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Control Pathways (control + pathway)
Selected AbstractsEffects of Chronic Oestrogen Replacement on Stress-Induced Activation of Hypothalamic-Pituitary-Adrenal Axis Control PathwaysJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2000C. V. Dayas Abstract Oestrogen replacement therapy reportedly suppresses hypothalamic-pituitary-adrenal (HPA) axis responses to an emotional stressor in postmenopausal women. However, most studies in the rat suggest a facilitatory role for oestrogen in the control of HPA axis function. One explanation for this difference may be the regimen of oestrogen replacement: during oestrogen replacement therapy, oestrogen levels are low and constant whereas most animal studies examined the HPA axis response when oestrogen levels are rising. In the present study, we assessed HPA axis stress responses in mature ovariectomized rats after plasma oestrogen levels had been maintained at physiological levels for a prolonged period (25 or 100 pg/ml for 7 days). In the case of both an emotional stressor (noise) and a physical stressor (immune challenge by systemic interleukin-1, administration), oestrogen replacement suppressed stress-related Fos-like immunolabelling, in hypothalamic neuroendocrine cells and plasma adrenocorticotropin hormone responses. From the present data, and past reports, it appears unlikely that these effects of oestrogen are due to a direct action on corticotropin-releasing factor or oxytocin cells. Therefore, to obtain some indication of oestrogen's possible site(s) of action, Fos-like immunolabelling was mapped in the amygdala and in brainstem catecholamine groups, which are neuronal populations demonstrating substantial evidence of involvement in the generation of HPA axis stress responses. In the amygdala, oestrogen replacement suppressed central nucleus responses to immune challenge, but not to noise. Amongst catecholamine cells, oestrogen replacement was more effective against responses to noise than immune challenge, suppressing A1 and A2 (noradrenergic) and C2 (adrenergic) responses to noise, but only A1 responses to immune challenge. These data suggest that, as in postmenopausal women on oestrogen replacement therapy, chronic low-level oestrogen replacement can suppress HPA axis stress responses in the rat. Moreover, oestrogen appears to exert effects at multiple sites within putative HPA axis control pathways, even though most of the relevant neuronal populations do not contain genomic receptors for this gonadal steroid and the pattern of oestrogen action differs for an emotional vs a physical stressor. [source] Immediate early gene (ZENK, Arc) expression in the auditory forebrain of female canaries varies in response to male song qualityDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2005Stefan Leitner Abstract In male songbirds, the song control pathway in the forebrain is responsible for song production and learning, and in females it is associated with the perception and discrimination of male song. However, experiments using the expression of immediate early genes (IEGs) reveal the activation of brain regions outside the song control system, in particular the caudomedial nidopallium (NCM) and the caudomedial mesopallium (CMM). In this study on female canaries, we investigate the role of these two regions in relation to playback of male songs of different quality. Male canaries produce elaborate songs and some contain syllables with a more complex structure (sexy syllables) that induce females to perform copulation solicitation displays (CSD) as an invitation to mate. Females were first exposed to playback of a range of songs of different quality, before they were finally tested with playback of songs containing either sexy or nonsexy syllables. We then sectioned the brains and used in situ hybridization to reveal brain regions that express the IEGs ZENK or Arc. In CMM, expression of ZENK mRNA was significantly higher in females that last heard sexy syllables compared to those that last heard nonsexy syllables, but this was not the case for NCM. Expression of Arc mRNA revealed no differences in either CMM or NCM in both experimental groups. These results provide evidence that in female canaries CMM is involved in female perception and discrimination of male song quality through a mechanism of memory reconsolidation. The results also have further implications for the evolution of complex songs by sexual selection and female choice. © 2005 Wiley Periodicals, Inc. J Neurobiol, 2005 [source] Female canaries that respond and discriminate more between male songs of different quality have a larger song control nucleus (HVC) in the brainDEVELOPMENTAL NEUROBIOLOGY, Issue 4 2002Stefan Leitner Abstract In male songbirds the song control pathway in the forebrain is responsible for song production and learning. In most species, females do not sing and have smaller nuclei in the song control pathway. Although the function of the pathway in females is assumed to be associated with the perception of male song, there is little direct evidence to support this view. In this study on female canaries, we investigate the role of two key nuclei in the song control pathway (HVC and lMAN) in relation to playback of male song. Male canaries produce elaborate songs that function to attract and stimulate females. The songs are constructed from smaller units called syllables, and special syllables with a more complex structure (sexy syllables) are known to induce females to perform copulation solicitation displays (CSD) as an invitation to mate. By using computer-edited experimental songs, we first show that females discriminate between songs by producing significantly more CSD to those containing sexy syllables. We then sectioned the brains and used in situ hybridization to reveal song nuclei containing androgen receptors. We report positive correlations between the size of HVC and both total CSD response and the amount of discrimination between sexy and nonsexy songs. We found no such relationships between these measures and the size of lMAN. These results provide some evidence to support the view that, in female canaries HVC is involved in female perception and discrimination of male song. The results also have implications for the evolution of complex male songs by sexual selection and female choice. © 2002 Wiley Periodicals, Inc. J Neurobiol 52: 294,301, 2002 [source] The effect of intravesical electrical stimulation on bladder function and synaptic neurotransmission in the rat spinal cord after spinal cord injuryBJU INTERNATIONAL, Issue 8 2009Chang Hee Hong OBJECTIVE To investigate the effects of intravesical electrical stimulation (IVES) on bladder function and synaptic neurotransmission in the lumbosacral spinal cord in the spinalized rat, as the clinical benefits of IVES in patients with increased residual urine or reduced bladder capacity have been reported but studies on the mechanism of IVES have mainly focused on bladder A, afferents in central nervous system-intact rats. MATERIALS AND METHODS In all, 30 female Sprague-Dawley rats were divided equally into three groups: normal control rats, sham-stimulated spinalized rats and IVES-treated spinalized rats. IVES was started 5 weeks after spinal cord injury (SCI) and was performed 20 min a day for 5 consecutive days. At 7 days after IVES, conscious filling cystometry was performed. Sections from the L6 and S1 spinal cord segments were examined for n -methyl- d -aspartic acid receptor 1 (NMDAR1) subunit and ,-aminobutyric acid (GABA) immunoactivity. RESULTS In IVES-treated spinalized rats, the number and maximal pressure of nonvoiding detrusor contractions were significantly less than in sham-stimulated spinalized rats. The mean maximal voiding pressure was also lower in IVES-treated than in sham-stimulated spinalized rats. IVES significantly reduced the interval between voiding contractions compared with the untreated spinalized rats. There was an overall increase in NMDAR1 immunoactivity after SCI, which was significantly lower in IVES-treated spinalized rats. Immunoactivity of GABA after SCI was significantly lower than in the control group and was significantly higher in IVES-treated spinalized rats. CONCLUSION Our results suggest that IVES might affect voiding contractions in addition to inhibiting C-fibre activity and that IVES seems to have a more complex effect on the bladder control pathway. For synaptic neurotransmission in the spinal cord, IVES could possibly shift the balance between excitation and inhibition towards inhibition. [source] Genetic variants in cell cycle control pathway confer susceptibility to bladder cancerCANCER, Issue 11 2008Yuanqing Ye PhD Abstract BACKGROUND Cell cycle checkpoint regulation is crucial for the prevention of carcinogenesis in mammalian cells. METHODS To test the hypothesis that common sequence variants in the cell cycle control pathway may affect bladder cancer susceptibility, the effects of a panel of 10 potential functional single nucleotide polymorphisms (SNPs) from 7 cell cycle control genes, P53, P21, P27, CDK4, CDK6, CCND1, and STK15, were evaluated on bladder cancer risk in a case-control study of 696 bladder cancer cases and 629 healthy controls. RESULTS Overall, on individual SNP analysis only individuals with the p53 intron 3 16-bp duplication polymorphism variant allele had a significantly reduced bladder cancer risk (odds ratio [OR] = 0.74, 95% confidence interval [CI], 0.56,0.96). This effect was more evident in former smokers and younger subjects. We then applied the Classification and Regression Tree (CART) statistical approach to explore the high-order gene-gene and gene-smoking interactions. In the CART analysis, smoking status was identified as the most influential factor for bladder cancer susceptibility. The final decision tree by CART contained 6 terminal nodes. Compared with the second-lowest risk group the ORs for terminal nodes 1 and 3 to 6 ranged from 0.46 to 6.30. CONCLUSIONS These results suggest that cell cycle genetic polymorphisms may affect bladder cancer predisposition through modulation of host genome stability and confirm the importance of studying gene-gene and gene-environment interactions in bladder cancer risk assessment. Cancer 2008. © 2008 American Cancer Society. [source] Effects of Chronic Oestrogen Replacement on Stress-Induced Activation of Hypothalamic-Pituitary-Adrenal Axis Control PathwaysJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2000C. V. Dayas Abstract Oestrogen replacement therapy reportedly suppresses hypothalamic-pituitary-adrenal (HPA) axis responses to an emotional stressor in postmenopausal women. However, most studies in the rat suggest a facilitatory role for oestrogen in the control of HPA axis function. One explanation for this difference may be the regimen of oestrogen replacement: during oestrogen replacement therapy, oestrogen levels are low and constant whereas most animal studies examined the HPA axis response when oestrogen levels are rising. In the present study, we assessed HPA axis stress responses in mature ovariectomized rats after plasma oestrogen levels had been maintained at physiological levels for a prolonged period (25 or 100 pg/ml for 7 days). In the case of both an emotional stressor (noise) and a physical stressor (immune challenge by systemic interleukin-1, administration), oestrogen replacement suppressed stress-related Fos-like immunolabelling, in hypothalamic neuroendocrine cells and plasma adrenocorticotropin hormone responses. From the present data, and past reports, it appears unlikely that these effects of oestrogen are due to a direct action on corticotropin-releasing factor or oxytocin cells. Therefore, to obtain some indication of oestrogen's possible site(s) of action, Fos-like immunolabelling was mapped in the amygdala and in brainstem catecholamine groups, which are neuronal populations demonstrating substantial evidence of involvement in the generation of HPA axis stress responses. In the amygdala, oestrogen replacement suppressed central nucleus responses to immune challenge, but not to noise. Amongst catecholamine cells, oestrogen replacement was more effective against responses to noise than immune challenge, suppressing A1 and A2 (noradrenergic) and C2 (adrenergic) responses to noise, but only A1 responses to immune challenge. These data suggest that, as in postmenopausal women on oestrogen replacement therapy, chronic low-level oestrogen replacement can suppress HPA axis stress responses in the rat. Moreover, oestrogen appears to exert effects at multiple sites within putative HPA axis control pathways, even though most of the relevant neuronal populations do not contain genomic receptors for this gonadal steroid and the pattern of oestrogen action differs for an emotional vs a physical stressor. [source] Programmed responses to virus replication in plantsMOLECULAR PLANT PATHOLOGY, Issue 1 2000A. J. Maule Despite their economic importance, we understand very little about the mechanism leading to symptom formation in compatible virus infections. By applying a spatial analysis to advancing infection fronts, we have been able to relate molecular events in small groups of cells to a sequence of virus-induced changes. This sequence starts ahead of the main front of virus replication and virus protein accumulation and lasts beyond the time at which virus replication has ceased. The host changes include alterations in gene expression, physiology and cellular ultrastructure. The relationship between these effects has been analysed in comparative studies between different virus infections in different hosts and abiotic stress. The research points to there being common features for different viruses leading to common effects. Also, although many of the consequences of virus infection are similar to the effects of heat shock, there are sufficient differences to suggest that the two inducers use distinct control pathways. The immediate challenge for the future is to establish synchronous infections of tissues so that the complex relationship between the virus and the host can be investigated using temporal rather than spatial analyses. [source] Microstructural white matter changes in primary torsion dystoniaMOVEMENT DISORDERS, Issue 2 2008Maren Carbon MD Abstract Primary torsion dystonia (PTD) has been conceptualized as a disorder of the basal ganglia. However, recent data suggest a widespread pathology involving motor control pathways. In this report, we explored whether PTD is associated with abnormal anatomical connectivity within motor control pathways. We used diffusion tensor magnetic resonance imaging (DT-MRI) to assess the microstructure of white matter. We found that fractional anisotropy, a measure of axonal integrity and coherence, was significantly reduced in PTD patients in the pontine brainstem in the vicinity of the left superior cerebellar peduncle and bilaterally in the white matter of the sensorimotor region. Our data thus support the possibility of a disturbance in cerebello-thalamo-cortical pathways as a cause of the clinical manifestations of PTD. © 2007 Movement Disorder Society [source] The chemistry behind redox regulation with a focus on sulphur redox systemsPHYSIOLOGIA PLANTARUM, Issue 3 2008Claus Jacob Sulphur metabolism in plants provides a wealth of natural products, including several chemically unusual substances, such as thiosulphinates, polysulphides and isothiocyanates. Many of these reactive sulphur species (RSS) exhibit a distinct redox behaviour in vitro, which translates into a rather interesting biological activity in vivo, such as antibiotic, fungicidal, pesticidal or anticancer activity. While the molecular basis for such activity has long remained obscure, research into sulphur-based redox systems during the past 5,10 years has achieved a better knowledge of the in vitro properties of RSS and has led to an improved understanding of their impact on intracellular redox signalling and control pathways in living cells. It has become apparent that the redox chameleon sulphur occurs in biological systems in about 10 different oxidation states, which give rise to an extensive and complicated network of sulphur-based redox events. Together, natural sulphur products from plants and their intracellular targets provide the basis for innovative design of novel antibiotics, fungicides, pesticides and anticancer agents. [source] The excitatory thalamo-"cortical" projection within the song control system of zebra finches is formed by calbindin-expressing neuronsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2007Raphael Pinaud Abstract The learning and production of vocalizations in songbirds are controlled by a system of interconnected brain nuclei organized into a direct vocal motor pathway and an anterior forebrain (pallium-basal ganglia-thalamo-pallial) loop. Here we show that the thalamo-pallial ("thalamo-cortical") projection (from the medial part of the dorsolateral thalamic nucleus to the lateral magnocellular nucleus of the anterior nidopallium,DLM to LMAN) within the anterior forebrain loop is composed of cells positive for the calcium-binding protein calbindin. We show that the vast majority of cells within DLM express calbindin, based both on immunocytochemistry (ICC) for calbindin protein and in situ hybridization for calb mRNA. Using a combination of tract-tracing and ICC we show that the neurons that participate in the DLM-to-LMAN projection are calbindin-positive. We also demonstrate that DLM is devoid of cells expressing mRNA for the GABAergic marker zGAD65. This observation confirms that the calbindin-expressing cells in DLM are not GABAergic, in accordance with previous electrophysiological data indicating that the DLM-to-LMAN projection is excitatory. Furthermore, we use ICC to determine the trajectory of the fibers within the DLM-to-LMAN projection, and to demonstrate a sex difference in calbindin expression levels in the fibers of the DLM-to-LMAN projection. Our findings provide a clear-cut neurochemical signature for a critical projection in the songbird vocal control pathways that enable song learning. J. Comp. Neurol. 504:601,618, 2007. © 2007 Wiley-Liss, Inc. [source] RNA-mediated neurodegeneration in repeat expansion disordersANNALS OF NEUROLOGY, Issue 3 2010Peter K. Todd MD Most neurodegenerative disorders are thought to result primarily from the accumulation of misfolded proteins, which interfere with protein homeostasis in neurons. For a subset of diseases, however, noncoding regions of RNAs assume a primary toxic gain-of-function, leading to degeneration in many tissues, including the nervous system. Here we review a series of proposed mechanisms by which noncoding repeat expansions give rise to nervous system degeneration and dysfunction. These mechanisms include transcriptional alterations and the generation of antisense transcripts, sequestration of mRNA-associated protein complexes that lead to aberrant mRNA splicing and processing, and alterations in cellular processes, including activation of abnormal signaling cascades and failure of protein quality control pathways. We place these potential mechanisms in the context of known RNA-mediated disorders, including the myotonic dystrophies and fragile X tremor ataxia syndrome, and discuss recent results suggesting that mRNA toxicity may also play a role in some presumably protein-mediated neurodegenerative disorders. Lastly, we comment on recent progress in therapeutic development for these RNA-dominant diseases. ANN NEUROL 2010;67:291,300 [source] | |||||||||||||