
Oeltgen, P R; Nilekani, S P; Nuchols, P A; Spurrier, W A; Su, T P · Animal Study
RPEP-00086 · 1988Naloxone (100 to 1000 micrograms/kg) did not affect the initial stomach response to vagus nerve stimulation. But it dose-dependently enhanced the delayed response (from vagal afferent fibers). This means endogenous opioids normally restrain the delayed stomach excitation.
Met-enkephalin was markedly more potent than the mu-agonist DAGO and the kappa-agonist dynorphin A(1-13) at inhibiting both types of vagal stomach responses.
The delta-selective agonist DPDPE mimicked met-enkephalin's inhibitory effects. The delta-selective antagonist ICI 174,864 blocked DPDPE's effects. This confirmed delta-opioid receptors mediate the gastric inhibition.
The conclusion: natural opioid peptides (likely enkephalins) tonically restrain vagus nerve-driven stomach excitation through delta receptors.
Okamoto, T; Kurahashi, K; Fujiwara, M · Animal Study
RPEP-00087 · 1988Met-enkephalin, leu-enkephalin, dynorphin (1-13), DSLET (delta agonist), and DAGO (mu agonist) were tested on human NK cells from healthy donors after 18-hour incubation.
The results were bidirectional: populations with low baseline NK activity showed enhancement. Populations with high baseline NK activity showed suppression. This immunoregulatory pattern was consistent across different opioid peptides.
The effect was confirmed in a serum-free system with recombinant interferon-alpha, ruling out serum-factor interference.
Naloxone displayed both antagonist properties (blocking opioid effects) and direct immunomodulatory effects. This suggested lymphocytes themselves may produce opioid peptides in culture, creating an autocrine signaling loop.
Oleson, D R; Johnson, D R · 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-00089 · 1988DBA mice had higher baseline pain thresholds than C57 mice. But C57 mice showed much greater stress-induced analgesia (pain relief from stress).
The opioid systems differed genetically: DBA mice had significantly more dynorphin in the hypothalamus and neurointermediate pituitary. C57 mice had lower KD values (better affinity) for spinal mu receptors but higher KD (lower affinity) for cerebral kappa receptors.
Under stress, the two strains activated different opioid systems. C57 mice: beta-endorphin decreased in hypothalamus and increased in neurointermediate pituitary lobe. DBA mice: dynorphin decreased in hypothalamus and beta-endorphin increased in the anterior pituitary.
Both strains showed spinal cord dynorphin decreases under stress.
Przewłocka, B; Vetulani, J; Lasoń, W; Dziedzicka, M; Silberring, J; Castellano, C; Przewłocki, R · 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-00091 · 1988Radioactive beta-endorphin injected intravenously accumulated specifically in the lung and liver but not other tissues. Four lines of evidence confirmed this was specific receptor binding, not passive trapping.
First, adding excess unlabeled beta-endorphin reduced the labeled peptide in lung and liver.
Second, injecting unlabeled beta-endorphin via the femoral vein (which passes through the lungs first) rapidly increased blood levels of the pre-injected labeled peptide, displacing it from lung binding sites. Injection via the carotid artery (bypassing the lungs) did not have this effect.
Third, immunoreactive labeled peptide that had lost its receptor-binding ability did not accumulate in lung or liver.
Fourth, dynorphin (1-13) and ethylketocyclazocine (kappa agonist) displaced beta-endorphin from these sites, but DADLE (delta agonist) and naloxone (mu antagonist) did not. This pharmacological profile indicates kappa-type binding sites.
Sato, H; Sugiyama, Y; Sawada, Y; Iga, T; Hanano, M · Animal Study
RPEP-00092 · 1988Three opioid peptides caused dose-dependent contraction of isolated gallbladder muscle cells: met-enkephalin > dynorphin(1-13) > leu-enkephalin.
The contractions were blocked by the opioid antagonists naloxone and MR2266 but not by muscarinic, CCK/gastrin, or tachykinin antagonists. This confirmed the response was specifically through opioid receptors.
Differential sensitivity to preferential antagonists of mu (naloxone) and kappa (MR2266) receptors, combined with the different potencies of the three agonists, indicated the presence of mu, delta, and kappa opioid receptors on the gallbladder muscle cells.
These opioid peptides are known to be present in myenteric neurons of the gut, providing the natural source of opioid signals for gallbladder muscle.
Severi, C; Grider, J R; Makhlouf, G M · In Vitro
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-00094 · 1988Leu-enkephalin and leu-enkephalinamide inhibited electrical self-stimulation in the substantia nigra/ventral tegmental area (SN-VTA) but not the medial forebrain bundle/lateral hypothalamus (MFB-LH). However, injection into MFB-LH facilitated self-stimulation of the distant SN-VTA.
Ala-leu-enkephalin injected into SN-VTA actually facilitated its self-stimulation (opposite to leu-enkephalin). The same peptide in MFB-LH facilitated SN-VTA stimulation like the other enkephalins.
Dynorphin A(1-13) injected into SN-VTA facilitated its self-stimulation. Injection into MFB-LH had no effect.
Met-enkephalin had no direct or indirect effects in either region.
These differences likely reflect different receptor preferences in the SN-VTA neural organization.
Singh, J; Desiraju, T · Animal Study
RPEP-00095 · 1988Dynorphin A produced dose-related, naloxone-reversible analgesia via intracerebroventricular injection, confirming its function as an endogenous opioid painkiller acting through kappa receptors.
Tiseo, P J; Geller, E B; Adler, M W · Animal Study
RPEP-00096 · 1988CSF from rats that had just experienced an electroshock seizure significantly raised seizure thresholds in recipient rats when injected into their brain ventricles.
This anticonvulsant activity was blocked by high-dose naloxone and by the selective delta-opioid antagonist ICI 174,864. This identified delta-opioid receptors as the mediators.
The active substance was destroyed by heat (90°C) and by trypsin (a protein-digesting enzyme), confirming it is a peptide. It passed through 10,000 dalton membranes but not 5,000 dalton membranes, putting its size between 5,000-10,000 daltons.
Post-seizure CSF had increased beta-endorphin (31 amino acids, ~3,500 daltons) but not dynorphin A, leu-enkephalin, or met-enkephalin. However, hidden met-enkephalin sequences (released by trypsin digestion of larger peptides) were found.
The size (5,000-10,000 Da) and delta-receptor specificity do not match any known opioid peptide, suggesting an undiscovered anticonvulsant opioid peptide.
Tortella, F C; Long, J B · Animal Study
RPEP-00097 · 1988Cold swim stress caused opposite changes in opioid peptide levels depending on the body region. Beta-endorphin dropped in the pituitary but surged in blood plasma by over 3-fold.
Vaswani, K K; Richard, C W; Tejwani, G A · 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-00099 · 1988Chronic arthritis triggered spinal cord neurons to produce peptides from two different opioid precursor families in the same cells. All proenkephalin-positive cells also contained prodynorphin peptides.
Weihe, E; Millan, M J; Leibold, A; Nohr, D; Herz, A · Animal Study
RPEP-00100 · 1988Amniotic fluid thymosin alpha 1 levels were remarkably higher than newborn serum levels and increased in a logarithmic pattern with fetal age (r = 0.838).
Welch, R A; Lee, H H; Sokol, R J; Mutchnick, M G · Cross Sectional
RPEP-00102 · 1989Beta-endorphin had a dose-dependent biphasic effect on insulin secretion. Low doses inhibited and high doses stimulated insulin release. Met-enkephalin only inhibited. Dynorphin A had no effect.
Ahrén, B · 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-00104 · 1989The opioidergic system (beta-endorphin, enkephalin, dynorphin) is involved in both the pharmacological actions of alcohol and the craving/genetic predisposition toward alcohol abuse.
Blum, K; Briggs, A H; Trachtenberg, M C · Review
RPEP-00105 · 1989The cecropin A(1-13)-melittin(1-13) hybrid was 100-fold more active against S. aureus and 10-fold more antimalarial than parent peptides, with no toxicity to red blood cells.
Boman, H G; Wade, D; Boman, I A; Wåhlin, B; Merrifield, R B · In Vitro
RPEP-00106 · 1989Stress-induced analgesia in slugs appears mediated by endogenous opioid peptides, particularly enkephalins and beta-endorphin. The opioid pain system is evolutionarily ancient.
Dalton, L M; Widdowson, P S · Animal Study
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-00110 · 1989Pain modulation involves three opioid peptide families plus serotonin and norepinephrine. Different drug classes target different parts of this system.
Dubner, R; Hargreaves, K M · Review
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-00112 · 1989Ethanol modifies the biosynthesis, post-translational processing, and release of all three opioid peptide families differently depending on acute versus chronic exposure.
Gianoulakis, C · Review
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-00114 · 1989Electroacupuncture increased measurable opioid activity in spinal fluid, including beta-endorphin (80% of patients) and dynorphin (60% of patients), plus an unidentified opioid substance.
Ho, W K; Wen, H L · Cross Sectional
RPEP-00115 · 1989Rhinovirus infection triggered significant increases in thymosin alpha 1 (p < 0.001), thymosin beta 4 (p < 0.001), and multiple immune cell types by day 5 after inoculation.
Hsia, J; Sztein, M B; Naylor, P H; Simon, G L; Goldstein, A L; Hayden, F G · RCT
RPEP-00116 · 1989TF5 stimulated IL-1 alpha (not IL-1 beta) production from monocytes. The active component was a novel basic peptide, not thymosin alpha 1.
Hu, S K; Badamchian, M; Mitcho, Y L; Goldstein, A L · 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-00119 · 1989Lidocaine increased plasma beta-endorphin equally in patients and controls, but pain relief in diabetic neuropathy was not correlated with beta-endorphin changes.
Kastrup, J; Bach, F W; Petersen, P; Dejgård, A; Ekman, R; Jensen, S; Angelo, H · Cross Sectional
RPEP-00120 · 1989Genetically obese mice showed massive increases in opioid peptide levels and shifts in receptor types, with kappa receptors up 2.7-fold and mu receptors down 40%.
Khawaja, X Z; Bailey, C J; Green, I C · Animal Study
RPEP-00121 · 1989Cytolytic peptides from diverse species converge on a common structural motif: a cationic site flanked by a hydrophobic surface. This motif is necessary and sufficient for membrane-disrupting activity.
Kini, R M; Evans, H J · Review
RPEP-00122 · 1989In a 4-site binding model, both beta-endorphin and dynorphin peptides preferred mu and delta sites, with dynorphin additionally interacting significantly with kappa sites.
Landahl, H D; Garzon, J; Lee, N M · In Vitro
RPEP-00123 · 1989Beta-endorphin and dynorphin replicated melatonin's immunoenhancing and anti-stress effects, but with complementary roles: beta-endorphin for normal conditions, dynorphin for stress states. Effects were circadian and opioid-receptor-mediated.
Maestroni, G J; Conti, A · Animal Study
RPEP-00124 · 1989Milk proteins contain encrypted bioactive peptide sequences that are released during digestion, including opioid-like casomorphins, mineral-binding phosphopeptides, and immunostimulating peptides.
Meisel, H; Frister, H; Schlimme, E · Review
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