Long-lasting Changes (long-lasting + change)

Distribution by Scientific Domains


Selected Abstracts


Long-lasting changes in small intestinal transport following the recovery from Trichinella spiralis infection

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2006
K. Venkova
Abstract, Changes in intestinal motility and visceral sensitivity are found after resolution of acute enteric inflammation. The study investigates whether a transient nematode-induced intestinal inflammation may result in long-lasting remodelling of epithelial transport. Ferrets infected with Trichinella spiralis or sham-infected animals were euthanized on day 10, 30 or 60 postinfection (PI) and the jejunum was isolated. The net transport of electrolytes was measured electrophysiologically as transmucosal short-circuit current (Isc) and responses to electrical field stimulation (EFS: 1,32 Hz) or secretagogues were investigated. Myeloperoxidase (MPO) activity, a marker of mucosal inflammation, was maximal during the enteric stage of T. spiralis infection (day 10 PI) and returned to normal on days 30 and 60 PI. Mucosal inflammation caused a reduction in basal Isc, increased electrical conductance (G) and decreased the maximal responses to EFS, carbachol or histamine. On days 30 and 60 PI the inflammation resolved and basal electrogenic transport appeared normal; however, the secretion induced by EFS, carbachol or histamine remained suppressed. Moreover, EFS-induced responses were shifted from predominantly cholinergic in controls to non-cholinergic in the infected animals. The results suggest that a transient small intestinal inflammation causes a long-term remodelling of epithelial function. [source]


Teaching Culturally Appropriate Care: A Review of Educational Models and Methods

ACADEMIC EMERGENCY MEDICINE, Issue 12 2006
Cherri Hobgood MD
Abstract The disparities in health care and health outcomes between the majority population and cultural and racial minorities in the United States are a problem that likely is influenced by the lack of culturally competent care. Emergency medicine and other primary-care specialties remain on the front lines of this struggle because of the nature of their open-door practice. To provide culturally appropriate care, health care providers must recognize the factors impeding cultural awareness, seek to understand the biases and traditions in medical education potentially fueling this phenomenon, and create a health care community that is open to individuals' otherness, thus leading to better communication of ideas and information between patients and their health care providers. This article highlights the rationale for and current problems in teaching cultural competency and examines several different models implemented to teach and promote cultural competency along the continuum of emergency medicine learners. However, the literature addressing the true efficacy of such programs in leading to long-lasting change and improvement in minority patients' clinical outcomes remains insufficient. [source]


Activity- and age-dependent GABAergic synaptic plasticity in the developing rat hippocampus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001
Paolo Gubellini
Abstract Activity-dependent plasticity of GABAergic synaptic transmission was investigated in rat hippocampal slices obtained between postnatal day (P) 0,15 using the whole-cell patch-clamp recording technique. Spontaneous GABAA receptor-mediated postsynaptic currents (sGABAA -PSCs) were isolated in the presence of ionotropic glutamate receptor antagonists. A conditioning protocol relevant to the physiological condition, consisting of repetitive depolarizing pulses (DPs) at 0.1 Hz, was able to induce long-lasting changes in both frequency and amplitude of sGABAA -PSCs between P0 and P8. Starting from P12, DPs were unable to induce any form of synaptic plasticity. The effects of DPs were tightly keyed to the frequency at which they were delivered. When delivered at a lower (0.05 Hz) or higher (1 Hz) frequency, DPs failed to induce any long-lasting change in the frequency or amplitude of sGABAA -PSCs. In two cases, DPs were able to activate sGABAA -PSCs in previously synaptically silent cells at P0,1. These results show that long-term changes in GABAergic synaptic activity can be induced during a restricted period of development by a conditioning protocol relevant to the physiological condition. It is suggested that such activity-induced modifications may represent a physiological mechanism for the functional maturation of GABAergic synaptic transmission. [source]


PRECLINICAL STUDY: Acquisition and reinstatement of MDMA-induced conditioned place preference in mice pre-treated with MDMA or cocaine during adolescence

ADDICTION BIOLOGY, Issue 4 2009
Manuel Daza-Losada
ABSTRACT Those who take ecstasy are more likely to consume other drugs than non-users with cocaine abuse being reported by 75.5% of high school student MDMA (± 3,4-methylenedioxymetamphetamine hydrochloride) users. The aim of this work was to evaluate the effects of exposure during adolescence to MDMA, cocaine or to both drugs on the MDMA-induced conditioned place preference (CPP) in adult mice. Animals received two daily administrations of saline, 10 mg/kg of MDMA, 25 mg/kg of cocaine or 10 mg/kg of MDMA plus 25 mg/kg of cocaine over 3 days (from PD28 to 30). Three weeks after pre-treatment, the MDMA-induced CPP procedure was initiated (PD52). Acquisition of CPP was induced with a sub-threshold dose of MDMA (1.25 mg/kg) only in animals treated during adolescence with MDMA alone. Preference was established in all the groups after conditioning with 10 mg/kg of MDMA, while the time required to achieve extinction was longer in those pre-treated with cocaine or MDMA alone (46 and 28 sessions, respectively). Moreover, preference was reinstated with progressively lower priming doses of MDMA in mice pre-treated with MDMA or cocaine alone. These results demonstrate that early exposure to MDMA or cocaine induces long-lasting changes that last until adulthood and modify the response of animals to MDMA. [source]


Transient viral-mediated overexpression of ,-calcium/calmodulin-dependent protein kinase II in the nucleus accumbens shell leads to long-lasting functional upregulation of ,-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors: dopamine type-1 receptor and protein kinase A dependence

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010
B. F. Singer
Abstract Calcium/calmodulin-dependent protein kinase II (CaMKII) activity is necessary for the long-lasting expression of locomotor sensitization and enhanced drug-taking observed in rats previously exposed to psychostimulants. Exposure to these drugs also transiently increases ,CaMKII levels in the nucleus accumbens (NAcc), an effect that, when mimicked by transient viral-mediated overexpression of ,CaMKII in NAcc shell neurons, leads to long-lasting enhancement in locomotor responding to amphetamine and NAcc ,-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA). The present experiments characterized the dopamine (DA) dependence of the functional AMPA receptor upregulation observed long after transient overexpression of ,CaMKII. Rats infected with herpes simplex virus-,CaMKII in the NAcc shell showed a transient increase in ,CaMKII levels that peaked at 4 days post-infection and returned to baseline 8 days later. When challenged with AMPA (0.8 nmol/side) in the NAcc shell at 20 days post-infection, these rats showed enhanced locomotion compared with controls. This sensitized locomotor response was blocked when AMPA was coinfused with either the DA type-1 receptor antagonist SCH23390 (0.8 nmol/side) or the protein kinase A inhibitor Rp-cAMPS (80 nmol/side). Neither SCH23390 nor Rp-cAMPS produced locomotor effects when infused by itself into the NAcc shell. Furthermore, these antagonists did not block the acute non-sensitized locomotor response to AMPA observed in control rats. These findings show that transient viral-mediated overexpression of ,CaMKII in neurons of the NAcc shell leads to long-lasting functional upregulation of AMPA receptors that is DA type-1 receptor and protein kinase A dependent. Thus, transient increases in levels of ,CaMKII in the NAcc shell produce long-lasting changes in the way that DA and glutamate interact in this site to generate locomotor behavior. [source]


Cannabinoid modulation of limbic forebrain noradrenergic circuitry

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2010
Ana F. Carvalho
Abstract Both the endocannabinoid and noradrenergic systems have been implicated in neuropsychiatric disorders. Importantly, low levels of norepinephrine are seen in patients with depression, and antagonism of the cannabinoid receptor type 1 (CB1R) is able to induce depressive symptoms in rodents and humans. Whether the interaction between the two systems is important for the regulation of these behaviors is not known. In the present study, adult male Sprague,Dawley rats were acutely or chronically administered the CB1R synthetic agonist WIN 55,212-2, and ,2A and ,1 adrenergic receptors (AR) were quantified by Western blot. These AR have been shown to be altered in a number of psychiatric disorders and following antidepressant treatment. CB1R agonist treatment induced a differential decrease in ,2A- and ,1-ARs in the nucleus accumbens (Acb). Moreover, to assess long-lasting changes induced by CB1R activation, some of the chronically treated rats were killed 7 days following the last injection. This revealed a persistent effect on ,2A-AR levels. Furthermore, the localization of CB1R with respect to noradrenergic profiles was assessed in the Acb and in the nucleus of the solitary tract (NTS). Our results show a significant topographic distribution of CB1R and dopamine beta hydroxylase immunoreactivities (ir) in the Acb, with higher co-localization observed in the NTS. In the Acb, CB1R-ir was found in terminals forming either symmetric or asymmetric synapses. These results suggest that cannabinoids may modulate noradrenergic signaling in the Acb, directly by acting on noradrenergic neurons in the NTS or indirectly by modulating inhibitory and excitatory input in the Acb. [source]


Abnormal associative encoding in orbitofrontal neurons in cocaine-experienced rats during decision-making

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2006
Thomas A. Stalnaker
Abstract Recent evidence has linked exposure to addictive drugs to an inability to employ information about adverse consequences, or outcomes, to control behavior. For instance, addicts and drug-experienced animals fail to adapt their behavior to avoid adverse outcomes in gambling and reversal tasks or after changes in the value of expected rewards. These deficits are similar to those caused by damage to the orbitofrontal cortex, suggesting that addictive drugs may cause long-lasting changes in the representation of outcome associations in a circuit that includes the orbitofrontal cortex. Here we test this hypothesis by recording from orbitofrontal neurons in a discrimination task in rats previously exposed to cocaine (30 mg/kg i.p. for 14 days). We found that orbitofrontal neurons recorded in cocaine-experienced rats failed to signal the adverse outcome at the time a decision was made in the task. The loss of this signal was associated with abnormal changes in response latencies on aversive trials. Furthermore, upon reversal of the cue,outcome associations, orbitofrontal neurons in cocaine-treated rats with enduring reversal impairments failed to reverse their cue-selectivity, while orbitofrontal neurons in cocaine-treated rats with normal performance showed an increase in the plasticity of cue-selective firing after reversal. These results provide direct neurophysiological evidence that exposure to cocaine can cause behaviorally relevant changes in the processing of associative information in a circuit that includes the orbitofrontal cortex. [source]


Early life modulators and predictors of adult synaptic plasticity

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2006
Katherine G. Akers
Abstract Early life experience can induce long-lasting changes in brain and behaviour that are opposite in direction, such as enhancement or impairment in regulation of stress response, structural and functional integrity of the hippocampus, and learning and memory. To explore how multiple early life events jointly determine developmental outcome, we investigated the combined effects of neonatal trauma (anoxia on postnatal day 1, P1) and neonatal novelty exposure (P2,21) on adult social recognition memory (3 months of age) and synaptic plasticity in the CA1 of the rat hippocampus (4.5,8 months of age). While neonatal anoxia selectively reduced post-tetanic potentiation (PTP), neonatal novel exposure selectively increased long-term potentiation (LTP). No interaction between anoxia and novelty exposure was found on either PTP or LTP. These findings suggest that the two contrasting neonatal events have selective and distinct effects on two different forms of synaptic plasticity. At the level of behaviour, the effect of novelty exposure on LTP was associated with increased social memory, and the effect of anoxia on PTP was not accompanied by changes in social memory. Such a finding suggests a bias toward the involvement of LTP over PTP in social memory. Finally, we report a surprising finding that an early behavioural measure of emotional response to a novel environment obtained at 25 days of age can predict adult LTP measured several months later. Therefore, individual differences in emotional responses present during the juvenile stage may contribute to adult individual differences in cellular mechanisms that underlie learning and memory. [source]


Activity- and age-dependent GABAergic synaptic plasticity in the developing rat hippocampus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001
Paolo Gubellini
Abstract Activity-dependent plasticity of GABAergic synaptic transmission was investigated in rat hippocampal slices obtained between postnatal day (P) 0,15 using the whole-cell patch-clamp recording technique. Spontaneous GABAA receptor-mediated postsynaptic currents (sGABAA -PSCs) were isolated in the presence of ionotropic glutamate receptor antagonists. A conditioning protocol relevant to the physiological condition, consisting of repetitive depolarizing pulses (DPs) at 0.1 Hz, was able to induce long-lasting changes in both frequency and amplitude of sGABAA -PSCs between P0 and P8. Starting from P12, DPs were unable to induce any form of synaptic plasticity. The effects of DPs were tightly keyed to the frequency at which they were delivered. When delivered at a lower (0.05 Hz) or higher (1 Hz) frequency, DPs failed to induce any long-lasting change in the frequency or amplitude of sGABAA -PSCs. In two cases, DPs were able to activate sGABAA -PSCs in previously synaptically silent cells at P0,1. These results show that long-term changes in GABAergic synaptic activity can be induced during a restricted period of development by a conditioning protocol relevant to the physiological condition. It is suggested that such activity-induced modifications may represent a physiological mechanism for the functional maturation of GABAergic synaptic transmission. [source]


CN algorithm and long-lasting changes in reported magnitudes: the case of Italy

GEOPHYSICAL JOURNAL INTERNATIONAL, Issue 2 2000
A. Peresan
Prediction methods based on seismic precursors, and hence assuming that catalogues contain the necessary information to predict earthquakes, are sometimes criticised for their sensitivity to the unavoidable catalogue errors and possible undeclared variations in the evaluation of reported magnitudes. We consider a real example and we discuss the effect, on CN predictions, of a long-lasting underestimation of the reported magnitudes. Starting approximately in 1988, the CN functions in Central Italy evidence an anomalous behaviour, not associated with TIPs, that indicates an unusual absence of moderate events. To investigate this phenomenon, the magnitudes given in the catalogue used, which since 1980 is defined by the ING bulletins, are compared to the magnitudes reported by the global catalogue NEIC (National Earthquake Information Centre, USGS, USA) and by the regional LDG bulletins issued at the Laboratoire de Detection et de Geophysique, Bruyeres-le-Chatel, France. The comparison is performed between the ING bulletins and the NEIC catalogue, considering the local, ML,, and duration, Md,, magnitudes, first within the Central region, and then extended to the whole Italian territory. To check the consistency of the conclusions drawn from ING and NEIC data, the comparison of local magnitudes is extended to a third data set, the LDG bulletins. The differences between duration magnitudes Md that are reported by ING and NEIC since 1983 appear quite constant with time. Starting in 1987, an average underestimation of about 0.5 can be attributed to ML reported by ING for the Central region; this difference decreases to about 0.2 when the whole Italian territory is considered. The anomalous behaviour of the CN functions disappears if a magnitude correction of +0.5 is applied to ML reported in the ING bulletins. However, such a simple magnitude shift cannot restore the real features of the seismic flow, and ING bulletins are not suitable for CN algorithm application. [source]


Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

HIPPOCAMPUS, Issue 8 2005
David M. Diamond
Abstract This speculative review serves two purposes. First, it as an extension of the ideas we developed in a previous review (Diamond et al., Hippocampus, 2004;14:281,291), and second, it is a rebuttal to Abraham's (Hippocampus, 2004;14:675,676) critique of that review. We had speculated on the functional significance of the finding that post-training LTP induction produces retrograde amnesia. We noted the similarities between the findings that strong tetanizing stimulation can produce LTP and retrograde amnesia, and that a strong emotional experience can produce a long-lasting memory and retrograde amnesia, as well. The commonalities between LTP induction and emotional learning provided the basis of our hypothesis that an emotional experience generates endogenous LTD/depotentiation, which reverses synaptic plasticity formed during previous learning experiences, and endogenous LTP, which underlies the storage of new information. Abraham raised several concerns with our review, including the criticism that our speculation "falters because there is no evidence that stress causes LTD or depotentiation," and that research on stress and hippocampus has "failed to report any LTP-like changes." Abraham's points are well-taken because stress, in isolation, does not appear to generate long-lasting changes in baseline measures of hippocampal excitability. Here, within the context of a reply to Abraham's critique, we have provided a review of the literature on the influence of stress, novelty, fear conditioning, and the retrieval of emotional memories on cognitive and physiological measures of hippocampal functioning. An emphasis of this review is our hypothesis that endogenous forms of depotentiation, LTD and LTP are generated only when arousing experiences occur in conjunction with memory-related activation of the hippocampus and amygdala. We conclude with speculation that interactions among the different forms of endogenous plasticity underlie a form of competition by synapses and memories for access to retrieval resources. © 2005 Wiley-Liss, Inc. [source]


Intermittent hypoxia during sleep induces reactive gliosis and limited neuronal death in rats: implications for sleep apnea

JOURNAL OF NEUROCHEMISTRY, Issue 4 2010
Rolando Xavier Aviles-Reyes
J. Neurochem. (2010) 112, 854,869. Abstract Sleep apnea (SA) can be effectively managed in humans but it is recognized that when left untreated, SA causes long-lasting changes in neuronal circuitry in the brain. Recent neuroimaging studies gave suggested that these neuronal changes are also present even in patients successfully treated for the acute effects of SA. The cellular mechanisms that account for these changes are not certain but animal models of intermittent hypoxia (IH) during sleep have shown neuronal death and impairment in learning and memory. Reactive gliosis has a drastic effect on neuronal survival and circuitry and in this study we examined the neuro-glial response in brain areas affected by SA. Glial and neuronal alterations were analyzed after 1, 3, 5 and 10 days of exposure to IH (8 h/day during the sleep phase, cycles of 6 min each, 10,21% O2) and observed significant astroglial hyperplasia and hypertrophy in parietal brain cortex and hippocampus by studying gliofibrillary acidic protein, Vimentin, S100B and proliferating cell nuclear antigen expression. In addition, altered morphology, reduced dendrite branching and caspase activation were observed in the CA-1 hippocampal and cortical (layers IV,V) pyramidal neurons at short exposure times (1,3 days). Surprisingly, longer exposure to IH reduced the neuronal death rate and increased neuronal branching in the presence of persistent reactive gliosis. Up-regulation of hypoxia inducible factor 1 alpha (HIF-1,) and mdr-1, a HIF-1, target gene, were observed and increased expression of receptor for advanced end glycated products and its binding partner S100B were also noted. Our results show that a low number of hypoxic cycles induce reactive gliosis and neuronal death whereas continuous exposure to IH cycles reduced the rate of neuronal death and induced neuronal branching on surviving neurons. We hypothesize that HIF-1, and S100B glial factor may improve neuronal survival under hypoxic conditions and propose that the death/survival/re-growth process observed here may underlie brain circuitry changes in humans with SA. [source]


Regulation of mitogen-activated protein kinases by glutamate receptors

JOURNAL OF NEUROCHEMISTRY, Issue 1 2007
John Q. Wang
Abstract Glutamate receptors regulate gene expression in neurons by activating intracellular signaling cascades that phosphorylate transcription factors within the nucleus. The mitogen-activated protein kinase (MAPK) cascade is one of the best characterized cascades in this regulatory process. The Ca2+ -permeable ionotropic glutamate receptor, mainly the NMDA receptor subtype, activates MAPKs through a biochemical route involving the Ca2+ -sensitive Ras-guanine nucleotide releasing factor, Ca2+/calmodulin-dependent protein kinase II, and phosphoinositide 3-kinase. The metabotropic glutamate receptor (mGluR), however, activates MAPKs primarily through a Ca2+ -insensitve pathway involving the transactivation of receptor tyrosine kinases. The adaptor protein Homer also plays a role in this process. As an information superhighway between surface glutamate receptors and transcription factors in the nucleus, active MAPKs phosphorylate specific transcription factors (Elk-1 and CREB), and thereby regulate distinct programs of gene expression. The regulated gene expression contributes to the development of multiple forms of synaptic plasticity related to long-lasting changes in memory function and addictive properties of drugs of abuse. This review, by focusing on new data from recent years, discusses the signaling mechanisms by which different types of glutamate receptors activate MAPKs, features of each MAPK cascade in regulating gene expression, and the importance of glutamate/MAPK-dependent synaptic plasticity in memory and addiction. [source]


Land use legacies in post-agricultural forests in the Doupovské Mountains, Czech Republic

APPLIED VEGETATION SCIENCE, Issue 2 2009
Martin Kopecký
Abstract Questions: Do differences in previous land use cause long-lasting changes in soil chemistry? Is vegetation composition affected by the previous land use after 50 years of secondary succession? Is the effect of previous land use caused by pre-existing differences in environmental conditions or mediated through changes in soil chemistry? How important is the effect of previous land use in relation to other factors? Location: Doupovské Mountains, Czech Republic. Methods: A stratified random sampling design was used to collect 91 vegetation relevés with accompanying soil samples. The effects of previous land use (arable field, meadow, pasture) on soil pH, organic carbon (C), total nitrogen (N), C:N ratio and available phosphorus were tested by an analysis of covariance. A canonical correspondence analysis and variation partitioning procedure were used to reveal relationships among previous land use, environmental factors and species composition. Results: Organic C, total N and C:N ratio were significantly influenced by previous land use, while available phosphorus and soil pH were not. Previous land use explained a significant part of the variation in species composition and its effects only partly overlapped with the effects of soil chemistry and terrain attributes. However, the species composition of post-agricultural forests was mostly determined by environmental factors not modified by previous land use. Conclusions: Forest communities that originate on abandoned agricultural land are primarily determined by natural environmental conditions. Nevertheless, the type of previous land use also modifies the species assemblages of these forests and needs to be considered as an important determinant of their composition. [source]