β-Endorphin, but not substance-P, is increased by acute stress in humans

doi:10.1016/0306-4530(94)00048-4

Psychoneuroendocrinology

Volume 20, Issue 1, 1995, Pages 103-110

https://doi.org/10.1016/0306-4530(94)00048-4 Get rights and content

Abstract

The role of neuropeptides in the psychoneuroendocrinological stress response is largely unknown. In this study the effect of acute psychological stress on β-endorphin and substance-P plasma concentrations was investigated and further the effect of different anxiety levels or control attributions on β-endorphin or substance-P levels was determined. Blood samples were obtained from 47 inexperienced tandem-parachutists 2 h before, immediately after, and 1 h after a parachute jump and plasma concentrations of β-endorphin and substance-P were analysed. Anxiety levels and control attributions were assessed by psychometric scales. Whereas substance-P concentrations seemed to be unaffected by the jump stress, there was a transient but significant increase in β-endorphin levels immediately after jumping. However, subjects higher in state-anxiety at the point of jumping (exit) displayed higher substance-P values at all three time points compared to the “low-anxiety” jumpers. In addition, stress-induced β-endorphin secretion was dependent on subjective control attributions.

References (33)

P.F. Miller et al.
Beta endorphin response to exercise and mental stress in patients with ischemic heart disease
J Psychosom Res
(1993)
A. Mutti et al.
Endocrine effects of psychological stress associated with neurobehavioral performance testing
Life Sci
(1989)
M. Schedlowski et al.
Acute psychological stress increases plasma levels of cortisol, prolactin and TSH
Life Sci
(1992)
R.M. Swenson et al.
Plasma catecholamine and corticosterone as well as brain catecholamine changes during coping in rats exposed to stressful footshock
Pharmacol Biochem Behav
(1983)
E. Young et al.
Changes in releasability of ACTH and β-endorphin with chronic stress
Neuropeptides
(1985)
H. Akil et al.
Induction of the intermediate pituitary by stress: Synthesis and release of a nonopioid form of β-endorphin
Science
(1985)
P.I.M. Allen et al.
Dissociation between emotional and endocrine responses preceding an academic examination in male medical students
J Endocrinol
(1985)
S. Amir et al.
The role of endorphins in stress: Evidence and speculations
Neurosci Biobehav Rev
(1979)
F. Berkenbosch et al.
Beta-adrenoceptor activation mediates stress-induced secretion of beta-endorphin-related peptides from intermediate but not anterior pituitary
Nature
(1983)
U. Bolm-Audorff et al.
Hormonal and cardiovascular variations during a public lecture
Eur J Appl Physiol
(1986)

D.E. Darr et al.

Platlet peripheral benzodiazepine receptors in repeated stress

Life Sci

(1991)

E.B. De Souza et al.

Rate-sensitive glucocorticoid feedback inhibition of adrenocorticotropin and β-endorphin/β-lipotropin secretion in rats

Endocrinology

(1989)

J.E. Dimsdale et al.

Short-term catecholamine response to psychological stress

Psychosom Med

(1980)

J.E. Dimsdale et al.

Do plasma norepinephrine levels reflect behavioral stress?

Psychosom Med

(1987)

A. Grossman

Opioids and stress in man

J Endocrinol

(1988)

G. Johansson et al.

Examination stress affects plasma levels of TSH and thyroid hormones differently in females and males

Psychosom Med

(1987)

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Our finding that patients diagnosed with schizophrenia had significantly higher levels of β-endorphin levels is consistent with previous literature. Furthermore, the intermittent but inescapable psychotic symptoms of patients with schizophrenia might parallel the way intermittent forms of inescapable electric foot shock stress activates the opioid system in animal models (Schedlowski et al., 1995). On the other hand, patients diagnosed with Substance Use Disorders (SUD), which were mostly diagnosed with an AUD, had significantly lower levels of β-endorphin.
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Psychological stress is recognized as a key factor in the exacerbation of allergic asthma, whereby brain responses to stress act as immunomodulators for asthma. In particular, stress-induced enhanced type 2 T-helper (Th2)-type lung inflammation is strongly associated with asthma pathogenesis. Psychological stress leads to eosinophilic airway inflammation through activation of the hypothalamic-pituitary-adrenal pathway and autonomic nervous system. This is followed by the secretion of stress hormones into the blood, including glucocorticoids, epinephrine, and norepinephrine, which enhance Th2 and type 17 T-helper (Th17)-type asthma profiles in humans and rodents. Recent evidence has shown that a defect of the μ-opioid receptor in the brain along with a defect of the peripheral glucocorticoid receptor signaling completely disrupted stress-induced airway inflammation in mice. This suggests that the stress response facilitates events in the central nervous and endocrine systems, thus exacerbating asthma. In this review, we outline the recent findings on the interplay between stress and neuroendocrine activities followed by stress-induced enhanced Th2 and Th17 immune responses and attenuated regulatory T (Treg) cell responses that are closely linked with asthma exacerbation. We will place a special focus on our own data that has emphasized the continuity from central sensing of psychological stress to enhanced eosinophilic airway inflammation. The mechanism that modulates psychological stress-induced exacerbation of allergic asthma through neuroendocrine activities is thought to involve a series of consecutive pathological events from the brain to the lung, which implies there to be a “neuropsychiatry phenotype” in asthma.
Age Differences in the Time Course and Magnitude of Changes in Circulating Neuropeptides After Pain Evocation in Humans
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This study tested the hypothesis that older adults would have a stronger response for substance P (facilitatory) but weaker response to β-endorphin (inhibitory), in magnitude as well as time course. Eight younger and 9 older adults underwent 3 experimental sessions using well validated laboratory pain models: cold pressor task, contact heat pain, and a nonpainful control. Blood was collected through an indwelling catheter at baseline and 3, 15, 30, 45, and 60 minutes after stimuli administration. Older adults had higher baseline levels of both neuropeptides suggesting increased peripheral activity compared with younger adults. After the cold pressor task, older adults demonstrated a quick and strong release of substance P with dramatic recovery, whereas young adults maintained a constant low-grade response. Unlike substance P, β-endorphin increased between 3 and 15 minutes for both groups with the upsurge substantially higher for older adults. After heat pain, younger adults had an immediate surge in circulating substance P and β-endorphin that was more pronounced than among older adults. However, levels of substance P for younger adults slowly tapered whereas they continued to climb for the older adults through 30 minutes. β-endorphin peaked at 30 minutes for both groups and returned to baseline. No changes were observed during the nonpainful control session.
Older adults had higher baseline levels of substance P and β-endorphin suggesting increased peripheral activity compared with younger adults. After pain evocation, older adults demonstrated a more intense early response for both neuropeptides suggesting peripheral mechanisms involved in the response to pain may change with age.
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In this study, female βE-HT and βE-KO mice, but not B6 mice, increased alcohol consumption in response to the stress of having an appetitive activity wheel blocked, suggesting susceptibility to stress-induced drinking is linked to low β-endorphin levels. Clinical research shows that stress increases β-endorphin, which in turn negatively modulates the stress response (Schedlowski et al., 1995). Furthermore, β-endorphin levels have been correlated with excessive drinking in humans (Froehlich et al., 1990; Gianoulakis, Dai, & Brown, 2003; Wand et al., 1998).
Animal models have long been used to study the mechanisms underlying the complex association between alcohol and stress. Female mice prevented from running on a home–cage activity wheel increase voluntary ethanol consumption. β-endorphin is an endogenous opioid involved in negatively regulating the stress response and has also been implicated in the risk for excessive drinking. The present study investigates the role of β-endorphin in moderating free-choice consumption of ethanol in response to a blocked activity wheel. Female, transgenic mice with varying levels of the opioid peptide were given daily 2-h access to 20% ethanol with rotations on a running wheel blocked on alternate days. Subjects with low β-endorphin exhibited enhanced stress sensitivity by self-administering larger quantities of ethanol on days when wheel running was prevented. β-endorphin levels did not influence voluntary activity on the running wheel. There were genotypic differences in plasma corticosterone levels as well as corticotropin-releasing hormone mRNA content in multiple brain regions associated with the stress response in these free drinking and running subjects. Susceptibility to stress is enhanced in female mice with low levels of β-endorphin, and better understanding of the role for this opioid in mitigating the response to stressors may aid in the development of interventions and treatments for excessive use of alcohol in women.
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Citation Excerpt :
Although there was not a significant difference in pre- vs. post-competition beta-endorphin levels, pre-competition sampling pain increased when beta-endorphin levels in the blood increased. In humans, beta-endorphins in the blood are known to increase due to acute psychological stress (Schedlowski, 1995; Sheps et al., 1995) or increased pain (Johansen et al., 2003), indicating that beta-endorphin levels in the blood seem to be part of the response to pain and/or stress. Inescapable footshock-induced stress promotes a five- to six-fold increase in beta-endorphin levels in the blood but not in the brain (Rossier et al., 1977).
The psychological stress of competition is a powerful stimulus affecting numerous hormones, which in turn change how pain is perceived. This study investigated whether a kumdo (kendo) team competition may be related to changes in hormones and pain. Seventeen healthy male kumdo practitioners participated in this experiment. Pain experiments were conducted by applying noxious stimuli with a thermal stimulator 10 min before a kumdo competition and 30 min post-competition. Serum testosterone, cortisol, beta-endorphin levels, pain thresholds, pain ratings at 48 °C and during blood sampling (sampling pain), anxiety, blood pressure, and heart rate were measured pre- and post-competition. Anxiety, pain threshold, testosterone/cortisol ratio, and blood pressure were significantly higher pre-competition compared to post-competition, while cortisol and pain ratings were significantly lower pre-competition than post-competition. There were significant correlations between the number of previous competitions and testosterone levels both pre-competition and post-competition. In pre-competition measurements, sampling pain increased with an increase in systolic blood pressure, heart rate, and beta-endorphins, and a decrease in age. In post-competition measurements, sampling pain increased with an increase in diastolic blood pressure and a decrease in testosterone levels. These results indicate that severe psychological pre-competition stress was associated with reduced pain ratings, perhaps in order to improve athletic performance. This also suggests that competitors may be at risk of potential injury due to changes in pain perception, and careful consideration should be taken to avoid potential injury before and during competition.
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Zebrafish has emerged as an important vertebrate animal model for the study of human diseases and for developmental studies in mammals. Since there are few studies of the tachykinin 1 gene (TAC1), precursor of substance P (SP), in relation to embryonic development, we aimed to study the expression of SP transcript (mRNA) and determine the influence of cocaine and opioid receptors on the expression of this neuropeptide. In order to analyse the spatial and temporal SP mRNA expression in zebrafish, we cloned – based on human TAC1 sequence – the sequence that originates SP. Phylogenetic analyses of the precursor of SP, revealed an alignment in the fish cluster, with a clear distinction from other species (amphibians, birds and mammals). Real time PCR (qPCR) results showed that SP mRNA was expressed in several stages of embryonic development, where it increased progressively from gastrula-8 hpf (hour post-fertilisation) to the end of the embryogenesis-72 hpf. SP mRNA was expressed mainly in the spinal cord in embryos at 20–30 hpf, whereas at 36, 42 and 48 hpf embryos SP mRNA was expressed mainly in the CNS telencephalon, diencephalon, hypothalamus, rhombomeres, epiphysis and in peripheral areas (heart and somites). Exposure of embryos to 1.5 μM cocaine altered the SP mRNA expression at 24 (increasing) and 48 hpf (decreasing). We also report that knockdown of μ-opioid receptor induced an increase of SP mRNA expression while the knockdown of the two delta opioid receptors did not produce changes in SP mRNA expression.
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Articleβ-Endorphin, but not substance-P, is increased by acute stress in humans

Abstract

J Psychosom Res

Life Sci

Life Sci

Pharmacol Biochem Behav

Neuropeptides

Induction of the intermediate pituitary by stress: Synthesis and release of a nonopioid form of β-endorphin

Science

Dissociation between emotional and endocrine responses preceding an academic examination in male medical students

J Endocrinol

The role of endorphins in stress: Evidence and speculations

Neurosci Biobehav Rev

Beta-adrenoceptor activation mediates stress-induced secretion of beta-endorphin-related peptides from intermediate but not anterior pituitary

Nature

Hormonal and cardiovascular variations during a public lecture

Eur J Appl Physiol

Platlet peripheral benzodiazepine receptors in repeated stress

Life Sci

Rate-sensitive glucocorticoid feedback inhibition of adrenocorticotropin and β-endorphin/β-lipotropin secretion in rats

Endocrinology

Short-term catecholamine response to psychological stress

Psychosom Med

Do plasma norepinephrine levels reflect behavioral stress?

Psychosom Med

Opioids and stress in man

J Endocrinol

Examination stress affects plasma levels of TSH and thyroid hormones differently in females and males

Psychosom Med

Article
β-Endorphin, but not substance-P, is increased by acute stress in humans