beta-endorphin and Bipolar-Disorder

Topics: beta-Endorphin; Bipolar Disorder; Brain; Clinical Trials as Topic; Depressive Disorder; Double-Blind Method; Endorphins; Humans; Injections, Intravenous; Injections, Spinal; Renal Dialysis; Schizophrenia

Topics: Affective Disorders, Psychotic; Animals; beta-Endorphin; Bipolar Disorder; Clinical Trials as Topic; Double-Blind Method; Endorphins; Growth Hormone; Humans; Hydrocortisone; Methylphenidate; Models, Psychological; Naloxone; Prolactin; Schizophrenia

Previous studies by a number have investigators have documented a decreased adrenocortotropic hormone (ACTH) and beta-lipotropin/beta-endorphin (beta-End) response to ovine corticotropin-releasing factor (oCRF) in depressed patients. Since depressed patients demonstrate higher plasma cortisol concentrations at the time of oCRF challenge, it is difficult to determine if the decreased ACTH response is due to enhanced negative feedback of cortisol on ACTH release or an alteration in CRF receptors in depressed patients. To evaluate the response to oCRF in an "open feedback loop" system, we administered metyrapone 750 mg at 4 PM and 7:30 PM, followed by administration of oCRF 0.3 microgram/kg at 8 PM in 10 normal controls and 10 depressed patients. Administration of metyrapone at this time in the circadian rhythm clamped plasma cortisol concentrations to less than 2 micrograms/dl but did not result in rebound ACTH or beta-End secretion in control subjects. In control subjects, metyrapone administration produced a 85% blockade of the cortisol response as well as a 3-fold greater beta-End response compared to administration of the same dose of oCRF without metyrapone. The 10 depressed patients and their matched controls demonstrated identical beta-End responses (integrated response for controls = 291 +/- 61, for patients = 352 +/- 86) and cortisol responses (integrated response for controls = 187 +/- 38, for patients = 206 +/- 52) to oCRF following metyrapone pretreatment. These data confirm that corticotroph CRF receptors are normal in depressed patients, and that cortisol feedback plays an essential role in the abnormal ACTH and beta-End response to oCRF in depressed patients.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Circadian Rhythm; Corticotropin-Releasing Hormone; Depressive Disorder; Feedback; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Metyrapone; Personality Inventory; Pituitary-Adrenal System; Receptors, Corticotropin-Releasing Hormone; Reference Values

Topics: beta-Endorphin; Bipolar Disorder; Brain; Clinical Trials as Topic; Depressive Disorder; Double-Blind Method; Endorphins; Humans; Injections, Intravenous; Injections, Spinal; Renal Dialysis; Schizophrenia

Topics: Affective Disorders, Psychotic; Animals; beta-Endorphin; Bipolar Disorder; Clinical Trials as Topic; Double-Blind Method; Endorphins; Growth Hormone; Humans; Hydrocortisone; Methylphenidate; Models, Psychological; Naloxone; Prolactin; Schizophrenia

Topics: Adrenocorticotropic Hormone; beta-Endorphin; Bipolar Disorder; Clinical Trials as Topic; Depression; Dose-Response Relationship, Drug; Double-Blind Method; Endorphins; Half-Life; Humans; Kinetics; Prolactin; Psychiatric Status Rating Scales; Schizophrenia

We aimed to compare neuropeptide levels between patients with major psychiatric disorders and healthy controls and examine their association with symptoms and cognitive function.. The participants were 149 patients with schizophrenia, 115 patients with bipolar disorder (BD), 186 unremitted patients with major depressive disorder (MDD), and 350 healthy controls. Psychiatric (schizophrenic, manic, and depressive) symptoms, sleep state, and cognitive (premorbid intelligence quotient, general cognitive, and memory) functions were evaluated. A multiplex immunoassay kit was used to measure cerebrospinal fluid (CSF) and plasma α-melanocyte-stimulating hormone (MSH), β-endorphin, neurotensin, oxytocin, and substance P levels.. The verification assay revealed that CSF α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were too low to be reliably measured, while plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels could be successfully measured. Plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were not significantly different between patients with schizophrenia, BD, or MDD and healthy controls. Plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were not significantly correlated with psychiatric symptom scores in patients with schizophrenia, BD, or MDD and cognitive function scores in patients or healthy controls.. Our data suggest that plasma neuropeptide levels do not elucidate the involvement of neuropeptides in the pathology of schizophrenia, BD, or MDD.

Topics: alpha-MSH; beta-Endorphin; Bipolar Disorder; Depressive Disorder, Major; Humans; Immunoassay; Neurotensin; Oxytocin; Schizophrenia; Substance P

Despite the well-recognized effects of endogenous opioids on mood and behavior, research on its role in bipolar disorder (BD) is still limited to small or anecdotal reports. Considering that Beta-endorphins (β-END) and Mu-opioid receptors (MOR), in particular, have a crucial activity in affective modulation, we hypothesized their alteration in BD. A cross-sectional study was conducted. We compared: (1) BD type I (BD-I) patients (n = 50) vs healthy controls (n = 27), (2) two BD-I subject subgroups: manic (MAN; n = 25) vs depressed (DEP; n = 25) subjects. Plasma levels of β-END and MOR gene expression in peripheral blood mononuclear cells were analyzed using ELISA Immunoassay qRT-PCR. We found that subjects with BD exhibited a significant upregulation of MOR gene expression and a decrease of β-END (p<0.0001 for both). MAN display higher MOR levels than DEP (p<0.001) and HC (p<0.0001). Plasma levels of β-END were lower in DEP compared to MAN (p<0.05) and HC (p<0.0001). The main limitations are the cross-sectional design and the lack of a group of euthymic subjects. Although preliminary, our results suggest a dysregulation of the endogenous opioid systems in BD. In particular, both MAN and DEP showed a reduction of β-END levels, whereas MAN was associated with MOR gene overexpression.

Topics: beta-Endorphin; Bipolar Disorder; Cross-Sectional Studies; Gene Expression; Humans; Leukocytes, Mononuclear; Receptors, Opioid, mu

Alterations in prolactin and beta-endorphin serum levels after ECT are well-established findings in depression. The present study focuses on electroconvulsive therapy (ECT) response patterns of the mentioned parameters in patients suffering from acute mania.. Following the first three ECTs of a treatment series in 19 patients diagnosed according to DSM-III-R criteria as suffering from mania, blood samples were drawn before, and 20, 30 and 40 minutes after ECT. Serum prolactin and beta-endorphin levels were established in order to gain information about the effects of ECT on different neurotransmitter systems.. A significant transient increase in serum prolactin after ECT was found. Furthermore, in females but not males, delta(max)prolactin diminished over the course of treatment as prolactin baseline levels increased. beta-endorphin levels showed a stable transient increase after ECT stimulus regardless from sex or treatment.. The reported findings reflect those established in depression. This suggests that they are epiphenomenal to ECT.

Topics: Acute Disease; Adult; beta-Endorphin; Bipolar Disorder; Depression; Electroconvulsive Therapy; Female; Humans; Logistic Models; Male; Middle Aged; Prolactin

We studied glucocorticoid receptor autoregulation and corticotropin response to dexamethasone in depressed patients and controls, attempting to control for the confounding effect of endogenous glucocorticoids. After depletion of endogenous cortisol, depressed patients showed an attenuated suppressibility of corticotropin by dexamethasone in the face of unchanged dexamethasone plasma levels. Beta-endorphin levels were strongly correlated with adrenocorticotropic hormone (ACTH) concentrations. Although metyrapone administration resulted in a marked rise of glucocorticoid receptor sites per cell in controls, this effect was not present in depressives. These data support the hypothesis of a decreased glucocorticoid receptor plasticity and a partial steroid resistance in depression.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Dexamethasone; Female; Homeostasis; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Metyrapone; Middle Aged; Pituitary-Adrenal System; Premedication; Psychiatric Status Rating Scales; Receptors, Glucocorticoid

Topics: Adjustment Disorders; Adolescent; Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Dexamethasone; Female; Humans; Hydrocortisone; Male; Middle Aged

Topics: Adult; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Chronic Disease; Circadian Rhythm; Depressive Disorder; Dexamethasone; Endorphins; Female; Humans; Insulin; Male; Middle Aged; Schizophrenia

Topics: Adult; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Middle Aged; Somatostatin

Anomalous anterior pituitary hormone responses to acute administration of TRH and LRH have previously been observed in patients with primary affective disorders (PAD), with TRH eliciting GH, FSH and LH rises, and LRH eliciting GH and Prl rises. We examined whether the same unusual responses were present also for beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) in 15 PAD patients, in 9 patients with secondary affective disorders (SAD), and in 7 controls. TRH (500 micrograms iv) elicited rises of beta-EP plasma levels in 5 PAD and 2 SAD patients, and of beta-LPH in 4 PAD and 3 SAD patients. LRH (150 micrograms iv) elicited rises of plasma beta-EP levels in 2 PAD and 2 SAD patients, and of beta-LPH in 5 PAD and 2 SAD patients. No rises of beta-EP and beta-LPH plasma levels were observed in PAD patients after saline administration, nor in the controls after TRH, LRH or saline administration.

Topics: Adult; Aged; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Growth Hormone; Humans; Luteinizing Hormone; Middle Aged; Pituitary Hormones, Anterior; Prolactin; Thyrotropin-Releasing Hormone

Five peptide fragments of pro-opiomelanocortin (alpha-melanocyte-stimulating hormone, beta-lipoprotin, adrenocorticotropic hormone, beta-endorphin, and the N-terminal fragment of pro-opiomelanocortin) were measured by radioimmunoassay in cerebrospinal fluid (CSF) and plasma from 31 normal volunteers and 26 euthymic lithium-treated bipolar patients (14 of whom provided a second CSF sample in the unmedicated state). With the exception of alpha-melanocyte-stimulating hormone, in the normal volunteers' CSF, levels of these peptides were highly correlated with one another, suggesting that: (1) some common regulatory factor may control the levels of these four peptides in CSF; and (2) CSF alpha-melanocyte-stimulating hormone is independently regulated from the other pro-opiomelanocortin products. Some of these correlations were absent in the patient groups, suggesting subtle alterations in pro-opiomelanocortin processing in manic-depressive illness. No effect of lithium on the CSF levels of these peptides was observed. No group differences were found.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Endorphins; Female; Humans; Lithium; Male; Melanocyte-Stimulating Hormones; Middle Aged; Peptides; Pro-Opiomelanocortin

Topics: beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Psychotic Disorders; Radioligand Assay; Receptors, Opioid; Schizophrenia

Mean plasma levels of beta-endorphin (beta EP), beta-lipotropin (beta LPH) and ACTH were significantly higher in 22 patients with primary affective disorders (PAD) and in 2 schizoaffective subjects off therapy since 10 days than in 22 age- and sex-matched healthy controls. Desimipramine therapy (50-100 mg/day per os for 3-5 weeks) induced in parallel psychological improvement and fall in beta LPH-beta EP in 6 of 8 PAD patients treated, and a normalization of beta EP-beta LPH levels with minimal mood improvement in the 2 schizoaffective subjects. These results indicate that the opioid levels are increased in PAD and schizoaffective patients and normalized by the desimipramine therapy in those patients in whom the affective disorders improved.

Topics: Adrenocorticotropic Hormone; Adult; Affective Disorders, Psychotic; Aged; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Desipramine; Endorphins; Female; Humans; Male; Middle Aged; Psychotic Disorders

A patient with a disseminated malignancy received 3 mg of synthetic beta-endorphin administered intrathecally by lumbar puncture. A marked behavioral syndrome characterized by confusion, hypomanic/manic behavior, and psychosis followed drug administration and persisted for more than 2 days.

Topics: beta-Endorphin; Bipolar Disorder; Confusion; Endorphins; Female; Humans; Injections, Spinal; Middle Aged; Neoplasms; Palliative Care; Psychoses, Substance-Induced

beta-Endorphin immunoreactivity was measured in cerebrospinal fluid of 75 medication-free subjects: normal, depressed, schizophrenic, and anorexic. No significant differences in beta-endorphin immunoreactivity were found. Affinity extraction chromatography revealed beta-lipotropin and beta-endorphin, but no apparent precursors.

Topics: Adolescent; Adult; Affective Disorders, Psychotic; Aged; Anorexia Nervosa; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Middle Aged; Reference Values; Schizophrenia

Beta-Endorphin (0.3 or 0.6 nanomoles) was infused into the A10-ventral tegmental area (VTA) of male Wistar rats previously treated for 6 days with either morphine sulfate or lactose via subcutaneously implanted silastic pellets. Beta-Endorphin microinfusions occurred at 24 and 96 hours after pellets were removed. Profound changes in locomotor response to beta-endorphin were found, with morphine-pretreated rats showing a spontaneous switch from hyporesponsiveness to hyperresponsiveness over 72 hours, compared to lactose-pretreated controls. These findings may reflect on current biochemical theories regarding the "switch" process in bipolar affective disease. The data can be viewed within a heuristic model of receptor changes which may underlie the transition from depression to mania.

Topics: Affective Disorders, Psychotic; Animals; beta-Endorphin; Bipolar Disorder; Dextroamphetamine; Disease Models, Animal; Endorphins; Humans; Limbic System; Male; Morphine; Motor Activity; Naloxone; Neural Pathways; Rats; Rats, Inbred Strains; Receptors, Dopamine; Substance Withdrawal Syndrome; Tegmentum Mesencephali

In this paper we have reported the results of studies in psychiatric patient groups using the strategy of measuring opioid activity and beta-endorphin (ir) in CSF. Our findings do not lend support to the notion of excess endorphin activity in schizophrenia, but rather suggest the possibility of a decrease in endogenous opioid activity in some schizophrenic patients. In affectively ill patients our data suggest that there may be a relative change in endogenous opioid system activity across state change in manic-depressive illness. Who also found a relationship between nurses' ratings of anxiety and CSF opioid activity in depressed patients, although it is unknown whether this directly relates to the pathophysiology of this symptom, or is related to stress response. The relationship between CSF opioid activity and HPA axis activity, as reflected by urinary free cortisol excretion, supports the notion of important physiologic relationships between these systems and raises the issue of a role for the endogenous opioid system in the abnormal activation of this system in depression. Finally, the finding of increased CSF opioid activity in anorexia nervosa patients when a minimum weight coupled with data relating endogenous opioids to eating behavior raises interesting questions regarding a possible involvement of the endogenous opioid system involvement in this illness.

Topics: Adult; Anorexia Nervosa; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Psychotic Disorders; Schizophrenia

We investigated the relationship between hypothalamic-pituitary-adrenal (HPA) activity, as measured by 24-hour mean urinary free cortisol (MUFC), and cerebrospinal fluid (CSF) opioid activity in patients with major affective disorder and normal volunteers. Among depressed patients, but not normal volunteers, mean 24-hour urinary cortisol values were significantly correlated with CSF opioid activity measured by radioreceptor assay, but were not significantly correlated with beta-endorphin immunoreactivity measured by radioimmunoassay. MUFC, as expected, was significantly higher in depressed patients than in normal volunteers. Mean values of CSF opioid activity and beta-endorphin immunoreactivity did not differ significantly in the two groups. The positive opioid-MUFC correlation found in the depressed group appeared to depend on patients who were cortisol hypersecretors. These data, using relatively crude measures of cortisol and opioid activity, are suggestive of a relationship between these two systems, particularly under "activated" conditions such as those observed in depression.

Topics: Adult; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Hydrocortisone; Male; Radioimmunoassay; Radioligand Assay; Receptors, Opioid

The authors measured total opioid activity by radioreceptor assay in the CSF of 41 normal subjects and 89 unmedicated psychiatric patients, including schizophrenic, schizoaffective, depressed, and manic diagnostic groups. Schizophrenic men had significantly lower levels of opioid activity than the normal men, although these levels did not significantly differ from levels of other male patients. The authors observed higher opioid activity during mania than during depression in paired samples for 4 manic-depressive patients. beta-Endorphin immunoreactivity in a subsample of the same subjects was no different in the patient group than in the normal group, suggesting that the differences in CSF opioid activity between schizophrenic men and normal patients may be related to opioids other than beta-endorphin.

Topics: Adult; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Mental Disorders; Psychotic Disorders; Radioligand Assay; Receptors, Opioid; Schizophrenia