beta-endorphin and Nervous-System-Diseases

Repetitive transcranial magnetic stimulation (rTMS) is an evidenced based treatment for depression and an emerging treatment for several other neuropsychiatric disorders. The objective of this systematic review was to assess molecular changes produced by rTMS or molecular markers that predict treatment response in neuropsychiatric disorders.. PubMed, PsycINFO, and Embase were searched through July 2019 for studies published in peer-reviewed journals. Eighty-nine studies were identified examining healthy adults and patients with neuropsychiatric disorders including depression, chronic pain, post-stroke deficits, and movement disorders.. Our ability to synthesize the information was limited by the large variability in treatment parameters and a limited number of placebo-controlled studies. While few findings were replicated by multiple strong studies, brain derived neurotrophic factor (BDNF) and gamma aminobutyric acid (GABA) in depression, BDNF in post-stroke deficits, and β-endorphin in chronic pain may be altered by rTMS.. BDNF, GABA and β-endorphin were identified as potential molecular markers of rTMS and warrant further exploration.. This study, which is the first systematic review to examine molecular markers of rTMS in both neurological and psychiatric disorders, provides an updated review of this subject and highlight the need for more placebo-controlled and adequately powered studies to identify biomarkers of rTMS.

Topics: beta-Endorphin; Biomarkers; Brain-Derived Neurotrophic Factor; gamma-Aminobutyric Acid; Humans; Mental Disorders; Nervous System Diseases; Transcranial Magnetic Stimulation

Topics: Adult; Antipsychotic Agents; Apomorphine; beta-Endorphin; Drug Tolerance; Endocrine System Diseases; Endorphins; Female; Genetic Variation; Homovanillic Acid; Humans; Hydrocortisone; Hypothalamus; Luteinizing Hormone; Male; Methoxyhydroxyphenylglycol; Middle Aged; Nervous System Diseases; Norepinephrine; Prolactin; Receptors, Adrenergic, alpha; Receptors, Dopamine; Schizophrenia; Thyrotropin

This review highlights that essentially all of the recently discovered putative central nervous system (CNS) peptides and other peptide substances are measurable in human cerebrospinal fluid (CSF). Preliminary evidence also suggests that peptides in CSF may have an active regulatory role in relation to CNS function and behavior. Even if this is not the case, CSF peptides may prove to be a useful indirect marker of CNS peptide function and metabolism. Alterations in peptides have been reported in neurological and psychiatric illness, pain symptoms and their treatment, symptoms such as anxiety, and following treatment with CNS active drugs such as carbamazepine. CSF methodologies provide a strategy for the study of the interaction of classical neurotransmitters and peptide substances and their relationship to neural function and behavior in man. Assessment of peptides in CSF may supplement post mortem studies of peptide levels and receptor distribution and help lead to new diagnostic and treatment approaches in neuropsychiatric disorders.

Topics: Adrenocorticotropic Hormone; Angiotensins; beta-Endorphin; Calcitonin; Endorphins; Humans; Mental Disorders; Nervous System Diseases; Oxytocin; Peptides; Somatostatin; Substance P; Vasoactive Intestinal Peptide; Vasopressins; Vasotocin

To further investigate the efficacy of progesterone in the treatment of the symptoms of premenstrual syndrome (PMS).. From an initial cohort of 25 subjects diagnosed with moderate to severe PMS, 17 reproductive age females completed the 7-month, double-blind, placebo controlled trial using 200-mg vaginal progesterone suppositories. Multiple modalities for evaluating symptoms were employed, including the Spielberger self-evaluation rating, the Beck depression inventory, and the Hamilton anxiety scale. In addition, each subject was interviewed by a psychiatrist on a monthly basis; ovulation was determined monthly using a basal body temperature chart; serum hormonal assays included beta endorphin, progesterone, follicle stimulating hormone, luteinizing hormone, estradiol, and prolactin.. Hormonal assays confirmed no differences between treatment and control groups. Overall scores on all test vehicles were likewise not significantly different between the two groups; however, in the subcategory of nervous symptoms, a significant improvement was found in symptoms relating to tension, mood swings, irritability, anxiety and lack of control.. Metabolites of progesterone (pregnanolone and allopregnanolone) may play a physiologic role as anxiolytic agents, perhaps modifying mood and anxiety; the current study confirms the utility of twice daily, 200-mg progesterone vaginal suppositories, in the alleviation of some PMS symptoms relating to anxiety and irritability. Further evaluation may be warranted to ascertain which patients in the known heterogeneous PMS population may be most likely to benefit from such treatment.

Topics: Adult; Affect; Anxiety; beta-Endorphin; Body Temperature; Cohort Studies; Double-Blind Method; Estradiol; Female; Follicle Stimulating Hormone; Humans; Irritable Mood; Luteinizing Hormone; Middle Aged; Nervous System Diseases; Pessaries; Premenstrual Syndrome; Progesterone; Prolactin

Topics: Analgesics, Opioid; Animals; beta-Endorphin; Cerebrospinal Fluid; Cisterna Magna; Male; Morphine; Nervous System Diseases; Postoperative Complications; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Specimen Handling; Time Factors; Ultrasonography, Interventional

Plasma and cerebrospinal fluid beta-endorphin concentrations were radioimmunologically assayed in dogs subjected to spinal cord ischemia induced by infrarenal aortic ligature and in control sham-operated dogs. Plasma beta-endorphin levels rose significantly following surgery in control dogs but were unaffected by spinal ischemia. On the other hand, a significant increase in cerebrospinal fluid beta-endorphin concentration occurred after spinal ischemia, while surgical stress had no significant effect. Thus, the origins of plasma and cerebrospinal fluid beta-endorphin may be different, with the former secreted from the hypophysis and the latter from nervous tissue. Observed changes in cerebrospinal fluid beta-endorphin concentration could be related to the ischemic lesion of nervous tissue while the changes in plasma levels may reflect general stressing factors such as the surgery in our experiments.

Topics: Animals; beta-Endorphin; Dogs; Ischemia; Ligation; Nervous System Diseases; Osmolar Concentration; Spinal Cord

Neurological disorders, such as seizures, are not infrequently associated with anti-leukemic therapy. It has been hypothesized that a disrupted peptidergic transmission between neurons could be the cellular basis of the neurological dysfunction. Since endogenous opioids have been recently found to alter neuronal function and possess anticonvulsant properties, the cerebrospinal fluid (CSF) immunoreactive beta-endorphin levels in children with Acute Lymphoblastic Leukemia (ALL) during chemotherapy and cranial irradiation have been studied. Twenty-seven children, 2 at low, 20 at medium and 5 with high risk ALL, undergoing prophylactic treatment for meningeal leukemia, entered the study. Sequential lumbar punctures with introduction of MTX combined with oral prednisone therapy were performed; each lumbar puncture sample was collected and assayed for immunoreactive beta-endorphin. All the patients studied showed a biphasic profile of the peptide with the minimum levels reached during the induction (days 14-28) and the maximum levels detected at the end of the intensification chemotherapy (days 49-55). In the 3 groups the beta-endorphin decrease corresponded to the period of prednisone therapy; the increase was concomitant with the suspension of oral glucocorticoids. 3 patients showed tonic-clonic seizures which coincided with the lowest cerebrospinal fluid beta-endorphin levels and, in the follow-up, 13 out of 27 patients displayed EEG abnormalities. From these findings a relationship between cerebrospinal fluid beta-endorphin concentrations and neuronal excitability in patients with ALL can be suggested. It is also evidenced that oral glucocorticoid therapy has profound inhibitory effects on central beta-endorphin levels.

Topics: Adolescent; Antineoplastic Combined Chemotherapy Protocols; beta-Endorphin; Child; Child, Preschool; Female; Humans; Infant; Male; Nervous System Diseases; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Prednisone; Radioimmunoassay

A number of studies have indicated a relationship between brain peptide activity and sensitivity to the behavioral effects of ethanol. Specifically, it has been suggested that ethanol effects are mediated by changes in the endogenous opioid peptides derived from the proopiomelanocortin (POMC) precursor. Most cell bodies containing brain POMC-derived peptides are found in the arcuate nucleus of the hypothalamus. Neonatal administration of monosodium glutamate (MSG) has been reported to destroy cell bodies of the arcuate nucleus. We treated WSC strain mice on postnatal Day 4 with a single SC injection of 4 mg/g MSG or saline. When adult, MSG and control mice were challenged with an IP injection of ethanol and its effect on body temperature, open field activity, or duration of loss of righting reflex was assessed. Blood ethanol concentration (BEC) was measured and the hypothalamic content of beta-endorphin like immunoreactivity (beta-EP) was determined by radioimmunoassay. beta-EP was markedly reduced in both females and males by MSG treatment. MSG-treated animals of both sexes showed significantly less ethanol-induced hypothermia than controls. BEC was higher in MSG-treated animals of both sexes than in controls, so the differences were not due to ethanol pharmacokinetics. beta-EP was generally lower in males. Duration of righting reflex was prolonged in MSG treated animals, and the reduction in open field activity was potentiated. These latter effects may be in part attributable to the higher BECs achieved in lesioned animals. These data suggest that beta-EP cell bodies in the arcuate nucleus of the hypothalamus mediate neurosensitivity to some effects of ethanol in mice, but further experiments will be necessary to implicate beta-EP specifically.

Topics: Aging; Animals; Animals, Newborn; beta-Endorphin; Body Temperature; Electroshock; Endorphins; Ethanol; Female; Glutamates; Hypothalamus; Male; Mice; Nervous System Diseases; Postural Balance; Radioimmunoassay; Sodium Glutamate