UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The environmental context in which amphetamine or cocaine are administered modulates both their acute psychomotor activating effects and their ability to induce sensitization. Here we report that environmental context differentially affects patterns of amphetamine- and cocaine-induced c-fos mRNA expression in the bed nucleus of the stria terminalis (BST) and amygdala of male rats. In the medial amygdala and medial posterior BST, exposure to novelty resulted in a marked increase in c-fos mRNA. Amphetamine given at home did not induce c-fos mRNA, and when given in the novel environment, did not increase levels beyond that observed for novelty alone. In the basolateral and lateral amygdala, amphetamine or cocaine at home or exposure to novelty induced c-fos mRNA. When amphetamine or cocaine was given in a novel environment the c-fos mRNA response was significantly enhanced. In the central nucleus of the amygdala (CEA) and oval subnucleus of the BST (BSTov), amphetamine administration at home produced a robust increase in c-fos mRNA expression, whereas exposure to novelty had little effect. In contrast to other brain regions examined, the c-fos mRNA response to amphetamine in a novel versus home environment was significantly smaller. In both "home" and "novel" amphetamine groups, c-fos mRNA in the BSTov and CEA was predominantly expressed in enkephalin-containing cells; coexpression with corticotropin-releasing hormone was rare. These data suggest that the context in which psychostimulants are given powerfully and differentially alters the response of limbic structures that have been functionally implicated in drug reinforcement and emotional behaviors.
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PMID:Environmental novelty differentially affects c-fos mRNA expression induced by amphetamine or cocaine in subregions of the bed nucleus of the stria terminalis and amygdala. 1116 Apr 52

In G(0)/G(1) cell cycle-arrested mouse Y1 adrenocortical cells, short pulses (30 min to 2 h) of fibroblast growth factor-2 (FGF2) (5 pM to 1 nM) caused induction of cFos protein by 2 h and onset of DNA synthesis stimulation by 8-9 h. FGF2 dose-response curves for cFos induction (percent labeled nuclei with a specific anti-cFos antibody) and DNA synthesis stimulation (bromodeoxyuridine labeling index) were linearly correlated with a correlation coefficient of 0.969. Inhibition of cFos and cJun protein induction with antisense oligodeoxynucleotides (ODNs) to cfos and cjun mRNAs blocked DNA synthesis stimulation by FGF2. Pulses (up to 2 h) of synthetic ACTH(39) (1 pM to 1 nM) and natural porcine corticotropin A (10 pg/ml to 1 microg/ml) also induced cFos protein and DNA synthesis in G(0)/G(1)-arrested Y1 adrenal cells. ACTH dose-response curves for cFos induction and DNA synthesis stimulation were not correlated. But cfos and/or cjun antisense ODNs blocked DNA synthesis stimulation by ACTH. Thus, signals initiated in FGF2 and ACTH receptors appear to converge to the induction of cfos and cjun genes to trigger DNA synthesis stimulation.
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PMID:cfos and cjun antisense oligonucleotides block mitogenesis triggered by fibroblast growth factor-2 and ACTH in mouse Y1 adrenocortical cells. 1124 Nov 69

Medial parvocellular paraventricular corticotropin-releasing hormone (mPVN CRH) cells are critical in generating hypothalamic-pituitary-adrenal (HPA) axis responses to systemic interleukin-1beta (IL-1beta). However, although it is understood that catecholamine inputs are important in initiating mPVN CRH cell responses to IL-1beta, the contributions of distinct brainstem catecholamine cell groups are not known. We examined the role of nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) catecholamine cells in the activation of mPVN CRH, hypothalamic oxytocin (OT) and central amygdala cells in response to IL-1beta (1 microg/kg, i.a.). Immunolabelling for the expression of c-fos was used as a marker of neuronal activation in combination with appropriate cytoplasmic phenotypic markers. First we confirmed that PVN 6-hydroxydopamine lesions, which selectively depleted catecholaminergic terminals, significantly reduced IL-1beta-induced mPVN CRH cell activation. The contribution of VLM (A1/C1 cells) versus NTS (A2 cells) catecholamine cells to mPVN CRH cell responses was then examined by placing ibotenic acid lesions in either the VLM or NTS. The precise positioning of these lesions was guided by prior retrograde tracing studies in which we mapped the location of IL-1beta-activated VLM and NTS cells that project to the mPVN. Both VLM and NTS lesions reduced the mPVN CRH and OT cell responses to IL-1beta. Unlike VLM lesions, NTS lesions also suppressed the recruitment of central amygdala neurons. These studies provide novel evidence that both the NTS and VLM catecholamine cells have important, but differential, contributions to the generation of IL-1beta-induced HPA axis responses.
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PMID:Dorsal and ventral medullary catecholamine cell groups contribute differentially to systemic interleukin-1beta-induced hypothalamic pituitary adrenal axis responses. 1124

We have previously proposed the existence of ultrashort loop-positive feedback regulation of corticotropin-releasing hormone (CRH) in the hypothalamus. To gain a better understanding of this effect, we performed double-label in situ hybridization to identify the neurons in the paraventricular nucleus (PVN) that express CRH type 1 receptor (CRH-R1) following stress. We also conducted immunohistochemistry to determine whether CRH-R1 mRNA was translated to CRH-R1 protein in the PVN. Thirty-minute restraint stress given to male Wistar rats increased c-fos mRNA expression primarily in the CRH-producing neurons of the parvocellular PVN. Small numbers of vasopressin and oxytoxin-producing cells were also labeled by c-fos probes. Approximately 70% of CRH-R1 positive neurons exhibited CRH mRNA 2 h after the beginning of stress, while only a small percentage of the vasopressin and oxytocin-producing cells coexpressed CRH-R1 mRNA. CRH-R1 immunoreactivity, which was detected in the perikarya and fibers of PVN neurons, appeared to increase in response to stress, though this was not statistically significant. Pretreatment with a selective CRH-R1 antagonist, CP-154,526, significantly attenuated stress-induced corticotropin (ACTH) secretion as well as c-fos mRNA expression in the PVN. These results demonstrate that acute stress increases neuronal activation and CRH-R1 mRNA expression primarily in CRH-producing neurons of the parvocellular PVN, that CRH-R1 message is translated to CRH-R1 protein, and that PVN neurons are activated at least in part through CRH-R1 under acute stress. The data further support the possibility of feedback regulation of CRH itself in CRH-producing neurons.
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PMID:Expression of corticotropin-releasing hormone type 1 receptor in paraventricular nucleus after acute stress. 1139 2

In the developing rodent, there is a period from about days 4 to 14 when the adrenal response to stress is either minimal or non-existent. This has been designated as the stress hyporesponsive period (SHRP). Numerous experiments have demonstrated that maternal factors are critical for the regulation of the pup's hypothalamic--pituitary--adrenal (HPA) axis and the maintenance of the SHRP. Following 24 h of maternal deprivation, the neonatal rat shows elevated basal levels of corticosterone (CORT) and exhibits a robust CORT and ACTH response to mild stress. Further, c-fos mRNA in the paraventricular nucleus (PVN) is enhanced following stress in deprived pups. At least three aspects of maternal behavior play a role in the regulation of the HPA axis during development. Tactile stimulation appears capable of inhibiting most of the brain-related changes that occur following maternal deprivation. Feeding is essential for maintaining the adrenal-unresponsive and reduces the sensitivity of the adrenal to ACTH. Passive contact suppresses the response to stress. In the adult, corticotropin-releasing hormone (CRH) is the major neuropeptide that controls pituitary ACTH secretion. In the maternally deprived pup, CRH gene transcription is downregulated and arginine vasopressin (AVP) appears to assume the major regulatory hormone that modulates ACTH. These data all indicate that maternal factors are responsible for actively inhibiting the endocrine responses to stress postnatally. Thus, during development, most of the peripheral and central stress-responsive systems are capable of being activated. However, under conditions of normal dam-pup interactions, these responses are mostly suppressed by the dam's behavioral interaction with the pups.
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PMID:Primary social relationships influence the development of the hypothalamic--pituitary--adrenal axis in the rat. 1143 50

Using in situ hybridisation with oligonucleotide probes, an expression of immediate early genes c-fos, jun B, c-jun, and NGFIA in the rat brain was studied following intrastriatal microinjection of corticotropin-releasing hormone (CRH). The hormone induced expression of c-fos, jun B, and NGFIA mRNAs in the neostriatum as well as in its target brain areas, including nucleus accumbens and different cortical areas. The expression of c-jun mRNAs was unaffected. The findings indicate that neuronal activation of the neostriatum and its target brain areas provides one possible mechanism for mediating adaptive CRH actions in stress.
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PMID:[Early gene expression in the rat brain following administration of corticoliberin in the neostriatum]. 1153 7

Stressor or cytokine treatments, such as interleukin-1beta, promote time-dependent alterations of hypothalamic-pituitary-adrenal functioning, including increased arginine vasopressin stores within corticotropin-releasing hormone (CRH) terminals in the external zone of the median eminence. Likewise, we have previously shown that the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), provoked a time-dependent sensitization of neuroendocrine and brain monoamine activity. To further explore the protracted consequences of TNF-alpha, the present investigation determined whether the cytokine sensitized activity of neuroendocrine regulatory brain regions, as assessed by c-fos expression, and had protracted consequences on amygdaloid CRH, as well as hypothalamic corticotropin secretagogues. Indeed, immunoreactivity for arginine vasopressin and corticotropin-releasing hormone, and their colocalization within cell terminals of the median eminence, varied over time following an initial 4.0-microg tumor necrosis factor-alpha treatment, peaking after 7 days and normalizing within 28 days. Within the central amygdala, a sensitization effect was evident as reflected by increased CRH immunoreactivity, but this effect required re-exposure to the cytokine, unlike the median eminence changes that simply evolved with the passage of time. As well, tumor necrosis factor-alpha provoked a marked sensitization of c-fos staining within the paraventricular nucleus of the hypothalamus, supraoptic nucleus and the central amygdala. From these data we suggest that tumor necrosis factor-alpha influences responsivity of stressor-reactive brain regions and has protracted effects on central neuropeptide expression within the hypothalamus and central amygdala, although the time course for the effects vary across brain regions. Evidently, exposure to tumor necrosis factor-alpha may promote neuroplasticity of brain circuits involved in mediating neuroendocrine, sickness or inflammatory responses. It is suggested that such a sensitization may influence the response to immunological and traumatic insults and may thus be relevant to behavioral pathology.
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PMID:Time-dependent sensitization of corticotropin-releasing hormone, arginine vasopressin and c-fos immunoreactivity within the mouse brain in response to tumor necrosis factor-alpha. 1156 24

The present study was conducted to investigate the pattern of neuronal activation and corticotropin-releasing hormone (CRH) expression in fed, food deprived and refed lean (Fa/?) and obese (fa/fa) Zucker rats. The pattern of neuronal activation was studied by measuring the expression of the immediate-early gene c-fos. Expression of c-fos and CRH mRNA was determined by in situ hybridization histochemistry. In both lean and obese rats, one hour of refeeding led to a transient increase in c-fos mRNA levels which was detected in the paraventricular hypothalamic nucleus (PVH), the dorsomedial hypothalamic nucleus, the supraoptic nucleus, the paraventricular thalamic nucleus, the central nucleus of amygdala (CeA), the lateral and medial parabrachial nuclei, the nucleus of the solitary tract, and the area postrema. In addition, refeeding led to strong activation of the arginine-vasopressin neurons located in the magnocellular part of the PVH. Following 24 h of food deprivation, CRH expression in the parvocellular division of the PVH was significantly higher in obese rats compared to lean animals. During refeeding, PVH CRH mRNA levels in obese rats decreased to reach control values. The decrease in CRH expression in obese rats was accompanied by the alleviation of the hypercorticosteronemia that characterized obese Zucker rats. CRH mRNA levels in the central nucleus of the amygdala were significantly higher in lean rats than in obese animals, when the rats were fed ad libitum During food deprivation, CeA CRH mRNA levels decreased in lean rats and gradually returned to predeprivation values during refeeding. In refed obese rats, CeA levels of CRH mRNA were higher than those of ad libitum fed or food-deprived obese mutants. In the perifornical region of the lateral hypothalamic area (LHA), the expression of CRH mRNA rose significantly in response to refeeding in lean rats, but not in obese animals. Following the first hour of refeeding, the number of neurons expressing CRH mRNA in the LHA in lean rats almost doubled. The present results demonstrate that refeeding has a stimulating effect in obese Zucker rats in a pattern of activation similar to that seen in lean Fa/? rats. They also demonstrate differences in CRH expression between Fa/? and fa/fa rats after refeeding. The most apparent of these differences was seen in the lateral hypothalamus in which refeeding failed to up-regulate CRH expression in obese rats.
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PMID:Neuronal activation and corticotropin-releasing hormone expression in the brain of obese (fa/fa) and lean (fa/?) Zucker rats in response to refeeding. 1191 62

It is well known that stress affects the central nervous system (CNS), neuroendocrinoimmune system and other peripheral organs such as the gastrointestinal tract. However, the process of adaptation or recovery after acute stress reactions in these systems or organs during prolonged stress has not yet been adequately investigated. To clarify the process of adaptation or recovery in these systems and organs after acute stress reactions, the time course of these responses during a single long-duration restraint stress (RTS) was studied. The expression of c-fos in the hypothalamic paraventricular nucleus (PVN) region of the brain was induced and reached a peak at 0.5 hours for c-fos mRNA and 4 hours for c-fos protein (Fos), but disappeared at 2 hours for mRNA and 16 hours for Fos during continuous RTS. The activation of the hypothalamic-pituitary-adrenal (HPA) axis during stress resulted in rapid increases in the plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Whereas the increase in ACTH was transient, the rise in CORT was maintained throughout the duration of the stress. A rapid significant decrease after stress exposure and following a slow and complete or partial recovery were observed in a number of total white blood cells (WBC), lymphocytes (LYM), helper T cells (Th) and cytotoxic/suppressor T cells (CTL/Ts). A gastric ulcer was found in 1/6 and 6/6 rats at 8 hours and 16 hours RTS, respectively. These results suggest that adaptive changes may occur in c-fos expression in the PVN, ACTH release and immune response, but not for CORT release, following acute stress reaction during long-duration RTS. In addition, any associated organic damage, such as gastric ulceration, was also suggested to possibly be progressive according to the duration of RTS.
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PMID:PVN c-fos expression, HPA axis response and immune cell distribution during restraint stress. 1206 82

Specialized neurons utilize glucose as a signaling molecule to alter their firing rate. Glucose-excited (GE) neurons increase and glucose-inhibited (GI) neurons reduce activity as ambient glucose levels rise. Glucose-induced changes in the ATP-to-ADP ratio in GE neurons modulate the activity of the ATP-sensitive K(+) channel, which determines the rate of cell firing. The GI glucosensing mechanism is unknown. We postulated that glucokinase (GK), a high-Michaelis constant (K(m)) hexokinase expressed in brain areas containing populations of GE and GI neurons, is the controlling step in glucosensing. Double-label in situ hybridization demonstrated neuron-specific GK mRNA expression in locus ceruleus norepinephrine and in hypothalamic neuropeptide Y, pro-opiomelanocortin, and gamma-aminobutyric acid neurons, but it did not demonstrate this expression in orexin neurons. GK mRNA was also found in the area postrema/nucleus tractus solitarius region by RT-PCR. Intracarotid glucose infusions stimulated c-fos expression in the same areas that expressed GK. At 2.5 mmol/l glucose, fura-2 Ca(2+) imaging of dissociated ventromedial hypothalamic nucleus neurons demonstrated GE neurons whose intracellular Ca(2+) oscillations were inhibited and GI neurons whose Ca(2+) oscillations were stimulated by four selective GK inhibitors. Finally, GK expression was increased in rats with impaired central glucosensing (posthypoglycemia and diet-induced obesity) but was unaffected by a 48-h fast. These data suggest a critical role for GK as a regulator of glucosensing in both GE and GI neurons in the brain.
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PMID:Glucokinase is the likely mediator of glucosensing in both glucose-excited and glucose-inhibited central neurons. 1208 33

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