As the effects of the Global Climate Changes on the costal regions of Central and South Americas advance, there is proportionally little research being made to understand such impacts. This commentary puts forward a series of propositions of strategies to improve performance of Central and South American science and policy making in order to cope with the future impacts of the Global Climate Changes in their coastal habitats. 相似文献
Prenatal opiate exposure causes a series of neurobehavioral disturbances by affecting brain development. However, the question of whether prenatal opiate exposure increases vulnerability to memory‐related neuropsychiatric disorders in adult offspring remains largely unknown. Here, we found that rats prenatally exposed to morphine (PM) showed impaired acquisition but enhanced maintenance of contextual fear memory compared with control animals that were prenatally exposed to saline (PS). The impairment of acquisition was rescued by increasing the intensity of footshocks (1.2 mA rather than 0.8 mA). Meanwhile, we also found that PM rats exhibited impaired extinction of contextual fear, which is associated with enhanced maintenance of fear memory. The impaired extinction lasted for 1 week following extinction training. Furthermore, PM rats exhibited reduced anxiety‐like behavior in the elevated plus‐maze and light/dark box test without differences in locomotor activity. These alterations in PM rats were mirrored by abnormalities in synaptic plasticity in the Schaffer collateral‐CA1 synapses of the hippocampus in vivo. PS rats showed blocked long‐term potentiation and enabled long‐term depression in CA1 synapses following contextual fear conditioning, while prenatal morphine exposure restricted synaptic plasticity in CA1 synapses. The smaller long‐term potentiation in PM rats was not further blocked by contextual fear conditioning, and the long‐term depression enabled by contextual fear conditioning was abolished. Taken together, our results provide the first evidence suggesting that prenatal morphine exposure may increase vulnerability to fear memory‐related neuropsychiatric disorders in adulthood. 相似文献
Cdk5 (cyclin-dependent kinase 5) activity is dependent upon association with one of two neuron-specific activators, p35 or p39. Genetic deletion of Cdk5 causes perinatal lethality with severe defects in corticogenesis and neuronal positioning. p35(-/-) mice are viable with milder histological abnormalities. Although substantial evidence implicates Cdk5 in synaptic plasticity, its role in learning and memory has not been evaluated using mutant mouse models. We report here that p35(-/-) mice have deficiencies in spatial learning and memory. Close examination of hippocampal circuitry revealed subtle histological defects in CA1 pyramidal cells. Furthermore, p35(-/-) mice exhibit impaired long-term depression and depotentiation of long-term potentiation in the Schaeffer collateral CA1 pathway. Moreover, the Cdk5-dependent phosphorylation state of protein phosphatase inhibitor-1 was increased in 4-week-old mice due to increased levels of p39, which co-localized with inhibitor-1 and Cdk5 in the cytoplasm. These results demonstrate that p35-dependent Cdk5 activity is important to learning and synaptic plasticity. Deletion of p35 may shift the substrate specificity of Cdk5 due to compensatory expression of p39. 相似文献
A major goal of learning and memory research is to correlate the function of molecules with the behaviour of organisms. The beautiful laminar structure of the cerebellar cortex lends itself to the study of synaptic plasticity, because its clearly defined patterns of neurons and their synapses form circuits that have been implicated in simple motor behaviour paradigms. The best understood in terms of molecular mechanism is the parallel fibre-Purkinje cell synapse, where presynaptic long-term potentiation and postsynaptic long-term depression and potentiation finely tune cerebellar output. Our understanding of these forms of plasticity has mostly come from the electrophysiological and behavioural analysis of knockout mutant mice, but more recently the knock-in of synaptic molecules with mutated phosphorylation sites and binding domains has provided more detailed insights into the signalling events. The present review details the major forms of plasticity in the cerebellar cortex, with particular attention to the membrane trafficking and intracellular signalling responsible. This overview of the current literature suggests it will not be long before the involvement of the cerebellum in certain motor behaviours is fully explained in molecular terms. 相似文献
Murine polyomavirus is used in various models of persistent virus infection. This study was undertaken to assess the spatial and temporal patterns of MPyV infection in the brains of immunocompetent (BALB/c) and immunocompromised (KSN nude) mice. MPyV was stereotaxically microinfused into the brain parenchyma, and the kinetics of infection were examined by quantitative PCR. In BALB/c mice, the amount of viral DNA in the brain peaked at 4 days p.i. and then rapidly diminished. In contrast, MPyV DNA levels increased up to 4 days and then gradually decreased over the 30‐day observation period in the brain of KSN mice. In both mouse strains, viral DNA was readily detected around the sites of inoculation from 2 to 6 days p.i., and continued to be detected for up to 30 days p.i. In addition, MPyV infection did not lead to a drastic induction of innate immune response in the brains, nor did MPyV‐inoculated mice show any signs of disease. These results indicate that MPyV establishes an asymptomatic long‐term infection in the mouse brain. 相似文献
Ethanol (EtOH) induces cognitive impairment through modulation of synaptic plasticity notably in the hippocampus. The cellular mechanism(s) of these EtOH effects may range from synaptic signaling modulation to alterations of the epigenome. Previously, we reported that two binge‐like exposures to EtOH (3 g/kg, ip, 9 h apart) in adolescent rats abolished long‐term synaptic depression (LTD) in hippocampus slices, induced learning deficits, and increased N‐methyl‐d ‐aspartate (NMDA) receptor signaling through its GluN2B subunit after 48 hours. Here, we tested the hypothesis of EtOH‐induced epigenetic alterations leading to modulation of GluN2B and GluN2A NMDA receptor subunits. Forty‐two days old rats were treated with EtOH or the histone deacetylase inhibitor (HDACi) sodium butyrate (NaB, 600 mg/kg, ip) injected alone or 30 minutes before EtOH. After 48 hours, learning was tested with novel object recognition while synaptic plasticity and the role of GluN2A and GluN2B subunits in NMDA‐fEPSP were measured in CA1 field of hippocampus slices. LTD and memory were impaired 48 hours after EtOH and NMDA‐fEPSP analysis unraveled changes in the GluN2A/GluN2B balance. These results were associated with an increase in histone deacetylase (HDAC) activity and HDAC2 mRNA and protein while Ac‐H4K12 labelling was decreased. EtOH increases expression of HDAC2 and mRNA level for GluN2B subunit (but not GluN2A), while HDAC2 modulates the promoter of the gene encoding GluN2B. Interestingly, NaB pretreatment prevented all the cellular and memory‐impairing effects of EtOH. In conclusion, the memory‐impairing effects of two binge‐like EtOH exposure involve NMDA receptor‐dependent LTD deficits due to a GluN2A/GluN2B imbalance resulting from changes in GluN2B expression induced by HDAC2. 相似文献
Three individually housed bonnet macaque males were given 75 weeks of continuous access to a joystick task with a reward choice of either viewing live color video of a bonnet group or obtaining a banana-flavored food treat. Here we report data for weeks 44-75 following a change in the stimulus group displayed in the video. The new stimulus group enhanced responding to the video for two subjects over the entire 32 weeks of this study, although there was some decline across weeks, and the video continued to be an effective reward for the duration of the study for all subjects. 相似文献
Objective: The aim of this study was to evaluate how well prepregnancy BMI, gestational weight gain, and postpartum weight retention predict retention of weight 15 years later among parous women. Research Methods and Procedures: The Stockholm Pregnancy and Women's Nutrition (SPAWN) study is a long‐term follow‐up study of women who delivered children in 1984 to 1985 (n = 2342). The participants initially filled out questionnaires about their eating and exercise habits, social circumstances, etc. before, during, and at 1 year after pregnancy. Anthropometric data were also sampled. Fifteen years later, these women were invited to take part in the follow‐up study. Anthropometric measurements were collected, and similar questions were asked. Five hundred sixty‐three women participated in the SPAWN 15‐year follow‐up study. The sample was divided into groups to examine three presumably critical time periods: 1) overweight and normal weight before pregnancy; 2) low, intermediate, and high weight gainers during pregnancy; and 3) low, intermediate, and high weight retainers at 1 year after pregnancy. Results: The overweight women did not gain more weight during pregnancy or retain more weight at 1 year follow‐up. High weight gainers during pregnancy retained more weight at the 1‐year and the 15‐year follow‐ups. High weight retainers had gained more during pregnancy and retained it at the 15‐year follow‐up. Fifty‐six percent of the high weight gainers during pregnancy ended up in the high weight retainers group. Discussion: Women who are overweight before pregnancy do not have a higher risk of postpartum weight retention than normal weight women. Thus, it is not necessarily the initially overweight woman who should be the target or focus of weight control programs during or after pregnancy. Both high weight gainers and high weight retainers had higher BMI at the 15‐year follow‐up, although only 56% of the high weight gainers during pregnancy were also classified as high weight retainers at the 1‐year follow‐up. Weight retention at the end of the postpartum year predicts future overweight 15 years later. 相似文献
In the face of rapid environmental and cultural change, long‐term ecological research (LTER) and social‐ecological research (LTSER) are more important than ever. LTER contributes disproportionately to ecology and policy, evidenced by the greater proportion of LTER in higher impact journals and the disproportionate representation of LTER in reports informing policymaking. Historical evidence has played a significant role in restoration projects and it will continue to guide restoration into the future, but its use is often hampered by lack of information, leading to considerable uncertainties. By facilitating the storage and retrieval of historical information, LTSER will prove valuable for future restoration. 相似文献
Previous studies have implicated the role of Purkinje cells in motor learning and the underlying mechanisms have also been identified in great detail during the last decades. Here we report that cyclin‐dependent kinase 5 (Cdk5)/p35 in Purkinje cell also contributes to synaptic plasticity. We previously showed that p35?/? (p35 KO) mice exhibited a subtle abnormality in brain structure and impaired spatial learning and memory. Further behavioral analysis showed that p35 KO mice had a motor coordination defect, suggesting that p35, one of the activators of Cdk5, together with Cdk5 may play an important role in cerebellar motor learning. Therefore, we created Purkinje cell‐specific conditional Cdk5/p35 knockout (L7‐p35 cKO) mice, analyzed the cerebellar histology and Purkinje cell morphology of these mice, evaluated their performance with balance beam and rota‐rod test, and performed electrophysiological recordings to assess long‐term synaptic plasticity. Our analyses showed that Purkinje cell‐specific deletion of Cdk5/p35 resulted in no changes in Purkinje cell morphology but severely impaired motor coordination. Furthermore, disrupted cerebellar long‐term synaptic plasticity was observed at the parallel fiber‐Purkinje cell synapse in L7‐p35 cKO mice. These results indicate that Cdk5/p35 is required for motor learning and involved in long‐term synaptic plasticity.
doi: 10.1111/j.1741‐2358.2011.00513.x Health care professionals’ perspectives on oral care for long‐term care residents: Nursing staff, speech–language pathologists and dental hygienists Background: Oral health has been identified as a key factor in general health and systemic disease in long‐term care populations. To optimise oral health of this population, it is important to understand the oral care perspectives held by health care professionals involved in oral care provision. Objectives: To explore perspectives regarding oral care held by nursing staff, speech–language pathologists (SLPs) and dental hygienists (DHs) in long‐term care institutions and to understand how their perspectives impact activities and processes involved in the delivery of oral care. Methods: A focus group methodology was utilised. Separate focus groups for each targeted profession were held. Transcribed data were analysed using constant comparative analysis. Results: Daily oral health maintenance and monitoring was considered a role of nursing staff. SLPs and DHs have roles focusing on advocacy, education and supplemental care. Social factors motivate nursing staff to provide oral care, whereas factors related to the general health consequences of poor oral health underlined the motivations of SLPs and DHs. Conclusions: Education and training initiatives incorporating social aspects of oral health may be more effective for motivating nursing staff than approaches emphasising physical risk factors. Organisations can foster environments that support collaboration and communication amongst the members of multidisciplinary teams in order to promote oral health as a priority. 相似文献
Integrins are heterodimeric transmembrane cell adhesion receptors that are essential for a wide range of biological functions via cell–matrix and cell–cell interactions. Recent studies have provided evidence that some of the subunits in the integrin family are involved in synaptic and behavioral plasticity. To further understand the role of integrins in the mammalian central nervous system, we generated a postnatal forebrain and excitatory neuron‐specific knockout of α8‐integrin in the mouse. Behavioral studies showed that the mutant mice are normal in multiple hippocampal‐dependent learning tasks, including a T‐maze, non‐match‐to‐place working memory task for which other integrin subunits like α3‐ and β1‐integrin are required. In contrast, mice mutant for α8‐integrin exhibited a specific impairment of long‐term potentiation (LTP) at Schaffer collateral–CA1 synapses, whereas basal synaptic transmission, paired‐pulse facilitation and long‐term depression (LTD) remained unaffected. Because LTP is also impaired in the absence of α3‐integrin, our results indicate that multiple integrin molecules are required for the normal expression of LTP, and different integrins display distinct roles in behavioral and neurophysiological processes like synaptic plasticity. 相似文献
Methyl‐β‐cyclodextrin (MβCD) is a reagent that depletes cholesterol and disrupts lipid rafts, a type of cholesterol‐enriched cell membrane microdomain. Lipid rafts are essential for neuronal functions such as synaptic transmission and plasticity, which are sensitive to even low doses of MβCD. However, how MβCD changes synaptic function, such as N‐methyl‐d ‐aspartate receptor (NMDA‐R) activity, remains unclear. We monitored changes in synaptic transmission and plasticity after disrupting lipid rafts with MβCD. At low concentrations (0.5 mg/mL), MβCD decreased basal synaptic transmission and miniature excitatory post‐synaptic current without changing NMDA‐R‐mediated synaptic transmission and the paired‐pulse facilitation ratio. Interestingly, low doses of MβCD failed to deplete cholesterol or affect α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPA‐R) and NMDA‐R levels, while clearly reducing GluA1 levels selectively in the synaptosomal fraction. Low doses of MβCD decreased the inhibitory effects of NASPM, an inhibitor for GluA2‐lacking AMPA‐R. MβCD successfully decreased NMDA‐R‐mediated long‐term potentiation but did not affect the formation of either NMDA‐R‐mediated or group I metabotropic glutamate receptor‐dependent long‐term depression. MβCD inhibited de‐depression without affecting de‐potentiation. These results suggest that MβCD regulates GluA1‐dependent synaptic potentiation but not synaptic depression in a cholesterol‐independent manner.
