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)

[125I]Corticotropin-releasing factor binding was measured in membrane homogenates prepared from the anterior pituitary, frontal cortex, motor cortex, somatosensory cortex, mesolimbic area (olfactory tubercle and nucleus accumbens), caudate putamen, hypothalamus, midbrain, and cerebellum from control and chronically stressed rats. The stressor consisted of 3 or 14 days of around-the-clock intermittent foot-shock (approximately one trial per 5-min frequency) that could be avoided or escaped on 90% of the trials presented by pulling a ceiling chain. Plasma corticosterone levels were almost doubled in stressed rats following 3 days of chronic stress and remained significantly elevated in rats stressed for 14 days as compared to controls. Plasma corticotropin levels were similar in controls and stressed animals in both the 3- and 14-day experiments. [125I]Corticotropin-releasing factor binding was decreased in anterior pituitary and frontal cortex following 3 days of chronic stress; binding affinity of anterior pituitary membranes was not different between control and stressed animals. [125I]Corticotropin-releasing factor binding was similar in control and 3-day-stressed animals in the other brain areas examined. After 14 days of chronic stress, hypothalamic [125I]corticotropin-releasing factor binding was decreased in stressed rats as compared to control animals but no other differences were seen. The decrease in the apparent number of anterior pituitary corticotropin-releasing factor receptors following 3 days of stress may be due, in part, to increased plasma corticosterone levels and/or increased corticotropin-releasing factor secretion during that time.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of chronic stress on anterior pituitary and brain corticotropin-releasing factor receptors. 838 81

In order to elucidate the effects of MPTP on enkephalinergic neurons, dopamine (DA), norepinephrine (NE), proenkephalin (PE) mRNA and met-enkephalin (ME) were measured in striatum, olfactory tubercle, and prefrontal cortex of C57/B16 mice 1 day-2 weeks following treatment with 96 mg/kg MPTP HCl (24 mg/kg i.p., twice/day for 2 days). DA and its metabolites were depleted 70% in striatum and 40% in olfactory tubercle within 1 day. In cortex, DA was unchanged, whereas homovanillic acid and NE were depleted 50 and 40% respectively by 3 days. ME increased in all three brain regions at different times whereas PE mRNA showed a different pattern in each region, with an increase in olfactory tubercle, a decrease in cortex, and in striatum, a decrease at 1 day followed by an increase at 3 days. Thus enkephalinergic neurons in each region respond differently to MPTP treatment. In striatum and olfactory tubercle. DA is depleted sufficiently to release its tonic inhibition on the enkephalinergic neurons, thereby leading to increased enkephalin synthesis. In cortex, the change in NE metabolism appears to cause a decrease of ME release and thereby a depression of PE synthesis. The possible relationship between these results and the changes observed in Parkinson's disease are discussed.
 ...
PMID:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) effects on enkephalinergic neurons in various regions of mouse brain. 843 70

This paper addresses the evidence for the face, construct, and criterion-related validity of the olfactory-limbic/neural sensitization model for multiple chemical sensitivity (MCS). MCS is a poorly-understood, controversial condition in which low levels of environmental chemicals are reported to trigger disabling levels of illness in certain individuals. Neural sensitization processes could generate an endogenous amplification of responsivity to exogenous substances, thereby providing a plausible explanation for the apparent lack of a classical toxicological dose-response relationship in MCS. Convergent data from both survey and psychophysiological studies of MCS patients and of persons from the community without MCS, but who report elevated frequency of illness from chemical odors (cacosmics), support the involvement of the limbic system and the sensitizability of cacosmics, as predicted by the model. Recent studies show that cacosmics do sensitize their heart rate, blood pressure, and plasma beta-endorphin responses to repeated exposures to a novel laboratory procedure involving dietary manipulations over time. Cacosmia may represent a pathological form of neural plasticity. Taken together, the model and the available evidence suggest the need for more intensive investigation of MCS from the standpoint of possible neurobiological mechanisms affecting cognitive, emotional, and somatic functions.
 ...
PMID:Clinically relevant EEG studies and psychophysiological findings: possible neural mechanisms for multiple chemical sensitivity. 871 27

Melanocortin peptides are reported to antagonize opiate dependence and tolerance, but the neural substrates underlying these actions are unknown. In this study, we characterize the rat melanocortin-4 receptor (MC4-R) and demonstrate that this receptor is regulated by opiate administration. The rat MC4-R is 95% identical to the human MC4-R, and the potency of melanocortin peptides to stimulate cAMP production is similar in these two species homologs (alpha-melanocyte-stimulating hormone = adrenocorticotropic hormone > gamma-melanocyte-stimulating hormone). Expression of MC4-R mRNA was found to be enriched in the striatum, nucleus accumbens, and periaque-ductal gray, all of which are regions implicated in the behavioral effects of opiates. In contrast, MC1-, MC3-, and MC5-R are expressed at very low or undetectable levels in these brain regions. Chronic administration of morphine (5 days) resulted in a time-dependent down-regulation of MC4-R mRNA expression in the striatum and periaqueductal gray. Expression of MC4-R mRNA was also decreased in the nucleus accumbens/ olfactory tubercle, but this effect was observed after 1 or 3 days of morphine treatment. In the striatum, the reduction of MC4-R mRNA was accompanied by a concomitant decrease in melanocortin receptor levels, shown by quantitative radioligand binding and autoradiography. In contrast, morphine administration did not influence levels of MC4-R mRNA in several other brain regions, including frontal cortex, olfactory bulb, hypothalamus, and ventral tegmentum/substantia nigra. In light of previous findings that melanocortins antagonize opiate self-administration, analgesic tolerance, and physical dependence, we hypothesize that decreased melanocortin function, via down-regulation of MC4-R expression, may contribute to the development of these opiate-induced behaviors.
 ...
PMID:Morphine down-regulates melanocortin-4 receptor expression in brain regions that mediate opiate addiction. 879 97

Observations on developmental actions of melanotropic peptides in nervous system have been difficult to interpret in the absence of data on receptor ontogeny. We investigated binding of [125I]Nle4,D-Phe7-alpha-MSH ([125I]NDP) in developing Long Evans rats from gestational day (E) 13 by quantitative autoradiography. Regional [125I]NDP binding characteristics were assessed by competition experiments in early postnatal brain. The study revealed region- and stage-specific, often transient ontogenetic patterns. Sympathetic ganglia exhibit high [125I]NDP binding from E13, with a peak in superior cervical ganglion at E16-E18. The first central [125I]NDP binding sites transiently appear in parts of thalamus between E13 and E15. The early fetal period is characterized by prominent peaks of receptor density in somatosensory and viscerosensory nuclei (trigeminal sensory nuclei, solitary tract nucleus), paralleled by receptor expression in 5th, 7th, 9th and 10th cranial nerve ganglia. During late fetal life, receptor density peaks in dorsal motor nucleus of vagus and inferior olive; binding sites transiently appear in cerebellum. Caudate-putamen, nucleus accumbens, olfactory tubercle and septohippocampal nucleus show a high perinatal maximum. Starting with late fetal piriform cortex, [125I]NDP binding peaks sequentially in cerebral cortical areas, with highest levels in entorhinal cortex. Preoptic, septal, hypothalamic and amygdaloid areas known for elevated receptor densities in adulthood, exhibit a slow, peri- and postnatal receptor ontogeny. Temporal relations to regional developmental processes support the idea of a role of melanocortins during ontogeny.
 ...
PMID:Region- and stage-specific patterns of melanocortin receptor ontogeny in rat central nervous system, cranial nerve ganglia and sympathetic ganglia. 882 81

In recent years much has become known about the substrates in the brain involved in the regulation of masculine sexual behavior and the involvement of specific neurochemicals in these brain areas. In the present paper the experimental data concerning the involvement of a number of brain areas in sexual behavior are reviewed, in relation to an incentive motivational theory of sexual behavior. The review is restricted to the involvement of opioids and dopamine, of which the role in sexual motivation and behavior is best documented. Opioids in the medial preoptic area (mPOA) impair sexual performance, although the endogenous opioids systems may be quiescent in normal, sexually active rats. Dopamine in the mPOA has a facilitative role in the masculine sexual performance. The corticomedial amygdala is involved in processing of sensory information, especially olfactory stimuli, which are subsequently directed towards the mPOA. Local beta-endorphin infusion interferes with this processing. Endogenous opioids in the ventral tegmental area activate the mesoaccumbens dopamine system and stimulate the sexual motivation. Increased dopamine transmission in the nucleus accumbens correlates with increased sexual motivation and vice versa. The basolateral amygdala plays an essential role in the association of environmental stimuli with reward and therefore in the expression of conditioned sexual motivation. Finally, the reviewed data are integrated and a comprehensive view on the relations between various neural substrates is composed.
 ...
PMID:Regulation of masculine sexual behavior: involvement of brain opioids and dopamine. 886 73

The sexual motivation and performance of male rats were observed in a bilevel testing chamber after bilateral infusion of 40 pmol beta-endorphin, 2.75 nmol naloxone or saline into the ventral tegmental area for four succeeding, weekly tests. In the 5 min prior to introduction of the female rat, the male rat explores the bilevel testing chamber. It was previously shown that the increase over tests of these anticipatory level changes is sexually motivated and a response to olfactory stimuli. Naloxone infusion into the VTA prevented the increase of anticipatory level changes. beta-Endorphin failed to affect the anticipatory level-changing behavior. The sexual performance was unaffected by naloxone or beta-endorphin treatment, but the number of ejaculating rats decreased with repeated testing after naloxone treatment. It is concluded that endogenous opioid systems in the ventral tegmental area contribute to the stimulation of sexual motivation and/or reward, presumably by stimulating the mesolimbic dopamine system in response to sex-related olfactory stimuli.
 ...
PMID:Sexual motivation: involvement of endogenous opioids in the ventral tegmental area. 887 73

Male Fischer rats received either methadone (a long-acting opioid agonist, 10 mg/kg/day) or saline (24 microliters/day) subcutaneously by osmotic minipumps for 7 days. Chronic steady-state methadone administration did not alter (a) corticotropin-releasing factor (CRF) mRNA in the hypothalamus, (b) proopiomelanocortin (POMC) and CRF type 1 receptor (CRF-R1) mRNAs in the anterior lobe and neurointermediate/posterior lobe of the pituitary, or (c) circulating levels of corticosterone. No change was found in levels of either POMC mRNA in the hypothalamus and amygdala, or CRF mRNA in the frontal cortex, olfactory bulb and amygdala. These results demonstrate that neither the activity of the hypothalamic-pituitary-adrenal axis, nor the beta-endorphin and CRF systems in the brain, are altered by steady-state occupancy of opioid receptors with the long-acting opioid agonist methadone.
 ...
PMID:Steady-state methadone in rats does not change mRNA levels of corticotropin-releasing factor, its pituitary receptor or proopiomelanocortin. 896 Aug 61

Alpha-melanocyte-stimulating hormone (alpha-MSH) and adrenocorticotropin (ACTH) promote habituation of prey-catching behavior in toads. We tested the hypothesis that habituation is associated with alterations in the activity of alpha-MSH neurons in a toad, Bufo cognatus. We used immunocytochemistry and RIA to determine the organization and distribution of alpha-MSH neurons in the brain. In addition, we measured brain alpha-MSH and plasma concentrations in toads at different times before and during stimulus specific habituation of the turning response to a rotating prey dummy. Cell groups immunoreactive for alpha-MSH-/and ACTH were detected only in the infundibular hypothalamus. Projections from these cells innervated the olfactory nucleus, nucleus accumbens, septum, habenular nucleus, the preoptic area, the hypothalamus, the caudal thalamus, optic tectum and brain stem. The rank order of alpha-MSH concentrations in the brain of Bufo cognatus was caudal thalamus/hypothalamus (T/HT) > preoptic area (PO) > or = rostral telencephalon (Tel) > brain stem (BS) > optic tectum (OT). The only difference observed in tissue alpha-MSH levels between habituated and non-habituated toads was an elevation in T/HT alpha-MSH levels in control toads after 20 min in the testing apparatus. In contrast, many differences were observed in both groups as a function of time spent in the test apparatus. Concentrations of alpha-MSH in the T/HT and PO increased while concentrations in the Tel decreased over time for both control and habituated toads. Plasma alpha-MSH titers rose over time in control toads but not in habituated toads. Our findings suggest that habituation per se is not associated with dramatic alterations in brain or plasma alpha-MSH levels. On the other hand, prolonged confinement causes pronounced alterations in the activity of brain and pituitary proopiomelanocortin cells.
 ...
PMID:Alterations in brain and plasma concentrations of alpha-melanocyte-stimulating hormone during habituation of prey-catching behavior in toads. 906 93

The data reviewed establish the presence and important role in body fluid homeostasis of brain atrial natriuretic peptide (ANP) in all vertebrate-species examined. The peptide is localized in neurons in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation, and its receptors are located in regions that contain the peptide. Most, if not all, of the actions of ANP are mediated by activation of particulate guanylyl cyclase with generation of guanosine 3',5'-cyclic monophosphate, which mediates its actions in brain as in the periphery. Although atrial stretch releases ANP from cardiac myocytes, the experiments indicate that the response to acute blood volume expansion is markedly reduced after elimination of neural control. Volume expansion distends baroreceptors in the right atria, carotid-aortic sinuses, and kidney, altering afferent input to the brain stem and hence the hypothalamus, resulting in stimulation via ANPergic neurons in the hypothalamus of oxytocin release from the neurohypophysis that circulates to the right atrium to stimulate ANP release. The ANP circulates to the kidney and induces natriuresis. Atrial natriuretic peptide also induces vasodilation compensating rapidly for increased blood volume by increased vascular capacity. Atrial natriuretic peptide released into hypophysial portal blood vessels inhibits release of adrenocorticotropic hormone (ACTH), thereby decreasing aldosterone release and enhancing natriuresis. Furthermore, the ANP neurons inhibit AVP release leading to diuresis and decreased ACTH release. Activation of hypothalamic ANPergic neurons via volume expansion also inhibits water and salt intake. These inhibitory actions may be partially mediated via ANP neurons in the olfactory system altering salt taste. Atrial natriuretic peptide neurons probably also alter fluid movement in the choroid plexus and in other brain vascular beds. Therefore, brain ANP neurons play an important role in modulating not only intake of body fluids, but their excretion to maintain body fluid homeostasis.
 ...
PMID:Atrial natriuretic peptide in brain and pituitary gland. 911 21


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