Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In earlier studies, we established that in rats, antagonism of corticotropin-releasing hormone (CRH) receptors reduced the occurrence of fear-motivated behavior displayed immediately after administration of electric foot shock. Because exposure to stress is reported to have long-term behavioral and physiological effects, we examined whether central administration of the synthetic CRH receptor antagonist, alpha-helical CRH(9-41), would also alter fear-motivated behavioral and hormonal responses occurring 24 h after exposure to electric foot shock. Adult male rats were placed in a shock box and administered three, 1.0 mA foot shocks. Twenty-four hours later, rats received an intracerebroventricular infusion of 20 micrograms of alpha-helical CRH(9-41) or vehicle 20 min before re-exposure to the shock box. Antagonism of CRH receptors produced a significant reduction in fear-motivated freezing. However, stress-induced analgesia and plasma adrenocorticotropin concentrations did not differ significantly from vehicle-treated animals. In order to assess whether the reduction in freezing was due to intrinsic actions of the CRH receptor antagonist, non-shocked rats received central infusions of alpha-helical CRH(9-41) prior to re-exposure to the test box. Under these conditions, behavior exhibited by antagonist- and vehicle-treated rats did not differ significantly. Results suggest that the reduction in fear-motivated behavior is mediated by antagonism of endogenous CRH receptors and occurs independently of analgesic and hormonal reactions induced by prior exposure to stress.
 ...
PMID:Fear-motivated behavior induced by prior shock experience is mediated by corticotropin-releasing hormone systems. 215 45

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.
 ...
PMID:Dexamethasone attenuates exercise-induced dental analgesia in man. 216 84

Somatostatin analogue (Sandostatin; SMS 201-995) is utilized as a therapy in acromegaly because of its efficiency in inhibiting GH secretion; it induces some clinical improvements, such as headache remission in acromegalic patient, which seem to be unrelated to Gh normalization. We have examined 8 acromegalic patients, suffering from headache, after injection of saline solution and subsequently of SMS 201-995 (100 y), in order to study the mechanism of analgesic effect induced by Sandostatin administration. Headache, by autovaluation test, heart rate frequency, PAO, sistolic and diastolic blood velocity in medial cerebral artery, by utilizing Transcranial Doppler Sonography (SDSV), have been measured before and after saline and after SMS 201-995. GH and beta-endorphin have been also assayed in plasma samples. All patients have shown a rapid and complete improvement in headache after Sandostatin administration. At the same time we have observed an increase in SDSV and a parallel slight increase in PAO values, more evident in the diastolic phase. Plasma beta-endorphin assay has shown rather conflicting results after SMS 201-995 administration. Our results confirm an important and rapid analgesis effect of Sandostatin on acromegaly headache unrelated to GH normalization. The cerebral emodinamic changes suggest their involvement in Sandostatin induced analgesia.
 ...
PMID:[Analgesic effect of Sandostatin (SMS 201-995) in acromegaly headache]. 227 13

The present work reviews neurochemical, physiological and behavioral data recorded from the attacked mouse and integrates them into a model of coping mechanisms during social conflict. More specifically, the possible relationships between systems of pain, memory and defense are presented, with special emphasis on the role of endogenous opioid peptides (EOPs). In recipients of attack, decreased beta-endorphin-like immunoreactivity and changes in opiate and benzodiazepine binding characteristics are found in structures of the brain defensive system. EOPs mediate the social conflict-induced increase of dopamine synthesis in the periaqueductal grey and frontal cortex. Social conflict analgesia in attacked mice is under the control of central opioid and nonopioid (e.g., benzodiazepine, glutamate) mechanisms, and is modified by experience (e.g., long-term analgesic reaction; tolerance). EOPs and pain-inhibitory mechanisms participate in the organization of behavioral defense, recuperative behavior and the memory of attack experience. The data are considered in relation to the perceptual-defensive-recuperative model of fear and pain, forwarded by Bolles and Fanselow.
 ...
PMID:An ethological model for the study of activation and interaction of pain, memory and defensive systems in the attacked mouse. Role of endogenous opioids. 228 85

We studied the cerebrospinal fluid (CSF) and plasma concentration-time profiles of morphine, methadone, and beta-endorphin after lumbar epidural or intrathecal injection in 17 patients with cancer. After epidural injection, all three drugs reached peak levels in lumbar CSF within 34 minutes that were 50 to 1300 times higher than free drug concentrations in plasma. The rate of decline of CSF levels correlated with drug lipid solubility (methadone [t1/2 = 73 minutes] greater than morphine [126 minutes] greater than beta-endorphin [317 minutes]). Plasma levels were comparable with those after intragluteal injection of the same dose. In four patients given intrathecal morphine or methadone, CSF at the C1-2 level contained high levels of morphine as early as 1 hour after injection, but levels of methadone were lower or undetectable. Three of 17 patients reported improved analgesia initially, but none were improved at 2 weeks after chronic therapy. We conclude that analgesia induced by intrathecal or epidural morphine injections is caused by drug acting at both spinal and supraspinal sites. The use of spinal opiates such as morphine is of limited value in patients whose pain is not adequately managed by high systemic doses of morphine-like drugs.
 ...
PMID:Epidural and intrathecal opiates: cerebrospinal fluid and plasma profiles in patients with chronic cancer pain. 241 86

Pain sensitivity of food and/or water-deprived male mice was tested on a hotplate. The most pronounced analgesia ensued in animals given no food and water, and no food but water ad libitum, the least one in water-deprived mice. The magnitude of the rise in pain threshold depended on the duration of deprivation and was correlated with the increase in the blood plasma beta-endorphin level. In the hypothalamus beta-endorphin level increased after 72-h food deprivation only. The level of dynorphin remained unchanged. Naloxone (10 mg/kg) almost completely reversed food or water-deprivation induced analgesia.
 ...
PMID:The effect of food and water deprivation on post-stress analgesia in mice and levels of beta-endorphin and dynorphin in blood plasma and hypothalamus. 242 64

Conjugate of horseradish peroxidase and wheat germ agglutinin (HRP-WGA conjugate) was injected into the midbrain central gray (MCG) of three adult rats. Frontal sections of the diencephalon were first treated with diaminobenzidine and hydrogen peroxide to detect the retrogradely transported conjugate. They were then stained immunohistochemically to detect pro-opiomelanocortin (POMC)-derived peptides (ACTH, beta-endorphin and alpha-MSH). The coexistence of the three POMC-derived peptides was confirmed by the immunohistochemistry of three consecutive sections stained with antiserum specific to each peptide. Some of the neuronal perikarya distributed in and around the arcuate nucleus were positive to the immunohistochemical stain for POMC-derived peptides, and, concomitantly, were labeled with HRP-WGA conjugate, which indicated that they projected to the MCG. They were mostly concentrated in the rostral three-fifths of the arcuate nucleus. The finding that some of the POMC neurons in the arcuate nucleus project to the midbrain central gray deserves interest, because the central gray is involved in analgesia induced by opioid peptides.
 ...
PMID:Projection of pro-opiomelanocortin neurons from the rat arcuate nucleus to the midbrain central gray as demonstrated by double staining with retrograde labeling and immunohistochemistry. 245 87

Substance P (SP) injected intracerebroventricularly (ICV) into rabbits caused dose-related thermal analgesia with the maximum effect after 2 micrograms. The analgesia was measured by timing the withdrawal of the rabbit's ear from an infrared beam. Equimolar amounts of the related peptides physalaemin and eledoisin-related peptide also caused analgesia, but the SP N-terminal fragment (1-9) was inactive. This suggests that the analgesic message of SP resides within the C-terminal fragment. The analgesia caused by each peptide developed more rapidly but did not last as long as that after central injection of beta-endorphin. In separate experiments, 2 micrograms SP injected ICV increased blood pressure and decreased heart rate. The analgesic, bradycardic and pressor responses to central administration of SP were opposite to effects of peripherally administered SP, described previously. These results indicate that the effect induced by SP depends upon its specific neuroanatomical site of action.
 ...
PMID:Analgesic and cardiovascular effects of centrally administered substance P. 245 73

Ten Type A and 10 Type B individuals exercised for 20 minutes on a bicycle ergometer at 40%, 60%, and 80% of maximal capacity to determine if differences in neuroendocrine reactivity exist. Pre-exercise plasma concentrations of beta-endorphin and epinephrine were similar for Type As and Type Bs. Pre-exercise plasma levels of norepinephrine tended to be higher for the Type As (p less than 0.07). Post-exercise plasma epinephrine concentrations were similar for As and Bs for all trials. The 40% and 60% trials resulted in no differences in post-exercise norepinephrine and beta-endorphin levels for the Type As and Bs. Conversely, the 80% trials resulted in significantly greater norepinephrine and beta-endorphin concentrations for the Type As (p less than 0.05). Plasma serotonin levels at rest and during exercise were always lower for the Type As (p less than 0.05). These results suggest that our Type As had a greater neuroendocrine response to high-intensity exercise than our Type Bs. The greater reactivity and analgesia may allow the Type A person to suppress feelings of fatigue, thus enduring higher levels of exertion for longer periods of time.
 ...
PMID:Neuroendocrine responses of type A individuals to exercise. 252 38

1. The antinociceptive effect of compound 48/80 was reversed by the pretreatment with an angiotensin-converting enzyme (ACE) inhibitor, Hoe 498, in a dose-dependent manner and with a opiate receptor antagonist, naloxone (5.0 mg/kg, s.c.) in rats. 2. The increase of plasma beta-endorphin-like immunoreactivity produced through s.c. administration of compound 48/80 was attenuated by the pretreatment with Hoe 498 but not with naloxone. 3. The present data suggest the possible involvement of renin-angiotensin system in compound 48/80-induced analgesia in rats.
 ...
PMID:The role of renin-angiotensin system in compound 48/80-induced analgesia in rats. 252 74


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>