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

Corticotropin-releasing factor (CRF) injected into the cerebral ventricles of small mammals induces EEG limbic seizures, behavioral excitability, stereotyped behavior, and tardive enhancement of hippocampal theta voltage and frequency. Because we addressed this phenomenon when we explained the pathogenesis of infantile spasms in children, we wished to study the interference exerted by some gamma-endorphin fragments on EEG epileptiform and behavioral symptoms induced by CRF in the rabbit. Animals were implanted intracerebroventricularly (i.c.v.) with semichronic cortical and hippocampal electrodes, together with a cannula into the left lateral ventricle. When some gamma-endorphin derivatives (DT gamma E, DE gamma E) were injected intravenously (i.v.) for 4 days (or hydrocortisone once), they prevented the EEG ictal seizures induced in the hippocampus of rabbits by CRF injected i.c.v. Hydrocortisone and DE gamma E also prevented the appearance of scattered spiking and partially prevented tardive enhancement of theta voltage in the hippocampal EEG. Finally, DE gamma E also prevented stereotyped behavior and excitability induced by CRF. These results confirm the regulatory role exerted by CRF in limbic structure excitability and suggest that the above peptides may be involved in a regulatory feedback mechanism of CRF metabolism or activity. The possibility that these peptides may also have interesting antiepileptogenic properties should be considered.
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PMID:Some endorphin derivatives and hydrocortisone prevent EEG limbic seizures induced by corticotropin-releasing factor in rabbits. 170 Sep 51

Cerebrospinal fluid (CSF) from 7 patients with infantile spasms (mean age: 6.7 months) was collected before and after treatment with adrenocorticotropic hormone (ACTH). The concentration of neurotransmitter metabolites was analyzed using high-performance liquid chromatography and compared to the metabolite concentration in the CSF from 7 age-matched controls (mean age: 6.1 months). Pretreatment levels of CSF 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid, 3-methoxy-4-hydroxyphenyl glycol (MHPG), and kynurenine were significantly lower in infantile spasm patients compared to controls. Following treatment, marked increases in 5-HIAA and decreases in kynurenine levels were observed in the CSF of the 5 infants whose seizures were eliminated or reduced by ACTH. In the 2 nonresponders 5-HIAA levels decreased. The level of MHPG was reduced slightly in 5 infants, including the 2 nonresponders, and was increased in 2 responders. CSF homovanillic acid levels increased in 4 infantile spasm infants and decreased in 3 following ACTH. These data demonstrate that the presence of seizures in infantile spasms is associated with a significant decrease in serotonergic activity and that elimination of seizures by ACTH is accompanied by increased serotonin turnover. The simultaneous increase of 5-HIAA and decrease of kynurenine, an alternate metabolite of tryptophan, suggests an underlying disturbance of tryptophan metabolism in infantile spasms. The possibility that elimination of seizures by ACTH may be related to decreased production of certain kynurenine metabolites, particularly quinolinic acid, is discussed.
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PMID:Changes in CSF neurotransmitters in infantile spasms. 172 2

By means of RIA, the contents of Leu-enkephalin, Met-enkephalin, and Beta-endorphin in CSF of 32 epileptic patients and 24 controls were determined. It was found that the mean Leu-enkephalin content in CSF of the epileptic patient group was significantly higher than that of the control group (P less than 0.01), whereas the mean contents of Met-enkephalin and Beta-endorphin in CSF showed no significant change as compared with those of the control group. The increase of Leu-enkephalin was not related to such factors as type of seizure, age of onset, length of time after the last seizure, taking of antiepileptic drugs, and abnormality in cranial CT manifestation. This suggested that endogenous opioid peptides might take part in the neurochemical mechanism of human epilepsy, and leu-enkephalin could play an important role in the development of epileptic episodes.
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PMID:[Opioid peptides in cerebrospinal fluids of epileptic patients]. 190 3

We have previously shown that procaine and lidocaine stimulate corticotropin-releasing hormone (CRH) secretion by explanted rat hypothalami. This effect was of interest in light of the fact that both lidocaine and CRH administration to experimental animals can produce kindled seizures which cross-sensitize with electrically kindled seizures, and of recent data suggesting that limbic hyperexcitability, perhaps mediated through CRH, may be involved in the pathophysiology of affective illness. Because a prominent effect of the local anesthetics is to decrease neuronal firing by blocking sodium conductance, we were surprised by the capacity of these agents to cause CRH secretion and pituitary-adrenal activation and wished to further elucidate the possible mechanism(s) of these effects. To accomplish this, we first explored the effect of the sodium channel blocker tetrodotoxin (TTX) on basal and stimulated immunoreactive CRH (iCRH) secretion by explanted rat hypothalami. In contrast to procaine and lidocaine, TTX inhibited rather than stimulated iCRH secretion. Moreover, TTX inhibited lidocaine-induced iCRH secretion but had no influence on the response of the CRH neuron to procaine. To explore other potential mechanisms of action, we examined the effect of the calcium channels blocker verapamil and of pharmacologic antagonists to serotonergic, alpha-adrenergic and cholinergic receptors. The latter was particularly of interest because of structural similarities between procaine or lidocaine and acetylcholine (ACh) and because it has been shown that these anesthetic agents interact with the ACh receptor. Verapamil and blockade of serotonergic, alpha-adrenergic and cholinergic receptors did not inhibit the effects of procaine or lidocaine on iCRH secretion, whereas both GABA and dexamethasone exerted inhibitory effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Procaine and lidocaine stimulate corticotropin-releasing hormone secretion by explanted rat hypothalami through a sodium conductance-independent mechanism. 196 16

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.
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PMID:Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy. 203 37

Whether endogenous opioid peptides were involved in the inhibitory action of the hippocampus (HPC) on luteinizing hormone (LH) release was studied examining the effect of naloxone, an opioid antagonist, on the inhibitory action of electrical stimulation of the HPC and also by examining the effect of metenkephalin administration in the HPC, on preovulatory release of LH in proestrous rats. In rats treated with saline at 13:00 h, either sham stimulation or electrical stimulation of the dorsal HPC, which was performed acutely under ether anesthesia, significantly inhibited the afternoon rise in serum LH. In animals treated with naloxone at a dose of 2.0 mg/kg body weight, the afternoon rise in LH appeared smaller than that in the control group. However, statistical analysis showed no significant difference in LH values compared to the control group. Direct administration of met-enkephalin at a dose of 10 micrograms at 13:00 h through a chronically implanted cannula in the HPC did not induce any significant change in the afternoon rise in LH, regardless of whether it induced behavioral seizures or not. The results suggest that opioid peptides in the HPC do not play a significant role in the inhibitory action of HPC on LH release. Opioids existing in areas other than the HPC may play a certain, but small role.
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PMID:The roles of endogenous opioids in the inhibitory action of the hippocampus on preovulatory luteinizing hormone in rats. 208 31

D-Tyr-Ser-Gly-Phe-Leu-Thr (DSLET), beta-endorphin, morphiceptin and morphine were microinjected at 48-h intervals into the amygdala or hippocampus of awake rats in an attempt to identify the opiate receptor types involved in opioid kindling. DSLET, beta-endorphin, morphiceptin and morphine were injected into the lateral ventricle to assess the possibility of kindling seizures by this route. The delta-receptor agonist DSLET effectively kindled convulsions when microinjected into amygdala or ventral hippocampus. The convulsions were suppressed or strongly attenuated by ICI 174,864, a specific antagonist of the delta-receptor, microinjected into the same brain site, but were not affected by ICI 174,864 administered peripherally. When microinjected into amygdala or hippocampus, beta-endorphin and morphiceptin also kindled convulsions, which were antagonized by naloxone but not by ICI 174,864. Morphine evoked EEG epileptiform activity but did not kindle convulsions from limbic brain sites. DSLET occasionally evoked epileptiform spiking and submaximal convulsions when injected into ventricle, and morphiceptin evoked epileptiform spiking only, but tolerance to these effects occurred after repetition of the injections. Thus, convulsions can be kindled by activation of either mu-, delta- or epsilon-receptors when opioids are injected directly into limbic tissue. However, the ability of these compounds to kindle seizures is markedly reduced when they are administered into ventricle. The striking differences between the present results and previous results obtained by peripheral or intraventricular administration of opioid peptides suggest that the route of administration, among other variables, is a crucial factor in assessing the epileptogenic properties of opioid peptides.
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PMID:Involvement of multiple opiate receptors in opioid kindling. 216 33

Propofol is a new anesthetic induction agent that reduces electroconvulsive therapy (ECT) seizure duration. To indirectly investigate the effect of propofol on ECT-induced acute central neurotransmitter changes, we studied neuroendocrine responses in 25 primary depressed subjects treated with ECT under either propofol or thiopentone anesthesia. Blood samples were taken prior to ECT, and then at regular intervals for 2 hr. Only the prolactin response correlated significantly with seizure duration (r = 0.52, p less than 0.01). Subjects given propofol had significantly reduced adrenocorticotropin (ACTH) (p less than 0.01) and cortisol (p less than 0.05) responses compared to thiopentone, which were independent of seizure duration. There was a trend towards a reduction in the prolactin response with propofol compared to thiopentone, but this was dependent upon the diminished seizure duration. The results indicate that propofol affects endocrine responses to ECT by two distinct mechanisms: decreasing prolactin by reducing the seizure duration and decreasing ACTH and cortisol by another process, possibly via a reduction in central noradrenergic activation.
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PMID:Effect of the anesthetic agent propofol on hormonal responses to ECT. 164 24

Corticotropin releasing factor (CRF), injected into the cerebral ventricles (i.c.v.) of rabbits, induced EEG limbic seizures, behavioural excitability, stereotyped behaviour and the tardive enhancement of hippocampal theta voltage and frequency. The beta-endorphin cleavage derivatives des-tyr-gamma-endorphin (DT gamma E) and des-enkephalin-gamma-endorphin (DE gamma E), when injected i.v. for 4 days prevented the EEG ictal seizures induced by CRF in the hippocampus of rabbits and partly prevented the tardive enhancement of theta wave amplitude and frequency. These results suggest the possibility that these peptides may have antiepileptogenic properties.
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PMID:Effects of endorphin derivatives on the EEG alterations induced by corticotropin releasing factor in the rabbit hippocampus. 227 3

The specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29


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