13 research outputs found

    Disparate Postsynaptic Induction Mechanisms Ultimately Converge to Drive the Retrograde Enhancement of Presynaptic Efficacy

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    Retrograde signaling systems are fundamental modes of communication synapses utilize to dynamically and adaptively modulate activity. However, the inductive mechanisms that gate retrograde communication in the postsynaptic compartment remain enigmatic. We have investigated retrograde signaling at the Drosophila neuromuscular junction, where three seemingly disparate perturbations to the postsynaptic cell trigger a similar enhancement in presynaptic neurotransmitter release. We show that the same presynaptic genetic machinery and enhancements in active zone structure are utilized by each inductive pathway. However, all three induction mechanisms differ in temporal, translational, and CamKII activity requirements to initiate retrograde signaling in the postsynaptic cell. Intriguingly, pharmacological blockade of postsynaptic glutamate receptors, and not calcium influx through these receptors, is necessary and sufficient to induce rapid retrograde homeostatic signaling through CamKII. Thus, three distinct induction mechanisms converge on the same retrograde signaling system to drive the homeostatic strengthening of presynaptic neurotransmitter release

    Spatial patterns of genome‐wide expression profiles reflect anatomic and fiber connectivity architecture of healthy human brain

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    Unraveling the relationship between molecular signatures in the brain and their functional, architectonic and anatomic correlates is an important neuroscientific goal. It is still not well understood whether the diversity demonstrated by histological studies in the human brain is reflected in the spatial patterning of whole brain transcriptional profiles. Using genome-wide maps of transcriptional distribution of the human brain by the Allen Brain Institute, we test the hypothesis that gene expression profiles are specific to anatomically described brain regions. In this work, we demonstrate that this is indeed the case by showing that gene similarity clusters appear to respect conventional basal-cortical and caudal-rostral gradients. To fully investigate the causes of this observed spatial clustering, we test a connectionist hypothesis that states that the spatial patterning of gene expression in the brain is simply reflective of the fiber tract connectivity between brain regions. We find that although gene expression and structural connectivity are not determined by each other, they do influence each other with a high statistical significance. This implies that spatial diversity of gene expressions is a result of mainly location-specific features, but is influenced by neuronal connectivity, such that like cellular species preferentially connects with like cells

    A Glutamate Homeostat Controls the Presynaptic Inhibition of Neurotransmitter Release

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    Summary: We have interrogated the synaptic dialog that enables the bi-directional, homeostatic control of presynaptic efficacy at the glutamatergic Drosophila neuromuscular junction (NMJ). We find that homeostatic depression and potentiation use disparate genetic, induction, and expression mechanisms. Specifically, homeostatic potentiation is achieved through reduced CaMKII activity postsynaptically and increased abundance of active zone material presynaptically at one of the two neuronal subtypes innervating the NMJ, while homeostatic depression occurs without alterations in CaMKII activity and is expressed at both neuronal subtypes. Furthermore, homeostatic depression is only induced through excess presynaptic glutamate release and operates with disregard to the postsynaptic response. We propose that two independent homeostats modulate presynaptic efficacy at the Drosophila NMJ: one is an intercellular signaling system that potentiates synaptic strength following diminished postsynaptic excitability, while the other adaptively modulates presynaptic glutamate release through an autocrine mechanism without feedback from the postsynaptic compartment. : Homeostatic mechanisms stabilize synaptic strength, but the signaling systems remain enigmatic. Li et al. suggest the existence of a homeostat operating at the Drosophila neuromuscular junction that responds to excess glutamate through an autocrine mechanism to adaptively inhibit presynaptic neurotransmitter release. This system parallels forms of plasticity at central synapses. Keywords: homeostatic synaptic plasticity, glutamate homeostasis, synaptic depression, Drosophila neuromuscular junctio

    Prevalence & perinatal outcome of GDM : a tertiary teaching hospital based study

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    Can we do something to improve outcomes of GDM?Much needs to be done to deal with epidemic of GDM in India as it affects both mother and fetus adversely.This study was aimed to find out the data pertaining to GDM.Using notional sampling frame 200 pregnant women  were offered  75 gm oral glucose tolerance test between 24 to 28 weeks of gestation,irrespective of the fasting status as recommended by DIPSI.Patients having values ≥140 mg/dl ,2 hrs after administration of 75 gm oral glucose were labelled as GDM.Whole cohort was followed during antenatal period and upto 7 days after delivery for fetomaternal outcome. Prevalence of GDM was 8% in our study. Statistically significant  increased rates of gestational hypertension,chronic hypertension, preeclampsia,UTI,preterm delivery,rate of caesarean section and polyhydramnios were found  in GDM patients.Statistically significant higher rates of metabolic complications,respiratory distress,admission to neonatal unit and macrosomia were found in neonates of GDM mothers.Hence there is a need for studying outcomes as well as cost effectiveness of different diagnostic criteria while simultaneously creating social awareness, training manpower, and sensitizing policymakers to make GDM testing and management mandatory during pregnancy at all levels

    Delayed post-hatch feeding affects the performance and immunocompetence differently in male and female broiler chickens

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    The effect of post-hatch (PH) feed deprival for 6, 12, 24 and 36 h was studied in male and female broiler chickens. At 21 d, lower body weight (BW) was recorded in 36 h feed-deprived (FD) birds; however, at 42 d PH, only 36 h FD female birds had lower BW compared to control and other FD birds. Feed intake during 0–21 d PH was lower in 36 h FD birds, but feed conversion ratio did not differ between control and FD birds. The H:L ratio significantly increased in 12–36 h FD male birds and 24–36 h FD females. The humoral immune response was similar in FD and control birds, but the cellular immune response was higher in 12 and 24 h FD female birds. At 36 h the expression of interleukin 6 (IL-6), toll-like receptor-2 (TLR-2) and tumour necrosis factor-α- gene was down-regulated in male birds only. However, the expression of IL-6 and TLR-2 was up-regulated in 12–36 h FD female birds at 7 and 14 d PH. It may be concluded that PH feed deprival for the first 24 h did not affect growth performance but improved immune response in slow-growing broiler females

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    No full text
    Not AvailableThe effect of post-hatch (PH) feed deprival for 6, 12, 24 and 36 h was studied in male and female broiler chickens. At 21 d, lower body weight (BW) was recorded in 36 h feed-deprived (FD) birds; however, at 42 d PH, only 36 h FD female birds had lower BW compared to control and other FD birds. Feed intake during 0–21 d PH was lower in 36 h FD birds, but feed conversion ratio did not differ between control and FD birds. The H:L ratio significantly increased in 12–36 h FD male birds and 24–36 h FD females. The humoral immune response was similar in FD and control birds, but the cellular immune response was higher in 12 and 24 h FD female birds. At 36 h the expression of interleukin 6 (IL-6), toll-like receptor-2 (TLR-2) and tumour necrosis factor-α- gene was down-regulated in male birds only. However, the expression of IL-6 and TLR-2 was up-regulated in 12–36 h FD female birds at 7 and 14 d PH. It may be concluded that PH feed deprival for the first 24 h did not affect growth performance but improved immune response in slow-growing broiler females.Not Availabl
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