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)

Administration of monosodium glutamate (MSG) in the neonatal period renders the rat to be alpha-MSH deficient later in life. In this study rats received MSG in their neonatal period and were examined at the age of 60 days. alpha-MSH caused hypothermia, potentiated induced hypothermia, blocked paradoxical behavioral thermoregulation, improved performance in the Morris water tank, but had no effect on pain threshold. Melanin only caused an increase in pain threshold. It is suggested that the differential effect of alpha-MSH and melanin is governed by the dopaminergic system.
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PMID:The facilitative effects of alpha-MSH and melanin on learning, thermoregulation, and pain in neonatal MSG-treated rats. 168 21

Neuroendocrine and autonomic responses were assessed in chloralose-anesthetized cats after chemical stimulation of medial brain-stem regions, including those that influence nociceptive input to the medullary or spinal dorsal horn. Microinjections of L-glutamate (0.5 M, 160 nl) were directed at the following rostral and caudal raphe nuclei: the periaqueductal gray (PAG), the dorsal raphe nucleus (DR), the raphe magnus (RM), and the raphe obscurus/raphe pallidus (Ro/Rpa). Activation of DR neurons evoked a significant increase in the adrenal secretion of epinephrine (+2.6 +/- 1.1 ng/min, P less than 0.01) that returned towards prestimulus values by 6 min, whereas microinjections into other raphe nuclei had no consistent effect. Activation of Ro/Rpa neurons evoked an increase in the plasma concentration of adrenocorticotropin (ACTH, +47.9 +/- 12.3 pg/ml, P less than 0.01), whereas microinjections into other raphe nuclei did not affect ACTH. Arterial pressure increased significantly after activation of PAG (+7.5 +/- 2.1 mm Hg, P less than 0.01) or of DR (+4.8 +/- 2.0 mm Hg, P less than 0.05) neurons, whereas heart rate increased significantly (P less than 0.05) after stimulation of cells within the Ro/Rpa. Glutamate microinjections within the RM, a raphe nucleus that exerts a significant descending influence on nociceptive input to the medullary and to the spinal dorsal horns, had no consistent effect on any measured variable. No evidence was seen to suggest that chemical activation of neurons within raphe nuclei inhibited the adrenal secretion of catecholamines or inhibited the release of ACTH. The results indicated that glutamate activation of neurons within different raphe nuclei evoked non-uniform effects on neuroendocrine and autonomic function. Further, these data suggested that the neural substrate underlying the control of the adrenal secretion of catecholamines and of the release of ACTH in response to activation of raphe neurons is likely distinct from that which contributes to the descending influence on nociceptive input to the medullary and spinal dorsal horn.
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PMID:Comparison of the influence of rostral and caudal raphe neurons on the adrenal secretion of catecholamines and on the release of adrenocorticotropin in the cat. 197 77

Corticotropin releasing factor, a 41 amino acid peptide, has been localized in climbing fibers and mossy fibers in the cat's cerebellar cortex. In the present study, corticotropin releasing factor was iontophoretically applied to Purkinje cells, isolated extracellularly, to assess the effect of this peptide on the firing rate of the neuron. By itself corticotropin releasing factor had little or no effect on cellular activity. However, this peptide potentiated the excitatory effects of aspartate and glutamate, the putative neurotransmitters of the climbing fiber and mossy fiber-parallel fiber systems, respectively. In addition, corticotropin releasing factor blocked the suppressive effects induced by the iontophoretic application of GABA. Finally, it shortened or eliminated the period of suppression produced by activation of climbing fibers in the cerebellar cortex. These data suggest that corticotropin releasing factor functions as a neuromodulator rather than as a neurotransmitter in cerebellar circuitry.
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PMID:Neuromodulatory effects of corticotropin releasing factor on cerebellar Purkinje cells: an in vivo study in the cat. 198 66

Despite the variability in sampling and methodology, the majority of the family, twin and adoption studies suggest that alcoholism is familial, a significant proportion of which can be attributed to genetic factors. However, the specific components of alcoholism that may be inherited have yet to be identified. To date, there are no biological trait markers for which there is evidence for specificity for alcoholism. The three major levels of enquiry regarding possible mechanisms for the transmission of alcoholism and the involvement of genes and gene products in its development are factors related to exposure, metabolism, or pharmacological effects of ethanol. Exposure to ethanol is an obvious precondition for the development of tolerance and/or dependence. Therefore, identification of factors which enhance (or decrease) exposure are important goals of studies of the pathogenesis of alcoholism. It is likely that demographic, cultural and environmental factors (i.e. sex, age, religious affiliation, social group influences, income, availability of alcohol, etc.) play a crucial role in mediating exposure to alcohol. The key to alcoholism is likely to reside in the effects of alcohol on the brain. In contrast to nicotine, the opioids, and catecholamines, no specific receptor for ethanol has been found. Thus, one major focus of current research on possible central nervous system (CNS) mechanisms for the effect of alcohol includes assessment of the role of alcohol in the stimulation of brain reward or reinforcement systems. Alternately, alcohol may produce dependence by normalizing abnormal baseline states such as irritability, hyperexcitability, dysphoria, impulsiveness, or stress/tension level. The results of animal studies have yielded information on the central effects of alcohol including sensitivity of neuronal membranes, proteins, and ion channels to alcohol, and factors related to the binding and release of neurotransmitters and neuromodulators including dopamine, norepinephrine, gamma aminobutyric acid, pro-opiomelanocortin, glutamate receptors and the endorphin system (Institute of Medicine, 1987). In addition to possible genetic explanations for the strong degree of familial aggregation of alcoholism, alternative explanations need to be further evaluated. These include: modelling of parental behaviour; possible changes in the susceptibility of the foetus to alcohol as a result of in utero maternal ingestion of alcohol; results of negligent rearing manifested in dietary deficiency, exposure to toxic substances, or brain trauma, which so often characterize the homes of alcoholic parents; or damage to paternal germ cells from alcohol.
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PMID:The genetic epidemiology of alcoholism. 218 16

The amino-terminal fragment of beta-lipotropin (i.e. beta-lipotropin (1-40)) and joining peptide portions of pro-opiomelanocortin have been purified from extracts of bovine posterior pituitaries. Peptides were purified using a combination of reversed-phase and ion-exchange batch extraction procedures followed by reversed-phase high performance liquid chromatography. beta-Lipotropin (1-40) was found to consist of four major components while joining peptide was found to consist of two major components. Fast atom bombardment-mass spectrometric analysis of the tryptic fragments of both peptides revealed that the observed heterogeneity could be explained in terms of post-translational modifications. beta-Lipotropin (1-40) was found to be sulfated at tyrosine residue 28 to an extent of about 50%. The tyrosine residue in beta-lipotropin (1-40) is situated within an amino acid sequence with a preponderance of glutamate residues. Sulfation of this amino acid residue is entirely compatible with the known primary structure requirements of the sulfotransferase enzyme located in the trans-Golgi fraction. Both beta-lipotropin (1-40) and joining peptide were found to have pyroglutamate at their amino termini to an extent of about 50%. The cDNA sequence for bovine pro-opiomelanocortin predicts the presence of glutamic acid at position 1 of both peptides. Pyroglutamate is normally formed through the cyclization of glutamine. This reaction is thought to be catalyzed by a pyroglutamate forming enzyme located within the secretory granule fraction. Under certain circumstances peptides with glutamate at their amino termini may act as substrates for this enzyme.
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PMID:Post-translational modification of bovine pro-opiomelanocortin. Tyrosine sulfation and pyroglutamate formation, a mass spectrometric study. 226 17

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.
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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

Pressor (VLPA) and depressor (VLDA) areas of the ventrolateral medulla were identified by microinjections of L-glutamate in urethane-anesthetized rats. Cardiovascular effects of opiate agonists microinjected into the same sites were then studied. Agents used to stimulate mu, delta, sigma, kappa, and beta-endorphin (epsilon) receptors were morphiceptin, D-Ala2-D-Leu5-enkephalin, N-allyl-normetazocine, dynorphin, and beta-endorphin, respectively. Opiate receptor stimulation in VLPA decreased blood pressure (BP) and heart rate (HR), while in VLDA it increased BP and HR. Thus, it is the site of injection rather than the type of opiate receptor that determines cardiovascular responses. Naloxone, an opiate antagonist, reversed and prevented these responses. Abolition of cardiovascular responses by spinal transection at the C1 level indicated that the sympathetic nervous system mediated these responses. The following mechanism is proposed for these actions of opiates: Cell bodies in VLPA, but not in VLDA, project to the intermediolateral cell column of the spinal cord. Opiates inhibit VLPA and lower BP and HR by decreasing sympathetic outflow. Opiate-induced inhibition of VLDA, which has an inhibitory effect on VLPA, results in an increase in BP and HR.
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PMID:Cardiovascular responses to medullary microinjections of opiate agonists in urethane-anesthetized rats. 242 96

We have developed a dissociated primary cell culture of noradrenergic neurons from the locus ceruleus of postnatal (1- to 5-d-old) mice or rats. Slices of the brain stem were made on a Vibratome. Then the region of locus ceruleus, which was identified by observing the slices under a dissecting microscope, was dissected out from the slices. The removed fragments of brain slices were dissociated and cultured up to 3 weeks on a non-neuronal feeder layer, which consisted predominantly of astroglial cells, or on a fibronectin-treated collagen substratum. After 2 weeks of culture, about 70% of total neuronlike cells revealed positive catecholamine histofluorescence, indicating that they were probably noradrenergic neurons. About 98% of large- and medium-sized cultured neurons (soma diameter greater than or equal to 20 microns) was histofluorescence positive. The fluorescence-positive cells had long processes rich in varicosities, and the shape of their soma was either multipolar or fusiform. Electron microscopy using permanganate fixation revealed that the varicosities along their processes had small granular vesicles, which may contain norepinephrine. Physiological properties of these noradrenergic neurons were investigated with intracellular microelectrodes or with the whole-cell version of the patch clamp. We observed that many cells were producing spontaneous firing. Many of these spontaneously firing cells had no obvious contact with neighboring cells. The neurons were depolarized when glutamate was applied by pressure ejection. They also responded to GABA and glycine with either hyperpolarization or depolarization, and these responses were antagonized by picrotoxin and strychnine. Application of substance P generally produced depolarization with an increase in input resistance. The neurons responded with hyperpolarization to somatostatin, beta-endorphin, and enkephalin. This culture system will become a useful tool for elucidating the cellular and molecular properties of the central noradrenergic neurons.
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PMID:Noradrenergic neurons from the locus ceruleus in dissociated cell culture: culture methods, morphology, and electrophysiology. 243 74

Intracellular recordings from primary mechanosensory neurones (dorsal cells) in the lamprey spinal cord were used to test the membrane effects of a variety of putative neuromodulatory agents. gamma-Aminobutyric acid (GABA) produced a dose-dependent increase in the duration of mixed Na-Ca or pure Ca action potentials in these cells. L-Glutamate and glycine produced minimal broadening of Ca action potentials. Acetylcholine, noradrenaline, serotonin, met-enkephalin, D-glutamate and dopamine had no effect. The pharmacology of GABA's action appeared to be complex. While the GABAA receptor antagonists, bicuculline, picrotoxin and curare, did not block GABA's effect, both the GABAA receptor agonist, muscimol, and the GABAB-receptor agonist, baclofen, occasionally broadened Ca action potentials in these cells. GABA had no effect on the resting potential, passive current-voltage (I-V) characteristics and pure Na action potential of dorsal cells, ruling out an action on passive membrane channels, transmitter-activated channels, or on those voltage-dependent channels activated during the Na action potential. Thus, GABA affected dorsal cells only when a significant Ca current was evident. GABA appeared not to increase the conductance of the Ca channels since its action was accompanied by an increase in input resistance, suggesting an inhibition of Ca-dependent conductance that normally acts to repolarize the membrane during a Ca action potential. An inhibitory effect of GABA on a Ca-dependent Cl conductance was ruled out in experiments where the Cl gradient was altered by removal of extracellular Cl without affecting GABA-induced Ca action potential prolongation. Dorsal cells have a prominent Ca-dependent K conductance (gK(Ca], and it is this conductance that GABA may inhibit. Consistent with this was the observation that the hyperpolarizing after-potential that follows Ca action potentials in dorsal cells, which reflects gK(Ca) in these cells and whose duration is normally increased when the Ca action potential duration increases, was not prolonged when the Ca action potential was broadened by GABA. Further, the failure of GABA to prolong Ba action potentials was consistent with this proposed mechanism of action, since Ba apparently does not activate gK(Ca) in these cells. Forskolin, a specific adenylate cyclase activator, caused broadening of Ca action potentials in lamprey dorsal cells comparable in magnitude to that of GABA. Thus, an increase in intracellular cyclic AMP is a candidate for the intracellular mediator of GABA's effect on these cells.
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PMID:Prolongation of calcium action potentials by gamma-aminobutyric acid in primary sensory neurones of lamprey. 243 26

1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) injection of beta-endorphin on arterial blood pressure (BP) in rats that received five intraperitoneal injections of monosodium glutamate (MSG) on alternate days in the first 10 days of life were studied. 2. beta-endorphin administered into the lateral ventricles caused a prolonged elevation in BP, whereas i.c. injection of the peptide resulted in an even longer lasting reduction in BP. In the MSG-treated rat, the prolonged hypertensive effect of i.c.v. injection of beta-endorphin was completely abolished, but the effect of i.c. injection of the peptide was the same as that in the control. Since MSG treatment destroyed selectively the structures around the third ventricle, it is suggested that these structures, including the arcuate nucleus, may be responsible for mediating the cardiovascular effects of beta-endorphin. 3. The effects of central administration of beta-endorphin were completely blocked by naloxone, which mainly antagonizes the actions of mu-receptor agonists and has no cardiovascular effects itself. The results suggest that mu-receptors may be involved in mediation of the effects of beta-endorphin on the cardiovascular system and that beta-endorphin in the brain may not exert a tonic influence on the cardiovascular functions.
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PMID:Cardiovascular effects of central administration of beta-endorphin in rats receiving neonatal injection of monosodium glutamate. 252 63


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