Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dysregulation of the immune response by malaria parasite has been considered as a possible constraint to the effectiveness of malaria vaccination. In spite of the important role interleukin-1 (IL-1) plays on the immunoregulation, and its ability to mimic various features of clinical malaria, reports on IL-1 in malaria are lacking. We found that only 2 out of 35 subjects with acute malaria showed increased levels of serum IL-1 alpha by enzyme immunoassay. To assess whether IL-1 could interfere with T-lymphocyte responses, blood mononuclear cells from patients infected with Plasmodium falciparum, P. vivax, or healthy subjects were cultured with phytohemagglutinin, and lymphocyte proliferation measured 72 h later by 3H-thymidine incorporation. Our data showed that T-lymphocyte responses are depressed both in P. falciparum (10,500 +/- 2,900) and P. vivax malaria (13,000 +/- 3,300), as compared to that of healthy individuals (27,000 +/- 3,000). Addition of IL-1 partially reversed depression of malaria lymphocytes, but had no effect on normal cells. On the other hand, T-lymphocytes from malaria infected-subjects presented a minimal decrease in proliferation, when cultured in the presence of exogenous PGE2. These data indicate the occurrence of two defects of immunoregulation in malaria: a deficiency of IL-1 production by monocytes/macrophages, and an increased resistance of lymphocytes to the antiproliferative effect of PGE2.
Mem Inst Oswaldo Cruz 1992
PMID:Cytokines and dysregulation of the immune response in human malaria. 134 9

Neurophysins are neuropeptides (MW +/- 10,000) synthetized together with active nonapeptides vasopressin (AVP) and oxytocin (OT). The original description of the radioimmunoassay for neurophysins in 1969 allowed us to demonstrate the concomitant, equimolecular, release of them together with AVP and OT, thus bringing strong arguments in favour of neurohypophyseal exocytosis. Beside the use of those RIAs as direct indexes of neurohypophyseal release in various physiological and pathological conditions, we have been interested these last two years, to the putative use of neurophysins RIA as direct neuroendocrine markers in various neuropsychiatric diseases (depression, mania, schizophrenia) and paraneoplastic syndromes (SIADH).
Bull Mem Acad R Med Belg 1990
PMID:[Neurophysins]. 209 28

Long-term potentiation (LTP) in the hippocampus and long-term depression (LTD) in the cerebellum are two forms of long-lasting synaptic plasticity that currently serve as our primary experimental models of learning and memory formation in mammals. In recent years, there have been considerable advances in our understanding of the cellular and molecular mechanisms of these and other forms of synaptic plasticity. This article presents an overview of these developments, considers the relationship of long-term synaptic plasticity mechanisms to learning and memory in view of these developments, and suggests future directions for research in this rapidly growing area of neuroscience.
Neurobiol Learn Mem 1995 Jan
PMID:Properties and mechanisms of long-term synaptic plasticity in the mammalian brain: relationships to learning and memory. 766 75

During Schistosoma mansoni infection, there is morphological evidence of involvement of various hematopoietic growth factors, which cause eosinophil, neutrophil, megakaryocytic and erythroid extramedullary foci in the liver, lymph nodes and omental and mesenteric milky spots. While the eosinophil metaplasia in the periphery of hepatic granulomas roughly reproduced the intensity of the medullary eosinopoiesis, the neutrophil metaplasia, on the contrary, was more intense during the period of neutrophil depression in the bone marrow. This fact suggests that extramedullary hematopoietic foci are locally regulated, and amplify and/or compensate the systemic hematopoietic response during the infection.
Mem Inst Oswaldo Cruz
PMID:Extramedullary hematopoiesis in murine schistosomiasis mansoni. 853 53

Triatoma jurbergi n. sp. is described based on nine specimens of both sexes deposited in the Rodolfo Carcavallo Collection in the Oswaldo Cruz Institute Entomological Collection. The new species can be separated from the closely related Triatoma guazu Lent & Wygodzinsky, 1979 by several characters. The most important are longer anteocular region; thin and pointed juga: the shape of the eyes without concavity in the posterior edge; much longer second rostral segment, passing the posterior edge of eye; the absence of a ventral longitudinal depression on the abdomen; the general color redish, brown and orange and the male genitalia, mainly in the vesical lightly chitinized and smaller, the phallosome with apical projection and the pointed apex of the endosome process.
Mem Inst Oswaldo Cruz
PMID:[Triatoma jurbergi sp. n. from the State of Mato Grosso, Brazil (Hemiptera, Reduviidae, Triatominae) with an updated list of synonyms and other taxa]. 971 34

We have found that two distinct forms of long-term depression (LTD), one dependent on the activation of NMDA receptors (NMDARs) and the other dependent on the activation of metabotropic glutamate receptors (mGluRs), coexist in pyramidal cells of the CA1 region of the hippocampus of juvenile rats (11-35 days). Both forms were pathway specific, required membrane depolarization, and were blocked by chelating postsynaptic Ca2+ with BAPTA. The mGluR-LTD, but not the NMDAR-LTD, was blocked by the T-type Ca2+ channel blocker Ni2+ and intracellular administration of a protein kinase C inhibitory peptide. In contrast, the protein phosphatase inhibitor Microcystin LR blocked NMDAR-LTD, but not mGluR-LTD. NMDAR-LTD is associated with a decrease in the size of quantal excitatory postsynaptic currents, whereas for mGluR-LTD there was no change in quantal size, but a large decrease in the frequency of events. While mGluR-LTD did not interact with NMDAR-dependent long term potentiation (LTP), NMDAR-LTD was capable of reversing LTP. Prior saturation of mGluR-LTD had no effect on NMDAR-LTD. NMDAR-LTD and mGluR-LTD thus appear to be mechanistically distinct forms of synaptic plasticity in that they share neither induction nor expression mechanisms.
Neurobiol Learn Mem
PMID:NMDA receptor-dependent and metabotropic glutamate receptor-dependent forms of long-term depression coexist in CA1 hippocampal pyramidal cells. 975 87

The coordinated activity of large numbers of adjacent parallel fiber synapses elevate calcium concentration locally in small regions of Purkinje cell dendrites. Such activity has also been reported to produce long-term depression of parallel fiber synaptic transmission. We have examined the relationship between these two events by combining patch clamp measurements of parallel fiber synaptic transmission with confocal microscopic imaging of the local calcium signals. We find that patterns of parallel fiber activity capable of evoking long-term depression invariably cause increases in Purkinje cell calcium concentration that are very spatially restricted. These results suggest that one function of the local dendritic calcium signals is to induce long-term depression of parallel fiber synapses.
Learn Mem
PMID:Local dendritic Ca2+ signaling induces cerebellar long-term depression. 1045 60

We present a model based on the synaptic and cellular organization of the cerebellum to derive a diverse range of phenomena observed in Pavlovian eyelid conditioning. These phenomena are addressed in terms of critical pathways and network properties, as well as the sites and rules for synaptic plasticity. The theory is based on four primary hypotheses: (1) Two cerebellar sites of plasticity are involved in conditioning: (a) bidirectional long-term depression/potentiation at granule cell synapses onto Purkinje cells (gr-->Pkj) in the cerebellar cortex and (b) bidirectional plasticity in the interpositus nucleus that is controlled by inhibitory inputs from Purkinje cells; (2) climbing fiber activity is regulated to an equilibrium level at which the net strength of gr-->Pkj synapses remains constant unless an unexpected unconditioned stimulus (US) is presented or an expected US is omitted; (3) a time-varying representation of the conditioned stimulus (CS) in the cerebellar cortex permits the temporal discrimination required for conditioned response timing; and (4) the ability of a particular segment of the CS to be represented consistently across trials varies as a function of time since CS onset. This variation in across-trials consistency is thought to contribute to the ISI function. The model suggests several empirically testable predictions, some of which have been tested recently.
Learn Mem
PMID:A model of Pavlovian eyelid conditioning based on the synaptic organization of the cerebellum. 1045 59

Extensive pharmacological evidence suggests that nitric oxide (NO) is a crucial transmitter for cerebellar long-term depression (LTD), a long-lasting decrease in efficacy of the synapses from parallel fibers onto Purkinje neurons, triggered by coincident presynaptic activity and postsynaptic depolarization. We now show that LTD cannot be induced in Purkinje neurons under whole-cell patch clamp in cerebellar slices from young adult mice genetically lacking neuronal nitric oxide synthase (nNOS). This genetic evidence confirms the essentiality of NO and nNOS for LTD in young adult rodents. Surprisingly, LTD in cells from nNOS knockout mice cannot be rescued by photolytic uncaging of NO and cGMP inside Purkinje neurons, although such stimuli circumvent acute pharmacological inhibition of nNOS and soluble guanylate cyclase in normal rodents. Also slices from knockout mice show no deficit in cGMP elevation in response to exogenous NO. Therefore, prolonged absence of nNOS allows atrophy of the signaling pathway downstream of cGMP.
Learn Mem
PMID:Absence of cerebellar long-term depression in mice lacking neuronal nitric oxide synthase. 1045 61

Previous studies have established that (1) a 1-min episode of theta pulse stimulation (TPS) is sufficient to reverse potentiation during the early phases of LTP in area CA1 without causing depression when administered to nonpotentiated pathways; (2) the magnitude of depotentiation is inversely related to the delay between LTP induction and reversal attempts; and (3) pharmacological facilitation of AMPA receptor-mediated currents significantly enhances the strength of the reversal mechanism. The present experiments confirm and extend these results by showing that the depotentiating action of TPS on prior LTP is antagonized by inhibitors of protein phosphatases and adenosine A1 receptors but is not affected by NMDA receptor blockade, and, moreover, that TPS interferes with subsequent LTP induction by triggering an inhibitory mechanism that is active for a few minutes and is blocked by phosphatase inhibition. The possible implications of these results are discussed.
Learn Mem
PMID:Proactive and retrograde effects on LTP produced by theta pulse stimulation: mechanisms and characteristics of LTP reversal in vitro. 1045 80


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