19 resultados para Tripartite synapse


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Quantum-state sharing is a protocol where perfect reconstruction of quantum states is achieved with incomplete or partial information in a multipartite quantum network. Quantum-state sharing allows for secure communication in a quantum network where partial information is lost or acquired by malicious parties. This protocol utilizes entanglement for the secret-state distribution and a class of quantum disentangling protocols for the state reconstruction. We demonstrate a quantum-state sharing protocol in which a tripartite entangled state is used to encode and distribute a secret state to three players. Any two of these players can collaborate to reconstruct the secret state, while individual players obtain no information. We investigate a number of quantum disentangling processes and experimentally demonstrate quantum-state reconstruction using two of these protocols. We experimentally measure a fidelity, averaged over all reconstruction permutations, of F=0.73 +/- 0.02. A result achievable only by using quantum resources.

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Objective: The tripartite model of anxiety and depression has been proposed as a representation of the structure of anxiety and depression symptoms. The Mood and Anxiety Symptom Questionnaire (MASQ) has been put forwards as a valid measure of the tripartite model of anxiety and depression symptoms. This research set out to examine the factor structure of anxiety and depression symptoms in a clinical sample to assess the MASQ's validity for use in this population. MethodsThe present study uses confirmatory factor analytic methods to examine the psychometric properties of the MASQ in 470 outpatients with anxiety and mood disorder. Results: The results showed that none of the previously reported two-factor, three-factor or five-factor models adequately fit the data, irrespective of whether items or subscales were used as the unit of analysis. Conclusions: It was concluded that the factor structure of the MASQ in a mixed anxiety/depression clinical sample does not support a structure consistent with the tripartite model. This suggests that researchers using the MASQ with anxious/depressed individuals should be mindful of the instrument's psychometric limitations.

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The goals of this study are to determine relationships between synaptogenesis and morphogenesis within the mushroom body calyx of the honeybee Apis mellifera and to find out how the microglomerular structure characteristic for the mature calyx is established during metamorphosis. We show that synaptogenesis in the mushroom body calycal neuropile starts in early metamorphosis (stages P1-P3), before the microglomerular structure of the neuropile is established. The initial step of synaptogenesis is characterized by the rare occurrence of distinct synaptic contacts. A massive synaptogenesis starts at stage P5, which coincides with the formation of microglomeruli, structural units of the calyx that are composed of centrally located presynaptic boutons surrounded by spiny postsynaptic endings. Microglomeruli are assembled either via accumulation of fine postsynaptic processes around preexisting presynaptic boutons or via ingrowth of thin neurites of presynaptic neurons into premicroglomeruli, tightly packed groups of spiny endings. During late pupal stages (P8-P9), addition of new synapses and microglomeruli is likely to continue. Most of the synaptic appositions formed there are made by boutons (putative extrinsic mushroom body neurons) into small postsynaptic profiles that do not exhibit presynaptic specializations (putative intrinsic mushroom body neurons). Synapses between presynaptic boutons characteristic of the adult calyx first appear at stage P8 but remain rare toward the end of metamorphosis. Our observations are consistent with the hypothesis that most of the synapses established during metamorphosis provide the structural basis for afferent information flow to calyces, whereas maturation of local synaptic circuitry is likely to occur after adult emergence.

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Agrin is a proteoglycan secreted by motor neurite terminals that functions to initiate and maintain AChR clusters at the nerve terminal. This led to the theory that neurite terminals decide where neuromuscular synapses form by secreting agrin. However, initiation of AChR clustering occurs in the absence of the innervating motoneuron and in the absence of agrin. In this instance, the muscle, not the nerve, is deciding the location of neuromuscular synapses by drawing neurite terminals towards pre-existing AChR clusters. If this were true, one would expect the initial innervation patterns to be the same in agrin-deficient mice and wild-type mice. To test this we quantified the intramuscular axonal branching and synapse formation in the diaphragm at E14.5 in agrin-deficient mice and wild-type mice. Heterozygote mothers were anaesthetised with Nembutal (30 mg) and killed via cervical dislocation. In the diaphragm, the nerve trunk runs down the centre of the muscle and extends branches primarily toward the lateral side. In agrin-deficient mice however, we found significantly more branches exited the phrenic nerve trunk, branched in the periphery and extended further on the medial side. Moreover, we found that the percentage α-bungarotoxin/synaptophysin colocalisations, markers of pre- and postsynaptic differentiation, respectively, was the same in agrin-deficient mice and wild-type mice. These results show that initial innervation patterns are not the same in agrin-deficient mice and wild-type mice indicating neurite terminals, not muscle, decide the placement of neuromuscular synapses in the absence of agrin.