Levels Of Immunoreactive Beta-endorphin Research Articles

Plasma β-endorphin levels in frequent and infrequent tanners before and after ultraviolet and non-ultraviolet stimuli

To the Editor: Ultraviolet (UV) exposure behavior exhibits similarities to other substance-related disorders.1Warthan M.M. Uchida T. Wagner Jr., R.F. UV light tanning as a type of substance-related disorder.Arch Dermatol. 2005; 141: 963-966Crossref PubMed Scopus (128) Google Scholar UV exposure has a direct reinforcing effect on frequent tanners.2Feldman S.R. Liguori A. Kucenic M. Rapp S.R. Fleischer Jr., A.B. Lang W. et al.Ultraviolet exposure is a reinforcing stimulus in frequent indoor tanners.J Am Acad Dermatol. 2004; 51: 45-51Abstract Full Text Full Text PDF PubMed Scopus (118) Google Scholar Cutaneous opioids are induced by UV exposure,3Wintzen M. Yaar M. Burbach J.P. Gilchrest B.A. Proopiomelanocortin gene product regulation in keratinocytes.J Invest Dermatol. 1996; 106: 673-678Crossref PubMed Scopus (128) Google Scholar but whether the reinforcement seen with UV exposure is caused by opioid release is unknown. The potential relationship is complicated, as larger studies have not found an effect of UV on plasma β-endorphin levels.4Wintzen M. Ostijn D.M. Polderman M.C. le Cessie S. Burbach J.P. Vermeer B.J. Total body exposure to ultraviolet radiation does not influence plasma levels of immunoreactive beta-endorphin in man.Photodermatol Photoimmunol Photomed. 2001; 17: 256-260Crossref PubMed Scopus (36) Google Scholar These conflicting results could be caused by differences in UV dose and subject populations, because the tests were not done under conditions in which preference for the UV stimulus was known to occur. To better understand the relationship between cutaneous opioids and the reinforcing effect of UV exposure, we conducted a small double-blind, placebo-controlled, randomized trial and assessed plasma β-endorphin levels in 3 frequent and 3 infrequent adult female tanners, between 25 and 32 years of age and skin types III and IV, before and after non-UV and UV exposures (10 min for frequent tanners and 5-9 min for infrequent tanners based on minimal erythema dose testing). The study was approved by the Institutional Review Board (IRB). Infrequent tanners were defined as individuals who had tanned intermittently in the past (fewer than 8 times per year) but who are not regular tanners. Frequent tanners were defined as tanners who tan more often than is necessary to maintain a tan (8-15 times per month). Commercial indoor tanning beds with Speed 175 and 205 bulbs were used. The bulbs have a UV output of 4% in the UVB range and 96% in the UVA range (estimate dosage of 22.4 j/cm2). Plasma β-endorphin levels were measured on the same day by enzyme-linked immunosorbent assay (MD Biosciences Inc, St Paul, Minn) from blood samples drawn 3 times: before exposure, immediately after non-UV bed, and immediately after UV bed. No discernable trend in plasma β-endorphin levels was observed among the 6 subjects (Fig 1), though the mean plasma β-endorphin level was slightly higher in frequent tanners exposed to UV as compared to baseline. Baseline β-endorphin levels vary and exhibit no distinct pattern of response to UV exposure (at one exposure time in these 6 subjects). The variability in plasma β-endorphin levels complicates attempts to understand the role of endorphins in mediating the preference for UV. Even anxiety about the blood draw could affect endorphin levels. Opioid inhibitor studies may be a better approach to characterize the role of endorphin related effects in mediating physiologic responses to UV.

Total body exposure to ultraviolet radiation does not influence plasma levels of immunoreactive beta-endorphin in man.

A growing number of reports support evidence of proopiomelanocortin (POMC)-derived peptides in human skin cells, although not consistently. Also the effect of ultraviolet radiation (UVR) on cutaneous and plasma levels of these POMC peptides has not been established unequivocally. We hypothesized that production of beta-endorphin (betaE) may explain the sense of well-being many people experience when sun-bathing. The aim of the present study was to investigate whether exposure of the skin to UVR elevates plasma betaE. Healthy volunteers (n=26) received a single, weighted dose of 15 J/cm2 of UVA. Several times during the hour following irradiation, plasma betaE- immunoreactivity (betaE-IR) was determined by radioimmunoassay. The effect of repeated exposure was assessed in 35 patients treated with UVB, UVA, or UVA-1. Plasma ACTH-IR was monitored in parallel. Overall, plasma levels of betaE-IR and ACTH-IR showed no significant changes during the experiment, indicating that these peptides are not influenced by single or repeated exposures to UVR of different wavelengths. On the basis of these results, the skin does not appear to contribute significantly to the levels of circulating betaE or ACTH. These data offer no support for the hypothesis that exposure to UVR leads to an increased concentration of circulating betaE, which could contribute to the feeling of well-being that often accompanies sun-bathing.

CORRELATION OF β-ENDORPHIN AND PROSTAGLANDIN E2 LEVELS IN PROSTATIC FLUID OF PATIENTS WITH CHRONIC PROSTATITIS WITH DIAGNOSIS AND TREATMENT RESPONSE

The chronic pelvic pain syndrome is a clinically defined symptom complex of unclear etiology. We have noted increased oxidative stress in the prostatic fluid of these patients, implying an active inflammatory response. Immune cells can produce the natural opioid beta-endorphin at the site of injury, which may modulate pain. We measured beta-endorphin and the inflammatory marker prostaglandin E2 in the expressed prostatic secretions of men with prostatitis, and correlated the results with symptoms. Expressed prostatic secretions samples from 70 patients and 8 asymptomatic controls were collected and frozen. beta-Endorphin and prostaglandin E2 were measured by enzyme-linked immunosorbent assay. Results were stratified according to prostatitis category and compared in individuals before and after therapy. In symptomatic patients beta-endorphin and prostaglandin E2 were not significantly different in categories II, IIIa and IIIb expressed prostatic secretions but they were higher than in controls. The mean beta-endorphin level plus or minus standard error of mean in symptomatic patients was significantly higher (23.8 +/- 11 ng./ml. versus 8.7 +/- 4.7, p = 0.0001) and mean prostaglandin E2 was lower (6.01 +/- 2.9 ng./ml. versus 3.01 +/- 2.9, p = 0.001) after successful therapy with antibiotics or antioxidant phytotherapy, Prosta-Q (Farr Laboratories, Santa Clarita, California). We observed a correlation of higher prostaglandin E2 and lower beta-endorphin in symptomatic men with chronic prostatitis. Increased oxidative stress and inflammation may induce prostaglandin E2 production that would inhibit beta-endorphin release. Treatment with therapeutic agents that decrease oxidative stress, such as antibiotics and antioxidant phytotherapy, may function at least partially by increasing beta-endorphin and decreasing prostaglandin E2.

Beta-endorphin immunoreactivity levels in CSF after laryngeal chemoreflex activation correlate with apnoea duration in piglets.

The activation of the laryngeal chemoreflex may be a pathogenic mechanism in apnoea, apparent life threatening events, and SIDS. Infants with apnoea and increased levels of beta-endorphin immunoreactivity in CSF have been successfully treated with naloxone. Beta-endorphin may induce respiratory depression, and naloxone is a beta-endorphin antagonist. We therefore wanted to measure beta-endorphin levels in CSF before and after the chemoreflex induced apnoea. This study includes 13 piglets, 5-10 days of age, treated with and without naloxone. Respiration, blood pressure, and heart rate were monitored. CSF was sampled before and after the laryngeal chemoreflex induced apnoea. We found a shorter duration of apnoea in the piglets which had received naloxone than in those which did not (p = 0.02). The beta-endorphin immunoreactivity levels in CSF increased after apnoea, and the increased levels correlated positively with the duration of the apnoea in the piglets which had not received naloxone (r = 0.94, p = 0.02), but not in those pretreated with naloxone (r = 0.1, p = 0.8). The median amount of beta-endorphin immunoreactivity in CSF after apnoea in the naloxone-treated piglets was not significantly different from that in the non-treated piglets: 615 +/- 589 (n = 7) fmol/ml CSF and 984 +/- 851 (n = 6) fmol/ml CSF, respectively. The beta-endorphin immunoreactivity levels measured before the apnoea were less than 4.3 fmol/ml CSF. The laryngeal chemoreflex induced apnoea may possible be partly mediated by beta-endorphin.

Comparison of the effects of immobilization and pressure overload induced cardiac hypertrophy on immunoreactive beta-endorphin

Acute physical stress in the form of immobilization resulted in a decrease in the concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary (AP) and an increase in the concentration of IR-BE in the neurointermediate lobe of the pituitary (NIL) and the plasma. Hypothalamic IR-BE was not influenced by immobilization. In response to chronic cardiovascular (physiological) stress resulting from constriction of the aorta (aortic banding) and subsequent pressure overload, the concentration of IR-BE in the AP was increased as was the concentration of IR-BE in the plasma. The concentration of IR-BE in the NIL and the hypothalamus was not affected. These findings suggest that physical stress and cardiovascular stress have the same affect on IR-BE levels in the plasma but differ in their respective effects on IR-BE in the AP and NIL and do not affect the concentration of IR-BE in the hypothalamus. The difference in the effects of each form of stress on the AP and the NIL respectively, may be attributed to either the type of stress employed (physical versus physiological), the duration of the stress (acute vs chronic), or both.

Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death

In nucleus tractus solitarius (NTS) beta-endorphin (BEND) induces bradycardia and respiratory depression which have been reported to precede death in sudden infant death (SID). Of SID victims, 50% have elevated levels of beta-endorphin immunoreactivity (BENDI) in the cerebrospinal fluid (CSF), and 50% had undetectable levels. We therefore investigated the relationship of BENDI in the CSF to BENDI levels in the NTS area. This study included SID victims (CSF from n = 47, brain stem from n = 16), borderline SID victims (CSF and brain stem from n = 2), sudden death in childhood (CSF and brain stem from n = 1), and controls (CSF from n = 32, brain stem from n = 11). BEND in CSF and NTS area, after extraction, was measured by radioimmunoassay. High performance liquid chromatography was used for closer identification of BENDI. We found that the SID victims divided into two subpopulations, one having a relatively high BENDI level in CSF and one having no detectable level (P < 0.01). Furthermore, an inverse relationship was found between BENDI level in CSF and BENDI level in NTS area in the SID victims (P < 0.05). We conclude that increased BENDI level in CSF is associated with low BENDI level in the NTS area in 50% of SID victims. The low BENDI level in the NTS area may be due to increased release of BEND.

MAY APNEA REFLEX INDUCE SUDDEN INFANT DEATH?

Beta-endorphin may induce respiratory depression and bradycardia. Elevated hypoxanthine (HX) level in corpus vitreum humor (CVH) indicates hypoxia before death. We measured beta-endorphin immunoreactivity (BEI) in CSF and HX in CVH in SIDS victims (n=27) and in control infants (n=12). In a pilot study we measured BEI in CSF in piglets where the larynx reflex was induced by ammonium gas (n=4). BEI in CSF was also measured after brain hypoxia in piglets (n=6). The BEI levels in CSF divided the SIDS victims into two subpopulations: one half with undetectable level <4.3 fmol/ml CSF, and the other half with high level 247 fmol/ml CSF (range 160-400). All the SIDS victims had elevated levels of HX in CVH 209 mikromol/l (range 53-419) compared with the controls that died a sudden death (accidental, cardial or strangled), which had 54 mikromol/l (range 0-188). In the subpopulation of SIDS victims with elevated BEI in CSF, we found a positive correlation between BEI in CSF and Hx levels in CVH r=0.92 (p<0.001). In the control infants no correlation between BSI in CSF and HX in CVH was found. In piglets where the larynx reflex was excited, we found increased levels of BEI in CSF which correlated with the duration of the apneas r=0.84 (p=0.16). In the control piglets undetectable levels of BEI in CSF was found. Conclusion: In SIDS victims with elevated levels of BEI in CSF, the BEI correlated with HX in CVH. The larynx reflex induced apneas, induced BEI increase in CSF in piglets.

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n = 19) and controls (n = 18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P < 0.01); one with undetectable levels (< 4.3 fmol/ml) (n = 10) and one with high levels (160-400 fmol/ml) (n = 9). In the SID subpopulation with high levels of BENDI in CSF, we found a correlation between BENDI in CSF and HX in VH (r = 0.92). Control infants who died a stressful death, such as during heart operations (n = 2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n = 11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Elevated CSF beta‐endorphin immunoreactivity in Rett's syndrome

Because some symptoms of Rett's syndrome are suggestive of excessive endogenous opioid activity, we measured the levels of beta-endorphin-like immunoreactivity in lumbar CSF from 158 affected female patients and from 13 female controls. The mean (+/- SE) control level of beta-endorphin immunoreactivity in CSF was 35.3 +/- 2.8 pg/ml (range, 23 to 48 pg/ml), whereas those with Rett's syndrome had a mean level of 95.3 +/- 3.6 pg/ml (range, 31 to 293 pg/ml). The levels of beta-endorphin immunoreactivity in initial CSF samples exceeded the control range in 90% of the patients with Rett's syndrome. The mean beta-endorphin immunoreactivity was also elevated in CSF from leukemic children (119.2 +/- 16.9 pg/ml; range, 40 to 159 pg/ml), relative to the control group. These results are consistent with the hypothesis that some symptoms of Rett's syndrome may be associated with excessive endogenous opioid levels in the CNS.

Effect of oral contraceptives on plasma beta-endorphin and corticotropin at rest and during exercise.

Concentrations of immunoreactive beta-endorphin and corticotropin in plasma were studied in 27 healthy physically active women at rest and after the exercise test on a treadmill requiring 60% and 90% of the maximal oxygen consumption. Eleven of the subjects were on a combination-type of oral contraceptive pills, and the remaining 16 did not use any pills. Plasma immunoreactive beta-endorphin levels at rest were higher in pill non-users than in pill users. Corticotropin levels at rest did not differ between the pill users and non-users. After the 60% exercise test a slight increase was found in the concentrations of corticotropin and beta-endorphin in the pill non-users but not in the pill users. In the 90% exercise test, plasma beta-endorphin and corticotropin levels increased significantly in both groups. We conclude that the use of oral contraceptives may elevate the threshold of the intensity of exercise required to increase beta-endorphin and corticotropin secretion. Decreased resting concentration of beta-endorphin in pill users can be explained by suppression of normal cyclic ovarian function.

Effects of Alcohol on β‐Endorphin and Reproductive Hormones in the Male Rat

In an attempt to examine the relationship between alcohol-induced alterations in immunoreactive beta-endorphin (i-beta E) levels in the hypothalamic-pituitary-gonadal axis and the synthesis and release of reproductive hormones, male rats were treated with either an acute intraperitoneal injection of alcohol or were chronically exposed to an alcohol-containing liquid diet. Hypothalamic, pituitary, serum, and testicular levels of immunoreactive beta-endorphin (i-beta E) and serum levels of luteinizing hormone (LH) and testosterone were measured at various times after initiation of these treatments. Testicular interstitial fluid (TIF) volumes and levels of TIF i-beta E and testosterone were also measured 4 hr after acute treatment as an index of testicular release of these substances. Acute alcohol decreased pituitary levels of i-beta E and increased serum levels of the peptide for up to 1 hr after its injection, but did not alter hypothalamic or testicular levels. Acute alcohol markedly increased TIF i-beta E and decreased TIF testosterone and TIF volume. Sharp decreases in serum LH and testosterone were observed in association with these acute changes in i-beta E levels in the pituitary, blood, and testes. During chronic alcohol exposure serum testosterone levels were substantially depressed, but tolerance appeared to develop quickly to the chronic effects of alcohol on serum LH. Similarly, tolerance to alcohol's effects on i-beta E levels in the pituitary and serum also appeared to develop during chronic alcohol administration. However, hypothalamic and testicular i-beta E levels were markedly suppressed by chronic alcohol administration in contrast to the lack of effect observed after acute alcohol administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Beta-endorphin in cerebrospinal fluid and serum after severe head injury

Endogenous opioids have been implicated as a cause of secondary damage after neural injury. The basis for this statement is primarily indirect evidence from studies that demonstrate neurological or physiological improvement when opiate antagonists are given. This study directly evaluates the level of the endogenous opioid beta-endorphin in 15 patients with severe head injury. Levels of immunoreactive beta-endorphin (ir-beta E) from ventricular cerebrospinal fluid (vCSF) and serum were determined less than 24 hours after trauma. No significant correlation was found with the degree of initial injury, age, sex, or either 6- or 12-month outcome. Levels of ir-beta E from vCSF were significantly lower in patients who had received intravenous administration of morphine sulfate (48.4 +/- 5.8 versus 85.9 +/- 10.1 pg/ml, P = 0.008). No correlation was found between vCSF levels of ir-beta E and elapsed time after injury. Although vCSF and serum ir-beta E were correlated (r = 0.532, P = 0.050), the latter exhibited a different profile; the mean level of serum ir-beta E was not significantly different in those patients who received morphine, and serum ir-beta E had a significant negative correlation with time after injury (r = -0.587, P = 0.03). These results do not support a relationship between acute levels of vCSF or serum ir-beta E and the degree of neurological injury or outcome after severe head trauma. This article, therefore, is a contribution to the body of literature in which the purported detrimental effect of beta-endorphin was not demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

The elevation of immunoreactive beta-endorphin in old male rats is related to alterations in dopamine and serotonin

The concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary (AP) and the neurointermediate lobe of the pituitary (NIL) was elevated in old as compared to young male rats. Treatment of old male rats with the dopamine precursor, L-DOPA, did not affect the concentration of IR-BE in the AP and produced a significant reduction in the concentration of IR-BE in the NIL. By contrast, administration of the serotonergic neurotoxin, p-CPA, significantly diminished the concentration of IR-BE in the AP of old male rats, while the concentration of IR-BE in the NIL remained unchanged. Hypothalamic IR-BE was decreased in old male rats and was not influenced by administration of L-DOPA or p-CPA. Chromatographic analysis indicated that in the AP of old animals the amount of beta-endorphin relative to beta-lipotropin was increased and was diminished slightly by the treatments. Alterations in IR-BE in the NIL and hypothalamus were represented solely by beta-endorphin. These data suggest that in old male rats, a decrease in dopaminergic activity contributes to the increase in IR-BE levels in the NIL, and an increase in serotonergic function, at least in part, is responsible for the elevation in the level of IR-BE in the AP.

Oocyte fertilization in vitro is associated with high follicular immunoreactive ß-endorphin levels

Follicular fluid (FF) levels of immuno reactive beta-Endorphin (i.r. beta-EP), i.r. gamma-Endorphin (i.r. gamma-EP), i.r. alpha-melanocyte-stimulating hormone (i.r. alpha-MSH), androgens and estrogens were measured in 76 preovulatory follicles obtained, after gonadotropin stimulation from 19 women undergoing in vitro fertilization (IVF). The aim of the study was to investigate the relationships existing between peptide contents of FF and both oocyte-cumulus-corona-complex (OCCC) maturity and the success of IVF. Peptides and steroids were measured by RIA after FF extraction with liquid chromatography and ethyl-ether, respectively. Out of the total of 76 oocytes, 52 were fertilized in vitro and 35 of them underwent normal cleavage and were transferred. Among the three peptides, only i.r. beta-EP levels were higher in FF from follicles which contained oocytes that were subsequently fertilized (127.6 +/- 16.2 pmol/L mean +/- SE) than in FF from follicles which contained oocytes that did not subsequently fertilized (62.9 +/- 8.4, p less than 0.04). Independent of subsequent fertilization, i.r. alpha-MSH values in FF were 5 times higher than those of i.r. beta-EP and i.r. gamma-EP. In the presence of a morphologically mature oocyte, FF i.r. gamma-EP levels (165.2 +/- 45.3 pmol/L) were higher than in FF from follicles yielding immature (63.6 +/- 13.5, p less than 0.01) or luteinized (32.7 +/- 9.2, p less than 0.01) oocytes. Steroid levels in FF did not change in relation to oocyte maturity or subsequent oocyte fertilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunoreactive beta-endorphin levels in cerebrospinal fluid of children with acute lymphoblastic leukemia: relationship with glucocorticoid therapy and neurological complications

Neurological disorders, such as seizures, are not infrequently associated with anti-leukemic therapy. It has been hypothesized that a disrupted peptidergic transmission between neurons could be the cellular basis of the neurological dysfunction. Since endogenous opioids have been recently found to alter neuronal function and possess anticonvulsant properties, the cerebrospinal fluid (CSF) immunoreactive beta-endorphin levels in children with Acute Lymphoblastic Leukemia (ALL) during chemotherapy and cranial irradiation have been studied. Twenty-seven children, 2 at low, 20 at medium and 5 with high risk ALL, undergoing prophylactic treatment for meningeal leukemia, entered the study. Sequential lumbar punctures with introduction of MTX combined with oral prednisone therapy were performed; each lumbar puncture sample was collected and assayed for immunoreactive beta-endorphin. All the patients studied showed a biphasic profile of the peptide with the minimum levels reached during the induction (days 14-28) and the maximum levels detected at the end of the intensification chemotherapy (days 49-55). In the 3 groups the beta-endorphin decrease corresponded to the period of prednisone therapy; the increase was concomitant with the suspension of oral glucocorticoids. 3 patients showed tonic-clonic seizures which coincided with the lowest cerebrospinal fluid beta-endorphin levels and, in the follow-up, 13 out of 27 patients displayed EEG abnormalities. From these findings a relationship between cerebrospinal fluid beta-endorphin concentrations and neuronal excitability in patients with ALL can be suggested. It is also evidenced that oral glucocorticoid therapy has profound inhibitory effects on central beta-endorphin levels.

Tolerance develops to the behavioural effects of ACTH-(1–24) during continuous I.C.V. infusion in rats, and is associated with increased hypothalamic levels of beta-endorphin

In rats, the continuous infusion of ACTH-(1–24) into a brain lateral ventricle (0.5 μg/h in the volume of 1.11 μl, for 7 days) caused a significant inhibition of the subsequent behavioural response to the acute intracerebroventricular injection of the same peptide. Tolerance developed to all the most typical signs of the ACTH-induced behavioural syndrome (grooming, stretching, yawning, penile erection, inhibition of food intake), and was associated with a significant increase in the hypothalamic levels of beta-endorphin immunoreactivity.

A D-2 Dopaminergic Agonist Stimulates Secretion of Anterior Pituitary Immunoreactive β-Endorphin in Rats

Hypothalamic dopamine neurons are known to control circulating levels of immunoreactive beta-endorphin (i beta-END) by inhibiting hormone secretion by the intermediate lobe (IL) of the pituitary gland. We examined the ability of the D-2 selective dopaminergic agonist, LY141865, to influence circulating levels of i beta-END in rats and found that in contrast to inhibiting IL secretion, LY141865 increased release of i beta-END from the anterior lobe (AL). Intraperitoneal injection of 1 mg/kg LY141865 transiently increased plasma levels of i beta-END by 7-30 min after drug treatment; plasma prolactin levels were maximally reduced within 15 min and throughout the remaining 2-hour time course of treatment. Doses of 0.3 and 1.0 mg/kg of LY141865 increased circulating i beta-END to 440 and 690%, respectively, of control levels (0.38 +/- 0.12 ng/ml, mean +/- SEM, n = 6). Lower doses of the D-2 agonist (0.01-0.1 mg/kg) failed to significantly affect plasma i beta-END. Sephadex G-50 chromatography of plasma pools revealed that virtually all of the increase due to LY141865 treatment was immunoreactivity resembling beta-lipotropin in molecular size, the principal component of AL secretion of i beta-END. Furthermore, LY141865-evoked release was blocked by pretreatment of rats with dexamethasone (50 micrograms/kg i.p., 4 h) which inhibits AL but not IL secretion of pro-opiomelanocortin-derived peptides. Stimulation of i beta-END release by LY141865 was also inhibited by the general dopamine antagonist, haloperidol, (0.1-3.0 mg/kg i.p., 2 h) and by the D-2 selective antagonist, sulpiride (100 micrograms/rat i.c.v., 4 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Eight weeks of streptozotocin-induced diabetes influences the effects of cold stress on immunoreactive beta-endorphin levels in female rats.

Cold stress produced a significant reduction in the concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary of diabetic female rats. IR-BE levels in the anterior pituitary of non-diabetic female rats were not affected by exposure to the cold. The effects of cold stress on IR-BE levels in the neurointermediate lobe of the pituitary and the hypothalamus were attenuated in diabetic as compared to control animals. These data suggest that in female rats, eight weeks of diabetes produced alterations in the neuroendocrine mechanisms which modulate IR-BE levels in the pituitary and hypothalamus in response to cold stress.

The effects of immobilization stress on beta-endorphin levels are modulated by testosterone

Immunoreactive beta-endorphin (IR-BE) levels were determined in the anterior pituitary (AP), neurointermediate lobe of the pituitary (NIL) and the hypothalamus of castrated male rats and castrated male rats treated with testosterone proprionate (TP), subsequent to exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute stress resulted in a reduction in the concentration of IR-BE in the AP of castrated male rats, which was potentiated by TP. The concentration of IR-BE in the NIL was elevated by acute stress in castrated male rats and was not affected by acute stress in castrated male rats administered TP. Exposure to chronic immobilization stress elevated the concentration of IR-BE in the AP of castrated animals and not animals treated with TP. The concentration of IR-BE in the NIL of castrated animals was not altered by chronic immobilization. Chronic stress did result in a significant rise in the level of IR-BE in the NIL of castrated male rats given TP. Hypothlamic IR-BE levels in castrated male rats were reduced by TP and were not influenced by acute or chronic stress. Chromatographic analysis indicated that acute and chronic stress promoted the accumulation of beta-lipotropin rather than beta-endorphin in the AP. This effect was attenuated by TP. Beta-endorphin was the only form of immunoreactivity detected in the NIL and hypothalamus. These findings indicate that immobilization stress affects IR-BE levels in the AP and the NIL, and that the effects of acute and chronic immobilization stress of IR-BE levels in the AP and the NIL are modulated by testosterone.

Estrogen influences the effect of immobilization stress on immunoreactive beta-endorphin levels in the female rat pituitary.

Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.