The effects of running and meditation on beta-endorphin, corticotropin-releasing hormone and cortisol in plasma, and on mood

The relations between three hormones of the hypothalamic-pituitary-adrenocortical (HPA) axis, beta-endorphin (β-EP), corticotropin-releasing hormone (CRH) and cortisol, and mood change were examined in 11 elite runners and 12 highly trained meditators matched in age, sex, and personality. Despite metabolic differences between running and meditation, we predicted that mood change after these activities would be similar when associated with similar hormonal change. Compared to pre-test and control values, mood was elevated after both activities but not significantly different between the two groups at post-test. There were significant elevations of β-EP and CRH after running and of CRH after meditation, but no significant differences in CRH increases between groups. CRH was correlated with positive mood changes after running and meditation. Cortisol levels were generally high but erratic in both groups. We conclude that positive affect is associated with plasma CRH immunoreactivity which itself is significantly associated with circulating β-EP supporting a role for CRH in the release of β-EP. Increased CRH immunoreactivity following meditation indicates, however, that physical exercise is not an essential requirement for CRH release.     

CSF neuropeptides in cancer pain: effects of spinal opioid therapy

The cerebrospinal fluid (CSF) levels of the opioid peptides met-enkephalin (ME), beta-endorphin (BE) and dynorphin (DYN) as well as the putative sensory neuropeptides substance P (SP), somatostatin (SOM), calcitonin gene related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were determined in 10 patients with severe nociceptive pain due to malignancy, before and after initiation of spinal opioid therapy, and in 10 control patients. Pain intensity, evaluated by means of a 100-mm visual analog scale (VAS), was reduced from 39 ± to 18±10 for continuous pain and from 70± 10 to 10 ± 8 for intermittent pain (means ± s.e.mean). Lumbar CSF immunoreactive ME and DYN concentrations were significantly increased (P = 0.05) and BE and VIP were significantly decreased (P < 0.05) in the pain patients. A slight, but nonsignificant (P = 0.06) decrease in SP-like immunoreactivity was found after initiation of spinal opioid therapy. Visceral pain seemed to be associated with low immunoreactive SP and ME concentrations compared to somatic pain. A highly significant correlation was found between SP and ME (P < 0.001) and to a lesser extent also between other peptides. We conclude that the concentrations of the endogenous opioids were more affected by nociceptive pain states than the non-opioid peptides. The origin of pain may also influence the results. The postulated inhibition of peptide release by spinal opioid application seemed to be present for SP, but could otherwise not be confirmed.     

Human EEG response to beta-endorphin.

Beta-endorphin, morphine, and saline were given intravenously to a single schizophrenic subject on separate occasions in a double-blind design. EEG spectral analyses performed on data collected before and after drug injection demonstrated that beta-endorphin and morphine produced similar increases in alpha power within 5 to 15 minutes after injection. This effect could be distinguished from two placebo (saline) injections. These data suggest that intravenous beta-endorphin can produce changes in the central nervous system in humans.     

Effect of acupotomy on nitric oxide synthase and beta-endorphin in third lumbar vertebrae transverse process syndrome model rats

Objective

To explore the long-term effects and pain relief mechanism of acupotomy by observing changes in nitric oxide synthase (NOS) and beta-endorphin (β-EP) in the hypothalamus, spinal cord, and peripheral blood of rats with third lumbar vertebrae (L3) transverse process syndrome.

Methods

Twenty-eight SD rats were randomly assigned to normal, model, electroacupuncture (EA), and acupotomy group. The last three groups were put through an operation to emulate L3 transverse process syndrome. Fourteen days after the simulation operation, EA and acupotomy treatments were applied to the respective groups. Fifty-six days after the simulation operation, biochemistry tests and enzyme-linked immunosorbent assay were used to measure NOS and β-EP in the hypothalamus, spinal cord, and peripheral blood.

Results

Rats with the simulation operation showed significantly higher levels of NOS and β-EP in the hypothalamus, spinal cord, and peripheral blood than those in the normal group. The EA and acupotomy groups had significantly lower levels of NOS and β-EP than those in the model group. There was no statistical difference between the EA and acupotomy groups.

Conclusion

EA and acupotomy treatments significantly lowered NOS and β-EP levels in the hypothalamus, spinal cord, and peripheral blood and alleviated L3 transverse process syndrome.     

海洛因依赖和戒断时大鼠脑区、垂体和血浆中β-内啡肽的变化

目的 研究海洛因依赖和戒断与β－内啡肽（β－ＥＰ）含量变化的关系。方法 ３０只ＳＤ大鼠随机分为海洛因依赖组,海洛因戒断组和对照组,各１０只,依赖组和戒断组大鼠腹腔内注射海洛因１０天建立海洛因依赖模型,对照组注射生理盐水,于第１０天末次用药３小时后（对照组和依赖组）或７２小时后（戒断组）将大鼠断头,收集躯干血,垂体和各脑区（包括桥延脑,下丘脑,中脑中央灰质,纹状体,海马和额叶皮质）标本,用放射免疫法     

Demonstration by in situ hybridization of the proopiomelanocortin gene in the rat heart

A biotinylated oligonucleotide probe was used to demonstrate the presence in the heart of the portion of the proopiomelanocortin messenger RNA which contains the sequence for beta-endorphin. The probe indicated the presence of beta-endorphin messenger RNA in cardiac tissue and specifically in the cardiac muscle cell. The probe also confirmed the well-documented presence of messenger RNA for beta-endorphin in the anterior and neurointermediate lobes of the pituitary. These findings indicate that in addition to the pituitary, beta-endorphin is produced in situ in the heart.     

Subjective correlates of cigarette-smoking-induced elevations of peripheral beta-endorphin and cortisol

Two experiments assessed subjective and hormonal effects of smoking cigarettes with three different nicotine deliveries. In experiment 1, 12 males smoked two cigarettes on three different occasions: (1) nicotine-free; (2) their own brand (1.0 mg FTC-estimated nicotine delivery); or (3) 2.4 mg FTC nicotine cigarettes. In experiment 2, 12 males smoked cigarettes of comparable nicotine yield using a quantified smoke delivery system (QSDS). Blood was sampled 2 min after each cigarette completion. Relative to nicotine-free smoking, plasma beta-endorphin (BE) and serum cortisol concentrations increased after quasi-ad libitum smoking of 2.4 mg, but not after 1.0 mg nicotine cigarettes. Self-reported malaise (nausea, sickness, and unpleasantness) also increased after smoking 2.4 mg nicotine cigarettes; subjective distress was correlated with changes in blood BE and cortisol, Smoking 1.0 mg cigarettes did not increase BE or cortisol, or subjective distress. QSDS smoking produced hormonal and subjective effects similar to quasi-ad libitum smoking; however, correlations between neuromodulator concentrations and mood were non-significant. These findings suggest that the elevated levels of plasma BE and cortisol reported in some smoking studies may not be characteristic effects of normal smoking.     

Selective potentiations in opioid analgesia following scopolamine pretreatment

The effects of the muscarinic receptor antagonist scopolamine upon analgesia induced by d-ala-d-leu-enkephalin (DADL), beta-endorphin (BEND) and morphine were examined. While scopolamine (10 mg/kg, IP) significantly potentiated the analgesic responses following DADL (40 g, ICV) and morphine (5 mg/kg, SC) on the jump test, it failed to alter significantly BEND (1 g, ICV) analgesia.