Sensitivity of T-Lymphocytes to Hormones of the Anterior Pituitary Gland.

The review provides information about the features of the sensitivity of thymocytes, lymphoid organs' cells and T-lymphocytes of peripheral blood to the hormones secreted by anterior pituitary gland's cells: growth hormone, thyrotropin, adrenocorticotropic hormone, prolactin and ß-endorphin. Some aspects of the T-lymphocytes's response to humoral signals from the hypophysis are shown in the article. Also the pituitary hormones' role in the regulation of proliferation, differentiation, and cytokine production of T-lymphocytes in normal and pathological conditions of the organism being discussed.

[Dynamics of pain tolerance thresholds and humoral immunity factors at dorsalgy].

OBJECTIVE: Our aim was to study the possible markers of pain syndrome--indicators of pain sensitivity--pain pressure tolerance thresholds (PPTT), and immuno-indicators--natural antibodies against pain processing mediators (eAb) for evaluation the possibility of its using for a objective pain assessment at chronic low back pain. METHODS: Pain sensitivity was assessed daily and nightly, by measuring the PPTT The natural antibody levels (eAb), were determined in serum by ELISA. Measurement of all parameters were performed at 1st, 10th and 21 days. RESULTS: 173 patients (93 women and 80 men) with chronic low back pain were included in the study. At 1st day most patients had lowered PPTT: 55% of men and 74% during the day, 72% of men and 89% of women at night. Dynamic study has shown a tendency of PPTT normalization in men. The study of diurnal PPTT variations have shown that night PPTT lower than day PPTT on 15-17%. We found gender PPTT differences: PPTT values in women 17-26% lower than in men. Analysis of individual eAb profiles has showed that elevated and high levels of eAb to ß-endorphin, orphanin and histamine have 84%, 78%, 84% women and 82%, 85 and 95% men, respectively. These indicators higher than those for serotonin, dopamine and angiotensin (55%, 65%, 70% in women and 65%, 66%, 66% in men, respectively; p < 0.05). Dynamic study of eAb levels have shown a significant anti-histamine eAbs decrease (23%; p = 0.015) only. CONCLUSION: The pathological changes in pain sensitivity and levels of eAbs to pain-processing mediatos are evidenced. Further investigations are necessary to clarify to role of these variations in pain processing and for use these indicators for objective pain assessment.

Endogenous µ-opioid peptides modulate immune response towards malignant melanoma.

Opioids exert major effects not only in the central nervous system but also in immune responses. We investigated the effects of µ-opioid peptides, secreted by tumor cells, on anti-tumor immune responses. For this purpose, tumor growth was studied in wild-type and µ-opioid receptor-deficient (MOR-/-) mice injected with B16 melanoma cells. The ability of these cells to produce opioids was studied by Western blots in vitro. Finally, biopsy material from human melanomas was investigated by immunohistochemistry for ß endorphin expression. Injection of B16 melanoma cells, producing endogenous ß endorphin, in the flank of MOR-/- mice revealed a profound reduction in tumor growth, paralleled by a significantly higher infiltration of immune cells into the tumors, when compared to tumor growth after injection of B16 melanoma cells into wild-type mice. Opioids present in B16 cell supernatant significantly reduced the proliferation of normal but not MOR-/- leucocytes. Immunohistochemical analyses of biopsies from human melanoma tissues showed a positive correlation between expression of ß endorphin and tumor progression. Our data provide evidence that µ-opioid peptides may play a major role in cancer progression by modulating immune response. This finding may have implications for the future optimization of immunointerventions for cancer.

Detection of a novel immunoreactive endomorphin 2-like peptide in rat brain extracts.

To pursue further the possible de novo biosynthetic pathway of endomorphins in rat brain we raised antibodies to endomorphin-2 conjugate in rabbits. Antiserum R1 recognized endomorphin-2 with good selectivity as compared to endomorphin-1 with a median detection value of 65.5+/-7.5 pg/tube (n=7), whereas R4 antiserum recognized both endomorphins with similar sensitivity. Neither antisera recognized YP-related di- or tripeptides or YGGF-related opioid sequences (enkephalins, beta-endorphin, dynorphin). Using the same rat brain extraction-RP-HPLC-gradient separation paradigm as previously, antisera detected 144.6+/-40.0 (n=3) pg/g wet brain weight endomorphin-2-like immunoreactivity in the fraction corresponding to standard endomorphin-2 retention time and also in the fraction matching endomorphin-2-OH standard retention time (179.1+/-30.1 pg/g). Since R1 failed to recognize authentic endomorphin-2-OH, the second immunoreactive species must be different from both endomorphin-2 and endomorphin-2-OH. Possible biosynthetic intermediates to endomorphins, synthetic YPFFG and YPWFG had retention times close to the parent endomorphin standards in RP-HPLC gradient separation profile. The former was a mu-opioid receptor agonist of medium potency in the in vitro assays (rat brain RBA>P gamma S binding and mouse vas deferens), whereas the latter was a weak mu-opioid receptor agonist with a significant delta-opioid receptorial action as well and a definite indication of partial agonism.

Increase of plasmatic beta-endorphin immunoreactive material in children in the perioperative period: the influence of the site of surgery.

BACKGROUND: The primary aim of the study was to confirm the increase of plasmatic IR beta-endorphin material during the perioperative period in children. The second was to search for the factors responsible for this increment. METHODS: Seventy-two consecutive children undergoing a surgical procedure were recruited. Pre-anaesthesia and anaesthesia were standardised. Plasmatic IR beta-endorphin material was measured at three timepoints: at baseline (t (0)), before induction (t (1)), and at the end of anaesthesia (t (2)). Two general linear models were set up to analyse the influence of demographics and clinics on the IR beta-endorphin variation between t (0) and t (1). A third model was established to process the possible surgical factors contributing to the IR beta-endorphin variation between t (1) and t (2). RESULTS: ANOVA showed that IR beta-endorphin concentrations increased significantly across the three timepoints (p < 0.0001). Wilcoxon test proved that the difference was significant both for t (0) vs. t (1) and for t (1) vs. t (2). None of the factors taken into account in the pre-operative period influenced the increase in IR beta-endorphin between t (0) and t (1). Of the factors taken into account in the surgical period, only the type of procedure was significant (p = 0.005). The t-test showed that IR beta-endorphin significantly increased during spermatic and epigastric anastomosis (p = 0.000), orchidopexy (p = 0.02), Van der Meulen urethroplasty (p = 0.004), and Duckett urethroplasty (p = 0.003). CONCLUSION: Plasmatic beta-endorphin increases during the perioperative period in children. The site of surgery is responsible for this increment during intervention.

Affinity-based screening of combinatorial libraries using automated, serial-column chromatography.

We have developed an automated serial chromatographic technique for screening a library of compounds based upon their relative affinity for a target molecule. A "target" column containing the immobilized target molecule is set in tandem with a reversed-phase column. A combinatorial peptide library is injected onto the target column. The target-bound peptides are eluted from the first column and transferred automatically to the reversed-phase column. The target-specific peptide peaks from the reversed-phase column are identified and sequenced. Using a monoclonal antibody (3E-7) against beta-endorphin as a target, we selected a single peptide with sequence YGGFL from approximately 5800 peptides present in a combinatorial library. We demonstrated the applicability of the technology towards selection of peptides with predetermined affinity for bacterial lipopolysaccharide (LPS, endotoxin). We expect that this technology will have broad applications for high throughout screening of chemical libraries or natural product extracts.

[A comparative study of immune and clinical indicators in radicular and myofascial back pain]. / Sravnitel'nyi analiz immunokhimicheskikh i klinicheskikh pokazatelei pri dorsalgiiakh koreshkovogo i reflektornogo geneza.

AIM: To compare immunochemical and clinical parameters in patients with chronic radicular and myofascial back pain. MATERIAL AND METHODS: A study included 92 patients (55 men and 37 women) with radicular pain syndrome and 97 patients (33 men and 64 women) with myofascial pain syndrome. Pain status was assessed with the differential visual analogous scale (at rest, on movement, at night and during spontaneous pain). Tensor algometry was used to measure pain intolerance thresholds at day and night. Levels of natural antibodies (nAB) to endogenous pain regulators (ß-endorphin, orphanin, serotonin, dopamine, histamine and angiotensin) were determined in the blood serum by ELISA. Patients were examined at admission to the hospital, on 10th and 21st days of treatment. RESULTS AND CONCLUSION: There was a significant decrease in pain syndrome in all patients to the 21st day. Pain intensity was higher in patients with radicular pain syndrome (р<0.05) in all functional states. Pain intolerance thresholds were initially reduced in both groups. No significant between-group differences in the dynamics were not found either in men or women. Women had lower pain intolerance thresholds compared to men. An analysis of nAB profiles to pain regulators showed that they were correlated with higher and high indices, with the predominance of nAB to ß-endorphin, orphanin and histamine in both groups. The increased levels of antibodies circulate in the blood serum of patients with dorsalgia for a long time can further be a factor of pain chronification.

Methodological aspects of rat beta-endorphin analysis-influence of diurnal variation.

Beta-endorphin radioimmunoassays (RIAs) are widely performed following physical, emotional and environmental challenges in the rat. In the literature, a wide range of techniques have been described, but in the present study, we have focused on methodological aspects of beta-endorphin RIAs, investigating various characteristics of human and rat specific antibodies. Initial studies verified that the RIA outcome was not appropriate when using non-species compatible components. Novel rat beta-endorphin antibodies, r 4114 and r 4268, were raised in rabbits and characterised in terms of specificity, avidity and titer. Both of the new antisera showed 68.1% cross-reactivity with human beta-endorphin. The ED50 was 50+/-8 pmol/l, and the mean ED80 was 17 pmol/l for r 4268 but three-fold higher for r 4114. The intra-assay coefficient of variation (CV) was 7% at 100 pmol/l and the inter-assay CV was 10% at the same level for r 4268 and similar for r 4114. Using this novel rat beta-endorphin RIA for analyses of diurnal influence and removal from the Animal House cage, no significant changes were observed in either the hypothalamus or peri-aqueductal grey regions. These results suggest that rat beta-endorphin concentrations in these brain areas are not affected by order of removal or diurnal variation.

Inflammation in low back pain may be detected from the peripheral blood: suggestions for biomarker.

Biomarker for prediction of development of low back pain, and disease progression in chronic conditions are virtually non-existent. In the present study, we examined evidence of inflammation in the peripheral blood and demonstrated significant changes in neuroinflammation markers in subjects with chronic low back pain in comparison with control subjects. The present study was performed using peripheral blood from subjects with chronic low back pain and age-matched control subjects. Western blotting, real-time RT-PCR, cell culture and in vitro assays were incorporated to perform the current study. We obtained evidence that the balance between proinflammatory and anti-inflammatory cytokines is misaligned, with decrease in interleukin-10 (IL-10) expression and increase in interleukin-6 (IL-6) expression. Furthermore, we demonstrated increase in CD16 monocyte expression. Cells were cultured under differential conditions to generate M1/M2 macrophages. In the macrophages, opioid secretory capacity was shown to be diminished. Finally, Dragon (repulsive guidance molecule b, RGMb) expression was shown diminished in M1 macrophages, which serves as a key transcriptional inhibitor of IL-6 expression. These biochemical and cellular alterations in chronic low back pain can serve as potential biomarkers for assessing disease initiation, intensity and progression.

17ß-estradiol effect on testicular ß-endorphin expression in Psammomys obesus.

INTRODUCTION: Testicular function in the sand rodent Psammomys obesus is subjected to seasonal alternations with a trigger of spermatogenesis in winter and a total quiescence which extends from late spring to summer. The aim of this study was to investigate the distribution of b-endorphin in the testis at the period of winter sexual activity and at its summer regression, and assess the effect of 17 ß-estradiol treatment on testicular morphology and b-endorphin expression. MATERIAL AND METHODS: The adult males were grouped into 4 groups (rest group, sexually active group, rest treated with 17ß-estradiol group and controls at sexual rest injected with olive oil, n = 5 in each group). Using anti-serum against b-endorphin, we studied its testicular expression by Western blot and cellular location by immunohistochemical (IHC) method, respectively. RESULTS: We detected by Western blot a peptide of 3.5 kDa molecular weight corresponding to b-endorphin only in sexually resting and control males. The 17ß-estradiol treatment induced a clear reduction in the b-endorphin band expression compared with the latter. These results were confirmed by the IHC analysis since b-endorphin was only observed in the testis at sexual rest and in controls, in majority of seminiferous tubules at the level of germ cells. The intensity of IHC labeling was significantly different between spermatogonia and spermatocytes I or round spermatids which revealed the strongest labeling. The intense immunoreactivity was also located in Leydig cells and highly significantly varied compared to the germ cells. The 17 ß-estradiol treatment decreased significantly the ß-endorphin signal in germ cells but not in Leydig cells. CONCLUSION: The 17ß-estradiol treatment induces a repressive effect on seasonal testicular endorphinergic system in P. obesus and this action targets exclusively the germ cells.

Identification and measurement of beta-endorphin levels in the skin during induced hair growth in mice.

We describe new and effective techniques for extracting proopiomelanocortin (POMC)-derived peptides from mammaliar skin. Using this methodology (hot-acid extraction) and two independent HPLC-controlled RIA systems, we identify beta-endorphin peptide in mammalian skin and demonstrate significant hair cycle-dependent fluctuations in both the skin concentration and the in situ expression pattern of beta-endorphin (sebaceous glands) during the entire murine hair cycle. The observed anagen (growth phase) associated increase in beta-endorphin concentration and its decline during the follicle involution (catagen) or resting (telogen) phase raise the possibility of a regulatory function of this neuropeptide in cyclic changes of skin physiology.

Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy.

Electroconvulsive therapy is accompanied by an activation of the hypothalamic-pituitary-adrenal axis, resulting in a release of beta-endorphin from the anterior pituitary corticotrophs of humans. As a group, patients in our study demonstrated similar plasma beta-endorphin immunoreactivity response to their initial and final treatments. However, approximately half of the patients demonstrated greater beta-endorphin immunoreactivity release with their first seizure compared with their last seizure, and half of the patients demonstrated the opposite pattern. This difference was not explained by age, sex, unilateral vs bilateral treatments, sine wave vs brief pulse, or psychotropic or anticholinergic medication. Patients with constant seizure duration during the first and final treatments demonstrated a greater release of beta-endorphin immunoreactivity with the final treatment compared with the first treatment. Individuals with decreasing seizure duration during the course of the electroconvulsive therapy demonstrated a decreased beta-endorphin immunoreactivity response during their final treatment.

Beta-endorphin prevents collagen induced arthritis by neuroimmuno-regulation pathway.

OBJECTIVE: To observe the effects and mechanisms of beta-endorphin (beta-END) preventing collagen induced arthritis (CIA) by neuroimmuno-regulating pathway. METHODS: Female wistar (Ws) rats were used in this study. CIA was induced by Native bovine type II collagen emulsified with complete Freund's adjuvant (CFA). Beta-END was administered i.p. to CIA rats every other day from the 14th day (secondary immunization) to the 35th day after primary immunization. Clinical assessments were performed by two independent, blinded examiners every other day. Pathological and radiological observations were taken on the 35th day after the primary immunization. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), regulated upon activation, normal T-cell expressed and secreted (RANTES), inducible NO syntheses (iNOS), matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA expression of synovium tissues of CIA rats was estimated by quantitative RT-PCR. The frequency of spleen Th1 and Th2 cells were assessed by fluorescence activated cell sorter (FACS) assay. RESULTS: Clinical manifestation of rats with CIA were significantly abrogated or ameliorated by treatment with beta-END. Beta-END treatment in vivo could down-regulate mRNA expression of several pro-inflammatory cytokines, chemokines and MMPs in CIA synovial, and polarize Th1/Th2 balance to Th2. CONCLUSION: Beta-END alleviates CIA through both depressing Th1 responses and down-regulating proinflammatory and other rheumatic factors, suggesting beta-END is a promising anti-inflammatory and anti-rheumatic agent in treating CIA.

[Anti-inflammatory and synovial-opioid system effects of electroacupuncture intervention on chronic pain in arthritic rats].

OBJECTIVE: To observe the analgesic effect of electroacupuncture (EA) on collagen-induced arthritis (CIA) rats and its regulating effect on inflammation reaction and the endogenous opioid system of synovial tissues. Methods A total of 30 healthy male Wistar rats were randomly divided into a control group, a model group and an EA group, 10 rats in each one. The chronic pain model of CIA rats was made by cattle type-II collagen in the model group and EA group. Rats in the EA group were treated with EA at "Zusanli" (ST 36) and "Kunlun" (BL 60) for 30 min from 16th day after model establishment, once a day for consecutive 10 days. Rats in the control group did not receive any treatment. Rats in the model group were treated with fixation as the EA group. Threshold of pain, arthritis index, paw swelling were measured before model establishment and 16 d, 20 d, 23 d and 25 d after model establishment. The levels of beta-endorphin (ß-END), met-enkephalin (met-ENK), dynorphin A (Dyn A) were measured by radioimmunoassay; the mRNA expressions of mu opioid receptor (MOR), kappa opioid receptor (KOR) and delta opioid receptor (DOR) in synovial tissues of CIA rats were detected by I quantitative polymerase chain reaction (qPCR). RESULTS: Compared with the control group, threshold of pain was reduced (all P<0. 01), arthritis index was increased (all P<0. 01) and paw swelling was increased (all P<0. 01) in the model group on the 16th day, 20th day, 23rd day, 25th day after model establishment. Compared with the model group, the threshold of pain was increased in the EA group (all P<0. 01), arthritis index and paw swelling were reduced (all P<0. 01) on the 23rd day and 25th day after model establishment. Compared with the control group, the level of Dyn A in synovial tissues of CIA rats was increased in the model group (P<0. 01); the mRNA expressions of MOR, KOR and DOR were down-regulated lower than 0. 5 fold of normal level. Compared with the model group, the level of ß-END in synovial tissues of the knee joint was increased in the EA group (P<0. 05), and the mRNA expressions of MOR, KOR and DOR in synovial tissues of CIA rats were up-regulated more than 2 folds of normal level. CONCLUSION: The intervention of EA on chronic pain of CIA rats is superior, which is likely to be related with effects of EA on anti-inflammation and up-regulation of synovial tissue ß-END and MOR, KOR, DOR.

Effects of immune neutralization of corticotropin-releasing hormone, adrenocorticotropin, and beta-endorphin in the surgically stressed rat.

Specific in vivo neutralization was used in an attempt to explore the roles of corticotropin-releasing hormone (CRH), ACTH, and beta-endorphin during surgical stress in Sprague-Dawley rats. Rats were randomly assigned to groups (n = 20-30/group) that received iv injections of rabbit antirat/human CRH (anti-r/hCRH), antihuman ACTH (anti-hACTH), antihuman beta-endorphin (anti-h beta-endorphin), or normal rabbit serum. Three hours later all animals were subjected to a uniform stress consisting of ether anesthesia, surgical laparotomy, and phlebotomy of 7 ml via the inferior vena cava. Survival rates were recorded, and RIAs were performed for ACTH, beta-endorphin, and corticosterone. Rats treated with anti-h beta-endorphin had a survival rate of 64%, which was significantly higher than that of the control group (33%; P less than 0.025, by analysis of variance). Anti-r/hCRH or anti-hACTH treatment was not associated with a change in survival rate. Plasma immunoreactive beta-endorphin levels were markedly decreased in the group treated with anti-h beta-endorphin (P less than 0.0001). Anti-r/hCRH had no effect on plasma immunoreactive ACTH or beta-endorphin. Plasma immunoreactive ACTH and corticosterone levels were decreased in the group treated with anti-hACTH (P less than 0.0001 and P less than 0.01, respectively). We conclude that 1) beta-endorphin immune neutralization is associated with a survival advantage during severe surgical stress, suggesting that circulating beta-endorphin might have deleterious effects during stress; 2) In severe stress, acute immune neutralization of CRH is not sufficient to inhibit ACTH, beta-endorphin, and corticosterone secretion, suggesting significant involvement of other secretagogues of the pituitary-adrenal axis; and 3) moderate decreases in corticosterone cannot affect survival, presumably because glucocorticoids play only a permissive role in maintaining cardiovascular stability during surgical stress.

Aging changes in the beta-endorphin neuronal system in the preoptic area of the C57BL/6J mouse: ultrastructural analysis.

In hypothalami of aging rodents, beta-endorphin (beta-EP) neuron number and content are reduced. The objectives of this study were: first, to analyze ultrastructurally the population of neuronal elements in a selected region of the preoptic area (POA) in young and old mice; second, to study the beta-EP neuronal system in the same region to determine whether or not this population remains stable with age. Vibratome sections from the most caudal POA through the diagonal band of Broca were examined by light microscopy and immunocytochemistry in mature, cycling (5-6 months old) and old, acyclic, disease-free (24-26 months old) mice. A subset of beta-EP-like perikarya and associated structures was observed in the periventricular POA. When this subregion was examined at the ultrastructural level, there was a significant decrease in the number of recipient dendrites [3.78 +/- 0.04 SEM/micron 2 young vs. 0.82 +/- 0.03/micron 2 old; p < 0.007, analysis of variance (ANOVA)], but a significant increase in the number of nonmyelinated axons (20.0 +/- 2.6/micron 2 young vs. 26.8 +/- 0.7/micron 2 old; p < 0.05). Immunolabeled terminals that contained a synapse comprised 2.56 +/- 0.08% of all terminals with synapses in young mice but only 0.34 +/- 0.04% in old ones when corrected for surface area examined (p < 0.03). A significant age-related loss was also observed in the nonmyelinated beta-EP-labeled axon population (1.50 +/- 0.10% young vs. 0.40 +/- 0.01% old; p < 0.009, ANOVA). We conclude that there are critical changes in the microenvironment of the POA in old, noncycling female mice that are likely to affect neuron function.

Discovery of D-amino-acid-containing ligands with selectide technology.

When all L-amino acid (aa) random peptide libraries synthesized on solid-phase particles were screened (Selectide Technology), we identified several peptide ligands (YG_F_) that interacted specifically with an anti-beta-endorphin monoclonal antibody (clone 3E7) (single-letter aa symbols; symbols '_' indicate variable aa). Here, we report on the screening of three different D-aa-containing pentapeptide libraries (XxXxX, xXxXx and xxxxx, wherein X = L-aa, and x = D-aa) with the same antibody, in which several D-aa-containing ligands were identified. The binding affinities of many of these D-aa-containing ligands were as least two orders of magnitude lower than that of YGGFL, for which the Ki is 17.5 nM.

Synthetic peptide combinatorial libraries (SPCLs): identification of the antigenic determinant of beta-endorphin recognized by monoclonal antibody 3E7.

The use of synthetic peptide combinatorial libraries (SPCLs), each composed of tens of millions of peptides, is described here for the identification of bioactive peptides. The identification of optimal peptide sequences is achieved through the screening of SPCLs in solution, each element of which is composed of more than 10(5) nonsupport-bound peptides in approximately equimolar representation, along with an iterative synthesis and screening process. Using an SPCL composed in total of 52 128 400 nonacetylated hexapeptides, along with an iterative selection process based on competitive ELISA, we identified the antigenic determinant of beta-endorphin recognized by monoclonal antibody (mAb) 3E7. These results will be compared with the results found by others investigating mAb 3E7 using different peptide library approaches.

Effects of estrogen on the number of neurons expressing beta-endorphin in the medial basal hypothalamus of the female guinea pig.

The distribution pattern of immunoreactive beta-endorphin neurons was studied in female guinea pigs that were ovariectomized, and one week later were injected with 25 micrograms estradiol benzoate or oil. The animals (5 from each group) were perfused after 24 hours with 4% paraformaldehyde. The locations of beta-endorphin cells and fibers were determined using avidin-biotin immunohistochemistry on free-floating vibratome sections. beta-endorphin-immunoreactive fibers were distributed widely throughout specific regions of the rostral forebrain, similar to what has been described in other species. beta-endorphin cell bodies were found in the arcuate nucleus and in adjacent ventrolateral areas throughout the rostrocaudal extent of the basal hypothalamus. Cells immunoreactive to beta-endorphin were also present in the caudal part of the ventromedial nucleus of the hypothalamus. The number of beta-endorphin neurons was quantified in anatomically matched sections through the rostral, medial and caudal basal hypothalamus of estradiol benzoate- and oil-treated guinea pigs. Analysis of variance revealed that the number of immunoreactive beta-endorphin cells was significantly increased in all regions of the basal hypothalamus of estrogen-treated guinea pigs as compared to vehicle-treated animals (P < 0.01). These data indicate that in the guinea pig, the number of neurons expressing beta-endorphin is increased in the arcuate nucleus 24 hours after estrogen treatment.

Beta-endorphin processing and cellular origins in rat spinal cord.

While enkephalin and dynorphin peptides have been well characterized in the spinal cord, the cellular localization of beta-endorphin (beta E) and the processing of pro-opiomelanocortin (POMC) to beta E and other non-opioid peptides in the cord have not been extensively investigated. Other investigators have characterized the various beta E forms present in rat spinal cord regions. Previous studies have also suggested that spinal POMC content is entirely derived from supraspinal sources. However, high proportions of beta E precursors present in spinal cord sieving profiles led us to suspect the presence of POMC cell bodies intrinsic to the cord. In this study, we performed thoracic spinal cord lesions on a group of animals and demonstrated the persistence of about one-third of control levels of beta E immunoreactivity (beta E-IR) below the level of the lesions. We also characterized POMC processing in various regions of the spinal cord both before and after lesioning. These data suggested that there may be intrinsic POMC/endorphinergic neuronal systems in the spinal cord.