Cause Of Suppression Research Articles

The main stages of development of agricultural nematology

Goal. Analyze the biological patterns underlying the principles of creating methods for monitoring and control of nematodes of field crops and woody plants, as well as the possibility of creating biological products based on EPN from local strains identified by the laboratory of nematology.
 Methods. Analysis of the results of laboratory developments for 30 years of research.
 Results. The high level of the number of parasitic species of nematodes (200—800 individuals in 100 cm3 of soil) has a significant impact on the growth, development and yield of the main field and flower ornamental crops. Losses can reach 35—55% of biomass (or ornamental) crops and 20—30% of the crop. Agrocenoses are more sensitive than natural coenoses to changes in the environment. Due to this, such agrotechnical measures as crop rotation, species and varietal composition of crops in crop rotation, fertilization system, tillage methods, etc. significantly affect the population density of parasitic nematodes, so they can be used to regulate their numbers. According to the results of laboratory tests in Ukraine, the pine wood nematode B. mucronatus was found, which is the cause of suppression and drying of Scots pine plantations. Methods for monitoring this new species of phytoparasitic nematodes have been developed. Long-term studies of the spread of entomopathogenic nematodes in Ukraine have made it possible to identify three species that quite densely (21.2% of the analyzed samples) inhabit the habitats of Ukraine, show high effectiveness against soil and other pests, so are promising for biopreparations based on entomopathogenic nematodes.
 Conclusions. The use of methods developed in the laboratory for monitoring and controlling the number of populations of phytopathogenic nematodes will keep the damage from this group of pathogens at a low level, preserving up to 20—30% of the crop, and prevent drying of coniferous forests from bursaphelenchosis.

Obtaining micro cuttings of potatoes by clonal micropropagation

At present, high-quality healthy planting material of potato tubers cannot be obtained without the use of clonal micropropagation technology, with the help of which, through micro-cuttings, it is possible to recover from viral, viroid, bacterial and fungal infections and mass propagation of economically valuable varieties. The wrong choice of explants and ineffective sterilization are the most common causes of suppression of the growth of microplants, bacterial infections, necrosis of shoot tips, habituation and growth of tissues, lack of rooting at the stage of rhizogenesis and successful acclimatization at the stage of adaptation to non-sterile conditions, etc.

The Study of effect of suppression of urge of micturition (Mutra vegadharan)

TITLE: Study of effect of suppression of urge of micturition (Mutra vegadharan)- A review study
 AUTHOR: Dr. Reshma .K. Mahale
 DESIGNATION : PG Scholar, Department of Kriya Sharir
 Abstract-
 Our body has to eliminate waste products from the body time to time. For this our body gives some signals which reminds us to remove this waste. These signals are called Natural urges or Vegas in Ayurveda. Vegas is the tendency to expel out1. These Vegas should not be hold or suppressed as it can cause severe effect on our body. There are various urges explained in Ayurvedic texts like urge of urine, faeces, vata, sneezing, sleep etc. Out of which is urge of micturition which is commonly seen to be suppressed by most of individuals. The major cause of suppression or Vegdharan of urine is bad life style habits, hectic schedules, heavy working hours, travelling, unavailability of proper facilities of urination and toilets etc. Hence urine should be eliminated according to its natural urge to prevent people from various disease.
 Key words- Vegas, Micturition, Vegadharan

The Trauma of Domestic Violence: A Study of Tehmina Durrani’s “My Feudal Lord”

The present paper is based on Tehmina Durrani’s novel, “My Feudal Lord”. The paper aims at studying various institutions like feudalism, patriarchy, religion and cultural mechanism which, according to the novelist, is the root cause of suppression, exploitation and subjugation of women in Pakistani society. The novel is a struggle by a woman towards the assertion of her identity. The present paper proposes to dismantle the existing female identity of submissive, meek, docile, weak, and passive to strong, active, speaking, and courageous as the novelist does.The main intention of the study is to emphasize the problems of women in the male dominated society and also to upgrade the condition of women. Women endures lot of physical and mental cruelties during the whole of their life in the male dominated society. Each and every woman should learn to challenge the disagreeable conceptions which have been considered as truths. Women should not tolerate violence, exploitation and subordination as part of their destiny. They should raise a voice against all kinds of suppression.

Suppressed Recombination of Sex Chromosomes Is Not Caused by Chromosomal Reciprocal Translocation in Spiny Frog (Quasipaa boulengeri).

Chromosome rearrangements (CRs) are perceived to be related to sex chromosome evolution, but it is a matter of controversy whether CRs are the initial causative mechanism of suppressed recombination for sex differentiation. The early stages of sex chromosome evolution in amphibians may represent intermediate states of differentiation, and if so, they potentially shed light on the ultimate cause of suppressed recombination and the role of CRs in sex chromosome differentiation. In this paper, we showed that sex determination differs among 16 populations of spiny frog (Quasipaa boulengeri), in which individuals have normal and rearranged chromosomes caused by reciprocal translocation. In eastern areas, without translocation, genetic differentiation between sexes was relatively low, suggesting unrestricted recombination. In comparison, in western populations that have both normal and translocated chromosomes, a male-heterogametic system and lack of X-Y recombination were identified by male-specific alleles and heterozygote excess. However, such genetic differentiation between sexes in western populations was not directly related to karyotypes, as it was found in individuals with both normal and translocated karyotypes. In the western Sichuan Basin, male-specific and translocation-specific allelic frequency distributions suggested that recombination of sex-differentiation ceased in all populations, but recombination suppression caused by translocation did not exist in some populations. Combined with phylogenetic inference, this indicated that the establishment of sex-linkage had taken place independently of reciprocal translocation, and translocation was not the ultimate cause of sex chromosome differentiation. Furthermore, comparison of the genetic diversity of alleles on Y chromosomes, X chromosomes, and autosomes in western populations showed a reduction of effective population size on sex chromosomes, which may be caused by reciprocal translocation. It indicates that, although it is not the ultimate cause of recombination suppression, reciprocal translocation may enhance sex chromosome differentiation.

Regulation of human stem and progenitor cells by acute myeloid leukaemia in the human niche

In acute myeloid leukemia (AML) the suppression of normal blood production is a major factor contributing to treatment complications and mortality rates. Recently it was demonstrated that cell cycle inhibition of haematopoietic stem and progenitor cells (HSPCs) may be the underlying cause of suppression in both AML xenograft and transgenic mouse models. However, the mechanism in human HSPCs is still poorly understood. Using a fully humanized ex vivo system comprising AML cell lines, umbilical cord blood derived CD34+ HSPCs and bone marrow mesenchymal stroma cells (MSCs), we studied the interactions between AML, normal HSPCs and their stromal niche. In our ex vivo system, AML but not normal white blood cells rapidly suppress the proliferation and differentiation of normal HSPCs via cell cycle inhibition of both (CD34+CD38+) progenitors and (CD34+CD38-CD45RA-CD90+) stem cells. In line with the finding of the in vivo AML models, AML did not induce apoptosis in HSPCs. Transcriptomic interrogation of a stroma cell line after AML exposure identified a hypoxia-response signature and an upregulation of Hypoxia inducible factor -1 alpha (HIF-1α) target genes. Hypoxia-induced stabilization of HIF-1α in MSCs recapitulated AML induced HSPC suppression, which was reversible by HIF-1α knockdown. Furthermore, we identified Stanniocalcin 1 (STC1), a small secreted glycoprotein, to be upregulated via HIF-1α dependent mechanisms in MSCs after AML exposure. Recombinant STC1 alone reduced HSPC proliferation and differentiation, using a STC1 neutralizing antibody, we were able to significantly reduce the AML-induced cell cycle inhibition of stem cells and increase the number of progenitors. In summary, we developed a fully humanized ex vivo system to study the interaction between AML, normal HSPCs and the stroma niche. We identified HIF-1α stabilization and its downstream target STC1 in MSCs as key contributors to the suppression of HSPC differentiation and proliferation, providing a potential route to release normal blood production from AML-induced suppression.

Abstract 2879: Dj-1 confers maintenance of stemness and radioresistance by regulating EGFRvIII expression in glioma stem cells

Abstract DJ-1 is involved in many key cellular processes including cell proliferation, transcriptional regulation, differentiation, oxidative stress protection, and mitochondrial function maintenance. Deregulation of DJ-1 has been implicated in the pathogenesis of many human diseases such as Parkinson's disease, amyotrophic lateral sclerosis, infertility, and cancer. DJ-1 was initially identified as an oncogene product involved in human tumorigenesis in numerous cancer types. Alteration in expression of DJ-1 is associated with tumorigenesis in several types of cancers. Herein, we aimed to clarify the effect of DJ-1 on stemness and radioresistance of glioma stem cells (GSCs). Firstly, we found that the reduction in expression of DJ-1 in brain tumor tissues when compared with tumor adjacent normal brain tissues, as indicated by reduced DJ-1 staining. Knock-down of DJ-1 inhibited self-renewal activity of GSCs in vitro as evidenced by neurosphere formation, limiting dilution, and soft agar clonogenic assays. DJ-1 knock-down suppressed maintenance of stemness by suppressing the expression of Notch intracellular domain, Sox2, and phosphorylated STAT3 proteins. Intriguingly, DJ-1 knock-down inhibited the expression of EGFRvIII in GSCs which might be the cause of suppression of stemness pathways. In addition, knockdown of DJ-1 induced apoptosis, reduced cell invasiveness, and sensitized GSCs to ionizing radiation. Based on these data, we propose that DJ-1 could be considered as a crucial diagnostics and therapeutics target for malignant glioma. Note: This abstract was not presented at the meeting. Citation Format: Myung-Jin Park, Jeong-Yub Kim, Hee-Jin Kim, Ji-Soo Kim, Jeong-Chul Kim, Dea-Hee Lee, Yoo-Jin Na. Dj-1 confers maintenance of stemness and radioresistance by regulating EGFRvIII expression in glioma stem cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2879. doi:10.1158/1538-7445.AM2017-2879

Effects of combined radiofrequency field exposure on amyloid-beta-induced cytotoxicity in HT22 mouse hippocampal neurones.

Alzheimer's disease (AD) is the most common progressive and irreversible neurodegenerative disease and it is caused by neuronal death in the brain. Recent studies have shown that non-ionizing radiofrequency (RF) radiation has some beneficial cognitive effects in animal models of AD. In this study, we examined the effect of combined RF radiation on amyloid-beta (Aβ)–induced cytotoxicity in HT22 rat hippocampal neurons. Treatment with Aβ suppressed HT22 cell proliferation in a concentration-dependent manner. RF exposure did not affect cell proliferation, and also had a marginal effect on Aβ-induced suppression of growth in HT22 cells. Cell cycle analysis showed that Aβ decreased the G1 fraction and increased the subG1 fraction, indicating increased apoptosis. Accordingly, Aβ increased the annexin V/propidium iodide (PI)–positive cell fraction and the degradation of poly (ADP ribose) polymerase and caspase-3 in HT22 cells. However, RF alone and the combination of Aβ and RF did not affect these events significantly. Aβ increased reactive oxygen species (ROS) generation, thereby suppressing cell proliferation. This was abrogated by N-acetylcysteine (NAC) treatment, indicating that Aβ-induced ROS generation is the main cause of suppression of proliferation. NAC also restored Aβ-induced annexin V/PI–positive cell populations. However, RF did not have a significant impact on these events. Finally, Aβ stimulated the ataxia telangiectasia and Rad3-related protein/checkpoint kinase 1 DNA single-strand breakage pathway, and enhanced beta-site amyloid precursor protein expression; RF had no effect on them. Taken together, our results demonstrate that RF exposure did not significantly affect the Aβ-induced decrease of cell proliferation, increase of ROS production, or induction of cell death in these cells.

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

The correct removal of 5'-flap structures by Rad27 and Dna2 during Okazaki fragment maturation is crucial for the stable maintenance of genetic materials and cell viability. In this study, we identified RAD52, a key recombination protein, as a multicopy suppressor of dna2-K1080E, a lethal helicase-negative mutant allele of DNA2 in yeasts. In contrast, the overexpression of Rad51, which works conjointly with Rad52 in canonical homologous recombination, failed to suppress the growth defect of the dna2-K1080E mutation, indicating that Rad52 plays a unique and distinct role in Okazaki fragment metabolism. We found that the recombination-defective Rad52-QDDD/AAAA mutant did not rescue dna2-K1080E, suggesting that Rad52-mediated recombination is important for suppression. The Rad52-mediated enzymatic stimulation of Dna2 or Rad27 is not a direct cause of suppression observed in vivo, as both Rad52 and Rad52-QDDD/AAAA proteins stimulated the endonuclease activities of both Dna2 and Rad27 to a similar extent. The recombination mediator activity of Rad52 was dispensable for the suppression, whereas both the DNA annealing activity and its ability to interact with Rad59 were essential. In addition, we found that several cohesion establishment factors, including Rsc2 and Elg1, were required for the Rad52-dependent suppression of dna2-K1080E. Our findings suggest a novel Rad52/Rad59-dependent, but Rad51-independent recombination pathway that could ultimately lead to the removal of faulty flaps in conjunction with cohesion establishment factors.

The effect of pre-strain on hydrogen embrittlement in 310S stainless steel

The effect of pre-strain on hydrogen embrittlement (HE) was investigated using STS 310S, considering its application to a ferrous cylinder liner for hydrogen storage. Whereas tensile strength was insignificantly influenced by hydrogen charging, elongation was decreased due to a ductile to brittle fracture transition. However, the degree of the reduction in elongation by hydrogen charging was decreased with increasing pre-strain, indicating that pre-straining improved the resistance to HE by suppressing the fracture transition. The cause for suppression of the fracture transition by pre-strain was investigated through the analyses of strain hardening behavior and thermal desorption of hydrogen. The strain hardening rate curves of annealed and pre-strained specimens was divided into several stages, which were greatly affected by primary and secondary twinning, regardless of hydrogen charging. This strain hardening analysis showed that pre-straining suppressed mechanical twinning during tensile deformation. The thermal desorption analysis revealed that the migration of diffusible hydrogen atoms to twin boundaries was hindered by pre-strain. Therefore, the reason why pre-strain suppressed the fracture transition to improve the resistance to HE was because pre-strain hindered both mechanical twinning during tensile deformation and hydrogen delivery to twin boundaries not to form highly hydrogen-concentrated twin boundaries.

T‐cell suppression by red blood cells is dependent on intact cells and is a consequence of blood bank processing

Red blood cells (RBCs) suppress T-cell responsiveness through a mechanism requiring cell-cell contact. Questions remain as to whether this effect is an allogeneic response, related to cell death, or dependent on particular components of the RBCs. Peripheral T cells were isolated from healthy donors and exposed to stored allogeneic RBCs or autologous RBCs after processing. RBCs were lysed by hypotonic solvent to produce cellular ghosts. Tritiated thymidine proliferation assays were utilized. Cultures were saturated with interleukin (IL)-2 to determine whether impaired IL-2 synthesis played a role. T-cell proliferation was suppressed by both autologous and allogeneic RBCs. RBC membrane integrity does enhance T-cell suppression. T-cell death is not responsible for the suppressive changes. IL-2 synthesis is suppressed in RBC-exposed T cells but addition of exogenous IL-2 does not rescue proliferative capabilities. Proliferation of T cells was inhibited with RBC exposure but mitigated with the addition of fresh RBCs. T-cell suppression is enhanced by intact RBCs but this effect is unrelated solely to alloantigens. Neither apoptosis nor necrosis of T cells contributes to this phenomenon. IL-2 synthesis is suppressed after RBC exposure as a consequence of T-cell inhibition, but is not the primary cause of suppression. Fresh RBCs do not mediate T-cell suppression, indicating that changes in the RBC and development of the storage lesion may occur during initial blood bank processing.

Role of Pr in Eu-123 high Tc nanometer-sized superconductors

Samples of Eu1−xPrxBa2Cu3O7−δ with compositions x=0.0, 0.1 and 0.3 were prepared by the solid state reaction route. The structural, electrical and microstructural properties were investigated by X-ray diffraction, Physical Property Measurement System (PPMS) and scanning electron microscopy (SEM) techniques respectively. The lattice parameters, oxygen deficiency, hole concentration in the CuO2 plane, average charge on Cu–O plane were evaluated from X-ray diffraction data. From XRD data, it is observed that the lattice parameters and oxygen deficiency increase with increasing Pr concentration. It was also observed that the hole concentration in CuO2 plane and average charge on Cu–O plane decrease with increasing Pr concentration. The electrical resistivity of all samples was measured in the temperature range 300 K to 4 K. It was found that the normalized transition temperature decreases with increasing Pr concentration. This may be due to reduction in hole concentration or average charge on Cu–O plane. From scanning electron microscopy images, it was observed that grain size increases with increasing Pr concentration. This increase may be the possible cause for suppression of Tc.

Quantitative relation between structure and thermal conductivity in type-I clathratesX8Ga16Ge30(X=Sr, Ba) based on electrostatic-potential analysis

In order to quantitatively characterize the effect of motion of the guest atom in type-I clathrates ${X}_{8}$Ga${}_{16}$Ge${}_{30}$ ($X$ $=$ Sr, Ba) on thermal conductivity, electrostatic potential in the crystal was visualized by synchrotron radiation x-ray diffraction. The obtained electrostatic potential clearly exhibited structural aspects of the guest atom, rattling, which is considered as a cause of suppression of thermal conductivity \ensuremath{\kappa}. The parameterized degree of rattling ``rattling factor,'' ${f}_{\mathrm{R}}$, being defined as a volume ratio of the electrostatic interaction region of the guest atom to the spherical volume estimated by the covalent radius of the guest atom, was found to well classify \ensuremath{\kappa}. The \ensuremath{\kappa} monotonously decreases with increasing the ${f}_{\mathrm{R}}$. Consequently, ${f}_{\mathrm{R}}$ was judged as a better criterion to explore high-performance thermoelectric system of the clathrates.

An analytical model of non‐photorespiratory CO2 release in the light and dark in leaves of C3 species based on stoichiometric flux balance

Leaf respiration continues in the light but at a reduced rate. This inhibition is highly variable, and the mechanisms are poorly known, partly due to the lack of a formal model that can generate testable hypotheses. We derived an analytical model for non-photorespiratory CO₂ release by solving steady-state supply/demand equations for ATP, NADH and NADPH, coupled to a widely used photosynthesis model. We used this model to evaluate causes for suppression of respiration by light. The model agrees with many observations, including highly variable suppression at saturating light, greater suppression in mature leaves, reduced assimilatory quotient (ratio of net CO₂ and O₂ exchange) concurrent with nitrate reduction and a Kok effect (discrete change in quantum yield at low light). The model predicts engagement of non-phosphorylating pathways at moderate to high light, or concurrent with processes that yield ATP and NADH, such as fatty acid or terpenoid synthesis. Suppression of respiration is governed largely by photosynthetic adenylate balance, although photorespiratory NADH may contribute at sub-saturating light. Key questions include the precise diel variation of anabolism and the ATP : 2e⁻ ratio for photophosphorylation. Our model can focus experimental research and is a step towards a fully process-based model of CO₂ exchange.

Exposure to non‐kin females rapidly affects testicular morphology in non‐reproductive male Damaraland mole‐rats

Damaraland mole-rats Fukomys damarensis are eusocial subterranean rodents that exhibit an extreme reproductive skew with one female and one or two males breeding. The non-reproductive individuals in the colony are reproductively suppressed, and yet show a rapid initiation of copulatory behaviour (within 1 h) when taken out of the colony and exposed to non-kin. Little is known about how these individuals can quickly become sexually active if the causes of suppression are removed. This study investigated circulating gonadotrophin concentrations [follicle stimulating hormone (FSH)] and testicular morphology and function in reproductive and non-reproductive male Damaraland mole-rats taken directly from their natal colonies and non-reproductive males that had been introduced to non-kin females outside their colony for 10 or 60 min. The main findings were that 60-min exposure males had a significantly heavier body mass-corrected testicular mass than reproductive males. In addition, the external seminiferous tubule diameter was significantly larger in reproductive males than in non-reproductive males, and the tubule lumen area was significantly greater in reproductive, 10 and 60-min exposure males than in non-reproductive males. Plasma concentrations of FSH were not different between the groups; however, the reproductive status significantly affected the area of testicular tissue stained immunopositive for the FSH receptor (FSH-R). Reproductive males had almost six times more FSH-R compared with non-reproductive males, and 60-min exposure males had eight times more FSH-R compared with non-reproductive males. In conclusion, the increase in the seminiferous tubular lumen area and the testicular FSH receptor content when non-reproductive male mole-rats come into contact with non-kin females indicates a rapid activation of testicular spermatogenic pathways to accompany the onset of copulatory behaviour, and is likely to be adaptive in allowing pairs formed of dispersing individuals from different colonies to rapidly bond and become fertile.

Suppression of Critical Current in Submicron Intrinsic Josephson Junction Fabricated in a Bi2Sr2Ca2Cu3O10+δ Single Crystal Whisker

We have fabricated intrinsic Josephson junction array stack in a Bi2Sr2Ca2Cu3O10+δ (Bi-2223) single crystal whisker using three dimensional focused ion beam milling technique. We report measurements of current density depend on junctions array at 30 K upon the junction cross-sectional area S showing a strong suppression in critical current density for junctions with S≤1 µm2. We discussed quantum fluctuations of phase in submicron junctions which is a cause for suppression of critical current density.

Involvement of Vts1, a structure-specific RNA-binding protein, in Okazaki fragment processing in yeast

The non-essential VTS1 gene of Saccharomyces cerevisiae is highly conserved in eukaryotes and encodes a sequence- and structure-specific RNA-binding protein. The Vts1 protein has been implicated in post-transcriptional regulation of a specific set of mRNAs that contains its-binding site at their 3′-untranslated region. In this study, we identified VTS1 as a multi-copy suppressor of dna2-K1080E, a lethal mutant allele of DNA2 that lacks DNA helicase activity. The suppression was allele-specific, since overexpression of Vts1 did not suppress the temperature-dependent growth defects of dna2Δ405N devoid of the N-terminal 405-amino-acid residues. Purified recombinant Vts1 stimulated the endonuclease activity of wild-type Dna2, but not the endonuclease activity of Dna2Δ405N, indicating that the activation requires the N-terminal domain of Dna2. Stimulation of Dna2 endonuclease activity by Vts1 appeared to be the direct cause of suppression, since the multi-copy expression of Dna2-K1080E suppressed the lethality observed with its single-copy expression. We found that vts1Δ dna2Δ405N and vts1Δdna2-7 double mutant cells displayed synergistic growth defects, in support of a functional interaction between two genes. Our results provide both in vivo and in vitro evidence that Vts1 is involved in lagging strand synthesis by modulating the Dna2 endonuclease activity that plays an essential role in Okazaki fragment processing.

Accumulation of the hormone abscisic acid (ABA) at the infection site of the fungus Cercospora beticola supports the role of ABA as a repressor of plant defence in sugar beet.

Inducible plant defence responses in sugar beet (Beta vulgaris L.) leaves are repressed during the early phase of infection by the fungus Cercospora beticola. In this report, we show that the concentration of the plant hormone abscisic acid (ABA) increases in sugar beet leaves during C. beticola infection. After an initial burst of ABA induced by inoculation of the fungus, elevated ABA concentrations were detected during the fungal penetration and colonization phases 3-9 days after inoculation. Fifteen days after inoculation, with visible onset of the necrotic phase of infection, the strongly elevated ABA concentrations in infected leaves were at levels similar to drought-stressed plants. A synthetic promoter composed of four copies of the ABA-responsive element (ABRE) A2 and the coupling element CE3 of the ABA-inducible barley gene HVA1 was strongly induced by ABA and C. beticola infection in transgenic sugar beet leaves. Analysis of the spatial pattern of promoter activity revealed that the ABA-inducible promoter was locally activated at the fungal infection sites. Furthermore, expression of the basic leucine zipper transcription factor AREB1 was induced by drought stress and fungal infection in the sugar beet. Application of ABA reduced the promoter activity of the phenylalanine ammonia lyase (BvPAL) gene, and this effect was observed with the -34 to +248 BvPAL promoter region. This region is equivalent to the core promoter, which is necessary for the suppression of BvPAL expression by C. beticola, as recently shown. These data indicate that ABA accumulation and activation of the ABA-dependent signalling cascade are the primary cause of suppression of BvPAL expression during infection of sugar beet leaves.

Acute β-adrenergic blockade: an unusual cause of suppression of spectral entropy values during isoflurane anaesthesia

Acta Anaesthesiologica ScandinavicaVolume 52, Issue 5 p. 718-719 Letters to the Editor Acute β-adrenergic blockade: an unusual cause of suppression of spectral entropy values during isoflurane anaesthesia M. Radhakrishnan, M. RadhakrishnanSearch for more papers by this authorS. Kumar, S. KumarSearch for more papers by this authorA. Jaganath, A. JaganathSearch for more papers by this authorG. S. Umamaheswara Rao, G. S. Umamaheswara RaoSearch for more papers by this author M. Radhakrishnan, M. RadhakrishnanSearch for more papers by this authorS. Kumar, S. KumarSearch for more papers by this authorA. Jaganath, A. JaganathSearch for more papers by this authorG. S. Umamaheswara Rao, G. S. Umamaheswara RaoSearch for more papers by this author First published: 15 April 2008 https://doi.org/10.1111/j.1399-6576.2008.01610.x Address:Dr G. S. Umamaheswara RaoNational Institute of Mental Health and Neurosciences (NIMHANS)Bangalore 560 029Indiae-mail: gsuma123@yahoo.com Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume52, Issue5May 2008Pages 718-719 RelatedInformation

Classical as well as novel antipsychotic drugs increase self-stimulation threshold in the rat — Similar mechanism of action?

Antipsychotic drugs given acutely increase the threshold for intracranial self-stimulation elicited from the ventral tegmental area. As all the antipsychotic drugs share the dopamine D 2-receptor antagonism it is reasonable to believe that this is the cause for suppression of intracranial self-stimulation behaviour. The objective of this investigation was to examine the effect of classical (haloperidol) as well as novel antipsychotic drugs (clozapine, olanzapine and sertindole) on intracranial self-stimulation behaviour. Furthermore, the effects of different specific receptor antagonists on intracranial self-stimulation behaviour were examined. Our results showed that both the classical (haloperidol) and the three novel antipsychotic drugs increase the threshold for intracranial self-stimulation. The results obtained with the receptor specific antagonists showed that dopamine D 2, α 1-adrenoceptor and serotonin 5-HT 2A receptor antagonisms inhibit intracranial self-stimulation behaviour and that muscarinic receptor antagonism is without effect. Even though all the tested antipsychotic drugs inhibited intracranial self-stimulation behaviour, there seems to be a difference in their ratio between doses that inhibits intracranial self-stimulation behaviour and those that produce antipsychotic effect in a preclinical model (amphetamine hyperactivity). Sertindole was the only antipsychotic drug able to produce antipsychotic effect without significant inhibition of intracranial self-stimulation behaviour at a narrow dose interval. The remaining antipsychotic drugs all inhibited intracranial self-stimulation behaviour at equal or lower doses than those producing antipsychotic effect.