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This paper presents a novel LoRa (Long Range) receiver operating in frequency selective Multi-Path Channel (MPC). The dechirped received LoRa wave-forms under MPC allows us to derive a simple and efficient LoRa receiver scheme by using a MF (Matched Filter) approach that aims to maximize the SNR (Signal-to-Noise Ratio) at the symbol index frequency of the DFT output. We show that the MF receiver can be seen as RAKE structure where interference peaks related to multipath, exhibited at DFT output, are recombined in a constructive way. Detection performance is driven by channel energy and the benefit of this novel MF/RAKE receiver over original coherent and non-coherent receiver appears only for MPC that exhibits significant paths energy. These two MF and RAKE receivers have however different implementation complexities that are studied in details. We provide in that sense recommendations on which receiver variant to use for real operations, depending on complexity constraints. Finally, the proposed MF/RAKE receiver outperforms previous results on TDEL (Time Delay Estimation LoRa) receiver over MPC, especially at low SNR and higher LoRa Spreading Factor (SF) parameter, at the cost of higher but reasonable complexity.

International audience; This paper presents a semi-analytical approximation of Symbol Error Rate (SER) for the well known LoRa Internet of Things (IoT) modulation scheme in the following two scenarios: 1) in multi-path frequency selective fading channel with Additive White Gaussian Noise (AW GN) and 2) in the presence of a second interfering LoRa user in flat-fading AW GN channel. Performances for both coherent and non-coherent cases are derived by considering the common Discrete Fourier transform (DF T) based detector on the received LoRa waveform. By considering these two scenarios, the detector exhibits parasitic peaks that severely degrade the performance of the LoRa receiver. We propose in that sense a theoretical expression for this result, from which a unified framework based on peak detection probabilities allows us to derive SER, which is validated by Monte Carlo simulations. Fast computation of the derived closedform SER allows to carry out deep performance analysis for these two scenarios.

In this paper, we present a new LoRa transceiver scheme to ensure discrete communications secure from potential eavesdroppers by leveraging a simple and elegant spread spectrum philosophy. The scheme modifies both preamble and payload waveforms by adapting a current state-of-the-art LoRa synchronization front-end. This scheme can also be seen as a self-jamming approach. Furthermore, we introduce a new payload demodulation method that avoids the adverse effects of the traditional cross-correlation solution that would otherwise be used. Our simulation results show that the self-jamming scheme exhibits very good symbol error rate (SER) performance with a loss of just 0.5 dB for a frequency spread factor of up to 10.

Significance Learning depends on synaptic plasticity. The signaling mechanisms that control induction of plasticity determine the learning rules at the specific synapse involved. Moreover, the relationship between the activity patterns of synaptic inputs and the type, direction, and level of plasticity induced may evolve during development. Here, we establish a key link between receptor activation presynaptic to cerebellar Purkinje cells, downstream signaling mechanisms, and the ability of adult animals to learn a cerebellar motor task., Long-term synaptic plasticity is believed to be the cellular substrate of learning and memory. Synaptic plasticity rules are defined by the specific complement of receptors at the synapse and the associated downstream signaling mechanisms. In young rodents, at the cerebellar synapse between granule cells (GC) and Purkinje cells (PC), bidirectional plasticity is shaped by the balance between transcellular nitric oxide (NO) driven by presynaptic N-methyl-D-aspartate receptor (NMDAR) activation and postsynaptic calcium dynamics. However, the role and the location of NMDAR activation in these pathways is still debated in mature animals. Here, we show in adult rodents that NMDARs are present and functional in presynaptic terminals where their activation triggers NO signaling. In addition, we find that selective genetic deletion of presynaptic, but not postsynaptic, NMDARs prevents synaptic plasticity at parallel fiber-PC (PF-PC) synapses. Consistent with this finding, the selective deletion of GC NMDARs affects adaptation of the vestibulo-ocular reflex. Thus, NMDARs presynaptic to PCs are required for bidirectional synaptic plasticity and cerebellar motor learning.

Precise quantitative information about the molecular architecture of synapses is essential to understanding the functional specificity and downstream signaling processes at specific populations of synapses. Glycine receptors (GlyRs) are the primary fast inhibitory neurotransmitter receptors in the spinal cord and brainstem. These inhibitory glycinergic networks crucially regulate motor and sensory processes. Thus far the nanoscale organization of GlyRs underlying the different network specificities has not been defined. Here, we have quantitatively characterized the molecular arrangement and ultra-structure of glycinergic synapses in spinal cord tissue using quantitative super-resolution correlative light and electron microscopy (SR-CLEM). We show that endogenous GlyRs exhibit equal receptor-scaffold occupancy and constant packing densities of about 2000 GlyRs μm-2 at synapses across the spinal cord and throughout adulthood, even though ventral horn synapses have twice the total copy numbers, larger postsynaptic domains and more convoluted morphologies than dorsal horn synapses. We demonstrate that this stereotypic molecular arrangement is maintained at glycinergic synapses in the oscillator mouse model of the neuromotor disease hyperekplexia despite a decrease in synapse size, indicating that the molecular organization of GlyRs is preserved in this hypomorph. We thus conclude that the morphology and size of inhibitory postsynaptic specializations rather than differences in GlyR packing determine the postsynaptic strength of glycinergic neurotransmission in motor and sensory spinal cord networks.

Long-term synaptic plasticity is believed to be the cellular substrate of learning and memory. Synaptic plasticity rules are defined by the specific complement of receptors at the synapse and the associated downstream signaling mechanisms. In young rodents, at the cerebellar synapse between granule cells (GC) and Purkinje cells (PC), bidirectional plasticity is shaped by the balance between transcellular nitric oxide (NO) driven by presynaptic NMDA receptor (NMDAR) activation and postsynaptic calcium dynamics. However, the role and the location of NMDAR activation in these pathways is still debated in mature animals. Here, we show in adult rodents that NMDARs are present and functional in presynaptic terminals where their activation triggers nitric oxide signaling. In addition, we find that selective genetic deletion of presynaptic, but not postsynaptic, NMDARs prevents synaptic plasticity at parallel fiber-Purkinje cell (PF-PC) synapses. Consistent with this finding, the selective deletion of GCs NMDARs affects adaptation of the vestibulo-ocular reflex. Thus, NMDARs presynaptic to PCs are required for bidirectional synaptic plasticity and cerebellar motor learning.Significance StatementLearning depends on synaptic plasticity. The signaling mechanisms that control induction of plasticity determine the learning rules at the specific synapse involved. Moreover, the relationship between the activity patterns of synaptic inputs and the type, direction, and level of plasticity induced may evolve during development. Here, we establish a key link between NMDA receptor activation presynaptic to cerebellar Purkinje cells, downstream signaling mechanisms, and the ability of adult animals to learn a cerebellar motor task.

Pyramidal neurons are covered by thousands of dendritic spines receiving excitatory synaptic inputs. The ultrastructure of dendritic spines shapes signal compartmentalization but ultrastructural diversity is rarely taken into account in computational models of synaptic integration. Here, we developed a 3D correlative light-electron microscopy (3D-CLEM) approach allowing the analysis of specific populations of synapses in genetically defined neuronal types in intact brain circuits. We used it to reconstruct segments of basal dendrites of layer 2/3 pyramidal neurons of adult mouse somatosensory cortex and quantify spine ultrastructural diversity. We found that 10% of spines were dually-innervated and 38% of inhibitory synapses localized to spines. Using our morphometric data to constrain a model of synaptic signal compartmentalization, we assessed the impact of spinous versus dendritic shaft inhibition. Our results indicate that spinous inhibition is locally more efficient than shaft inhibition and that it can decouple voltage and calcium signaling, potentially impacting synaptic plasticity.

Pyramidal neurons (PNs) are covered by thousands of dendritic spines receiving excitatory synaptic inputs. The ultrastructure of dendritic spines shapes signal compartmentalization, but ultrastructural diversity is rarely taken into account in computational models of synaptic integration. Here, we developed a 3D correlative light–electron microscopy (3D-CLEM) approach allowing the analysis of specific populations of synapses in genetically defined neuronal types in intact brain circuits. We used it to reconstruct segments of basal dendrites of layer 2/3 PNs of adult mouse somatosensory cortex and quantify spine ultrastructural diversity. We found that 10% of spines were dually innervated and 38% of inhibitory synapses localized to spines. Using our morphometric data to constrain a model of synaptic signal compartmentalization, we assessed the impact of spinous versus dendritic shaft inhibition. Our results indicate that spinous inhibition is locally more efficient than shaft inhibition and that it can decouple voltage and calcium signaling, potentially impacting synaptic plasticity., Pyramidal neurons are covered by thousands of dendritic spines receiving excitatory synaptic inputs. A new 3D correlative light-electron microscopy (3D-CLEM) approach enables the cartography of synaptic ultrastructure with cell type-, dendrite type- and synapse type-specific resolution in brain tissues, revealing unique properties of spines that receive dual innervation.

The marine pennate diatom Phaeodactylum tricornutum has become a model for diatom biology, due to its ease of culture and accessibility to reverse genetics approaches. While several features underlying the molecular mechanisms of cell division have been described, morphological analyses are less advanced than they are in other diatoms. We therefore examined cell ultrastructure changes prior to and during cytokinesis. Following chloroplast division, cleavage furrows are formed at both longitudinal ends of the cell and are accompanied by significant vesicle transport. Although neither spindle nor microtubules were observed, the nucleus appeared to be split by the furrow after duplication of the Golgi apparatus. Finally, centripetal cytokinesis was completed by fusion of the furrows. Additionally, F-actin formed a ring structure and its diameter became smaller, accompanying the ingrowing furrows. To further analyse vesicular transport during cytokinesis, we generated transgenic cells expressing yellow fluorescent protein (YFP) fusions with putative diatom orthologs of small GTPase Sec4 and t-SNARE protein SyntaxinA. Time-lapse observations revealed that SyntaxinA-YFP localization expands from both cell tips toward the center, whereas Sec4-YFP was found in the Golgi and subsequently relocalizes to the future division plane. This work provides fundamental new information about cell replication processes in P. tricornutum.

International audience; Dysfunction of microglia, the tissue macrophages of the brain, has been associated with the etiology of several neuropsychiatric disorders. Consistently, microglia have been shown to regulate neurogenesis and synaptic maturation at perinatal and postnatal stages. However, microglia invade the brain during mid-embryogenesis and thus could play an earlier prenatal role. Here, we show that embryonic microglia, which display a transiently uneven distribution, regulate the wiring of forebrain circuits. Using multiple mouse models, including cell-depletion approaches and cx3cr1−/−, CR3−/−, and DAP12−/− mutants, we find that perturbing microglial activity affects the outgrowth of dopaminergic axons in the forebrain and the laminar positioning of subsets of neocortical interneurons. Since defects in both dopamine innervation and cortical networks have been linked to neuropsychiatric diseases, our study provides insights into how microglial dysfunction can impact forebrain connectivity and reveals roles for immune cells during normal assembly of brain circuits.

The concatenation of multiple-input multiple-output (MIMO) linear precoder with an outer forward error correction (FEC) encoder is investigated at the transmitter. Turbo detection is applied at the receiver for the decoding. The bit-interleaved codeword is considered to be grouped and mapped directly onto the received constellation thanks to a MIMO symbol mapper. We exploit the optimal maximum squared Euclidean weight (MSEW) mappings for two forms of max-d min precoder to propose a novel precoder referred to as max-l min . The switching threshold between both forms is optimized by considering all received sequences whose binary mappings differ by exactly one bit and by first maximizing the minimum Euclidean distance within this set and then minimizing the number of pairs achieving it. Extrinsic information transfer (EXIT) chart is also used to validate the analysis. Simulation results show significant improvement, in terms of system error-rate performance, of the max-l min compared to the conventional max-d min .

Summary The density of GABA A receptors (GABA A Rs) at synapses regulates brain excitability, and altered inhibition may contribute to Huntington's disease, which is caused by a polyglutamine repeat in the protein huntingtin. However, the machinery that delivers GABA A Rs to synapses is unknown. We demonstrate that GABA A Rs are trafficked to synapses by the kinesin family motor protein 5 (KIF5). We identify the adaptor linking the receptors to KIF5 as the huntingtin-associated protein 1 (HAP1). Disrupting the HAP1-KIF5 complex decreases synaptic GABA A R number and reduces the amplitude of inhibitory postsynaptic currents. When huntingtin is mutated, as in Huntington's disease, GABA A R transport and inhibitory synaptic currents are reduced. Thus, HAP1-KIF5-dependent GABA A R trafficking is a fundamental mechanism controlling the strength of synaptic inhibition in the brain. Its disruption by mutant huntingtin may explain some of the defects in brain information processing occurring in Huntington's disease and provides a molecular target for therapeutic approaches.

International audience; This study deals with two linear precoders: the maximization of the minimum Euclidean distance between received symbol-vectors, called here max-dmin, and the maximization of the post-processing signal-to-noise ratio termed max-SNR or beamforming. Both have been designed for reliable MIMO transmissions operating over uncorrelated Rayleigh fading channels. Here, we will explain why performances in terms of bit error rates show a significant enhancement of the max-dmin over the max-SNR whenever the number of antennas is increased. Then, from theoretical developments, we will demonstrate that, like the max-SNR precoder, the max-dmin precoder achieves the maximum diversity order, which is warrant of reliable transmissions. The current theoretical knowledge will be applied to the case-study of a system with two transmit- or two receive-antennas to calculate the probability density functions of two channel parameters directly linked to precoder performances for uncorrelated Rayleigh fading channels. At last, this calculation will allow us to quickly get the BER of the max-dmin precoder further to the derivation of a tight semi-theoretical approximation.

In this paper, we focus on a multiple-input multiple-output (MIMO) linear precoder based on the minimum Euclidean distance criterion, the max- dmin precoder. We propose an optimization of this precoder for the case of an association with a non-binary low density parity check code (NB- LDPC). After recalling the well-known max-dmin precoder, we set forth an optimization of the mutual information of initial message, i.e. I(0), through the extrinsic information transfer (EXIT) analysis of the system. We present a new adaptive precoder whose forms are determined in function of an adaptive threshold angle, optimized in terms of the mutual information I(0), and depending on the signal-to-noise ratio at the reception (SNR_R). The performance of the new precoder is brought out through a theoretical study along with a series of numerical simulations.

Electron microscopy allows the analysis of synaptic ultrastructure and its modifications during learning or in pathological conditions. However, conventional electron microscopy uses aldehyde fixatives that alter the morphology of the synapse by changing osmolarity and collapsing its molecular components. We have used high-pressure freezing (HPF) to capture within a few milliseconds structural features without aldehyde fixative, and thus to provide a snapshot of living synapses. CA1 hippocampal area slices from P21 rats were frozen at −173 °C under high pressure to reduce crystal formation, and synapses on dendritic spines were analysed after cryosubstitution and embedding. Synaptic terminals were larger than after aldehyde fixation, and synaptic vesicles in these terminals were less densely packed. Small filaments linked the vesicles in subgroups. The postsynaptic densities (PSDs) exhibited filamentous projections extending into the spine cytoplasm. Tomographic analysis showed that these projections were connected with the spine cytoskeletal meshwork. Using immunocytochemistry, we found as expected GluR1 at the synaptic cleft and CaMKII in the PSD. Actin immunoreactivity (IR) labelled the cytoskeletal meshwork beneath the filamentous projections, but was very scarce within the PSD itself. ProSAP2/Shank3, cortactin and Ena/VASP-IRs were concentrated on the cytoplasmic face of the PSD, at the level of the PSD projections. Synaptic ultrastructure after HPF was different from that observed after aldehyde fixative. The boutons were larger, and filamentous components were preserved. Particularly, filamentous projections were observed linking the PSD to the actin cytoskeleton. Thus, synaptic ultrastructure can be analysed under more realistic conditions following HPF.

A first mammalian lysosomal transporter (LYAAT-1) was recently identified and functionally characterized. Preliminary immunocytochemical data revealed that LYAAT-1 localizes to lysosomes in some neurons. In order to determine whether it is expressed in specific neuron populations and other cell types, and to confirm whether it is localized at the membrane of lysosomes, we used in situ hybridization and immunohistochemistry methods in adult rat central nervous system (CNS). We found that LYAAT-1 is expressed in most areas of the CNS, specifically in neurons, but also in choroid plexus and ependymal epithelium cells. LYAAT-1-IR (immunoreactivity) levels varied among different neuroanatomical structures but were present in neurons independently of the neurotransmitter used (glutamate, GABA, acetylcholine, noradrenaline, serotonin, or glycine). Light and confocal microscopy demonstrated that LYAAT-1 and the lysosomal marker cathepsin D colocalized throughout the brain and electron microscopy showed that LYAAT-1-IR was associated with lysosomal membranes. In addition, LYAAT-1-IR was also found associated with other membranes belonging to the Golgi apparatus and lateral saccules and less frequently with multivesicular bodies, endoplasmic reticulum, and occasionally with the plasma membrane. The localization of LYAAT-1 at the lysosomal membrane is consistent with the view that it mediates amino acid efflux from lysosomes. Furthermore, its cell expression pattern suggests that it may contribute to specialized cellular function in the rat CNS such as neuronal metabolism, neurotransmission, and control of brain amino acid homeostasis.

GABA(A) receptors the major sites of fast synaptic inhibition in the brain are composed predominately of alpha, beta, and gamma2 subunits. The receptor gamma2 subunit interacts with a 17-kDa microtubule associated protein GABARAP, but the significance of this interaction remains unknown. Here we demonstrate that GABARAP, which immunoprecipitates with GABA(A) receptors, is not found at significant levels within inhibitory synapses, but is enriched within the Golgi apparatus and postsynaptic cisternae. We also demonstrate that GABARAP binds directly to N-ethylmaleimide-sensitive factor (NSF), a protein critical for intracellular membrane trafficking events. NSF and GABARAP complexes could be detected in neurons and these two proteins also colocalize within intracellular membrane compartments. Together our observations suggest that GABARAP may play a role in intracellular GABA(A) receptor transport but not synaptic anchoring, via its ability to interact with NSF. GABARAP may therefore have an important role in the production of GABAergic synapses.

Spinal muscular atrophy (SMA) is among the most common recessive autosomal diseases and is characterized by the loss of spinal motor neurons. A gene termed ‘Survival of Motor Neurons' (SMN) has been identified as the SMA-determining gene. Recent work indicates the involvement of the SMN protein and its associated protein SIP1 in spliceosomal snRNP biogenesis. However, the function of SMN remains unknown. Here, we have studied the subcellular localization of SMN in the rat spinal cord and more generally in the central nervous system (CNS), by light fluorescence and electron microscopy. SMN immunoreactivity (IR) was found in the different regions of the spinal cord but also in various regions of the CNS such as the brainstem, cerebellum, thalamus, cortex and hippocampus. In most neurons, we observed a speckled labelling of the cytoplasm and a discontinuous staining of the nuclear envelope. For some neurons (e.g. brainstem nuclei, dentate gyrus, cortex: layer V) and, in particular in motoneurons, SMN-IR was also present as prominent nuclear dot-like-structures. In these nuclear dots, SMN colocalized with SIP1 and with fibrillarin, a marker of coiled bodies. Ultrastructural studies in the anterior horn of the spinal cord confirmed the presence of SMN in the coiled bodies and also revealed the protein at the external side of nuclear pores complexes, in association with polyribosomes, and in dendrites, associated with microtubules. These localizations suggest that, in addition to its involvement in the spliceosome biogenesis, the SMN protein could also play a part in nucleocytoplasmic and dendritic transport.

In a previous study, miniature inhibitory synaptic events recorded in the Mauthner cell of the 52-hour-old zebrafish larvae (Brachydanio rerio) were found to be mainly glycinergic. Their amplitude distribution was not Gaussian and it was proposed that their large amplitude variation might reflect the activation of immature synapses. However, ultrastructural studies of the synaptic contacts over the M-cell soma of 52 h larvae described here, revealed that numerous synaptic contacts on this neuron are already mature at this developmental stage and that most of them already contain a single active zone. As in the adult goldfish, immunohistochemistry indicates the presence of both glycine- and GABA-immunoreactive boutons which establish synaptic contacts. We also found that, in addition to the predominant glycinergic postsynaptic inhibitory currents, some postsynaptic currents are also GABAergic since they are specifically inhibited by bicuculline (20 microM). GABAergic miniature events (time to peak close to 0.8 ms and decay time-constant close to 45 ms) were only detected in the presence of 11.5 mM [KCl]o. Their amplitude distributions were well fitted by one, or at most two, Gaussian curves. Outside-out recordings showed one class of GABA receptors with a main conductance state of 23 pS. This indicates that the smallest GABAergic miniature inhibitory synaptic events correspond to the opening of 14-20 chloride channels Pre- and postsynaptic factors which contribute to the predominance of glycinergic synaptic currents over GABAergic ones in untreated preparations and to the striking differences between their frequencies and their respective amplitude distribution histograms are discussed with reference to the morphological characteristics of the mature synaptic endings impinging on this still developing neuron.

In this paper, we present a transmission model for a multiple-input multiple-output (MIMO) channel with perfect channel state information (CSI). We intend to exploit the available CSI through the use of a precoder based on the minimum Euclidean distance (dmin) criterion. We also introduce a low density parity check coding block in order to improve the system performance. We consider a two-stream 4QAM-MIMO transmission scheme (4 bits per transmitted symbol vector) associated to a non-binary LDPC (NB-LDPC) code over GF(24). The addition of the precoder in this system is studied. Simulations are made in order to show the interest of the association of the dmin-based precoder with NB-LDPC codes, which is particularly well suited for LDPC codes with high rates.

International audience; Precoder optimization with full channel state in- formation (CSI) for finite alphabet signals over multiple-input multiple-output (MIMO) random channels is investigated in this paper. The precoder is represented by a product of power allocation matrix and constellation-forming matrix. There was an optimal algorithm introduced in literature to globally maximize the channel mutual information by iteratively optimizing these two matrices. However, the computational complexity of the optimal algorithm is painfully high, especially when it is used with high-order modulation and high data stream number. In this paper, we propose a novel sub-optimal low-complexity precoding algorithm and compare it with the optimal one. The new algorithm proceeds in two steps. First, the constellation-forming matrix is fixed in order to maximize the minimum Euclidean distance between the received symbols, which ensures high chan- nel mutual information. Then, given the constellation-forming matrix, an iterative algorithm searches for the power allocation matrix that maximizes the channel mutual information. Since optimizing only one matrix instead of two, the new algorithm not only achieves a lower computational complexity but also avoids the use of initial values, which must be carefully selected for each channel and signal-to-noise ratio for fast convergence. Another advantage of the new algorithm is that the resulting precoder has a fixed form of received constellation thanks to the fixed constellation-forming matrix. This allows us to optimize the symbol mapping on the received constellation. Simulation results show that the proposed low-complexity precoder achieves error- rate performance that is close to performance of the optimal one when the conventional mapping is used. In addition, the new precoder used with optimized mapping at received constellation shows significant error-rate performance improvement.

Miniature synaptic currents have long been known to represent random transmitter release under resting conditions, but much remains to be learned about their nature and function in central synapses. In this work, we describe a new class of miniature currents ("preminis") that arise by the autocrine activation of axonal receptors following random vesicular release. Preminis are prominent in gabaergic synapses made by cerebellar interneurons during the development of the molecular layer. Unlike ordinary miniature postsynaptic currents in the same cells, premini frequencies are strongly enhanced by subthreshold depolarization, suggesting that the membrane depolarization they produce belongs to a feedback loop regulating neurotransmitter release. Thus, preminis could guide the formation of the interneuron network by enhancing neurotransmitter release at recently formed synaptic contacts.

Presynaptic terminals are specialized for mediating rapid fusion of synaptic vesicles (SVs) after calcium influx. The regulated trafficking of SVs likely results from a highly organized cytomatrix. How this cytomatrix links SVs, maintains them near the active zones (AZs) of release, and organizes docked SVs at the release sites is not fully understood. To analyze the three-dimensional (3D) architecture of the presynaptic cytomatrix, electron tomography of presynaptic terminals contacting spines was performed in the stratum radiatum of the rat hippocampal CA1 area. To preserve the cytomatrix, hippocampal slices were immobilized using high-pressure freezing, followed by cryosubstitution and embedding. SVs are surrounded by a dense network of filaments. A given vesicle is connected to approximately 1.5 neighboring ones. SVs at the periphery of this network are also linked to the plasma membrane, by longer filaments. More of these filaments are found at the AZ. At the AZ, docked SVs are grouped around presynaptic densities. Filaments with adjacent SVs emerge from these densities. Immunogold localizations revealed that synapsin is located in the presynaptic bouton, whereas Bassoon and CAST (ERC2) are at focal points next to the AZ. In synapsin triple knock-out mice, the number of SVs is reduced by 63%, but the size of the boutons is reduced by only 18%, and the mean distance of SVs to the AZ is unchanged. This 3D analysis reveals the morphological constraints exerted by the presynaptic molecular scaffold. SVs are tightly interconnected in the axonal bouton, and this network is preferentially connected to the AZ.

International audience; This study deals with three transmission schemes because of their ability to achieve the maximum diversity order. Two of them are systems using the full channel state information at the transmitter side (Tx-CSI), i.e. the max-dmin precoder (maximization of minimum Euclidean distance (dmin) and max-SNR precoder (maximization of the received signal-to-noise ratio), whereas the last one is the Alamouti scheme belonging to the orthogonal space-time block code family which needs no Tx-CSI. Their performances are compared by using a dual-polarization channel model to take into account polarization diversity, transmit/receive correlation and estimation errors.

Inhibitory transmission in the hippocampus is predominantly GABAergic, but electrophysiological data evidenced strychnine-sensitive glycine-induced currents. However, synaptic currents have not been reported. Here, we describe, for the first time, the presence of GlyR clusters in several areas of the hippocampus as well as in cultured hippocampal neurons. In contrast with spinal cord, hippocampal GlyRs contain alpha2 but no alpha1 subunit. Optical and electron microscopy indicates that GlyRs can be synaptic as well as extrasynaptic. Synaptic GlyRs were apposed to glycinergic boutons characterized by the expression of the vesicular and the plasma membrane transporters of glycine (VIAAT and GlyT2, respectively). Double labeling with calcium-binding proteins showed that GlyT2 could be detected in boutons innervating both excitatory cells (soma and dendrites) and interneurons. Finally, GlyR clusters could be detected at synaptic sites with the GABAA receptor gamma2 subunit and gephyrin, suggesting that mixed GABA/glycine synapses might exist in the hippocampus.

Semiconductor quantum dots (QDs) are nanometer-sized fluorescent probes suitable for advanced biological imaging. We used QDs to track individual glycine receptors (GlyRs) and analyze their lateral dynamics in the neuronal membrane of living cells for periods ranging from milliseconds to minutes. We characterized multiple diffusion domains in relation to the synaptic, perisynaptic, or extrasynaptic GlyR localization. The entry of GlyRs into the synapse by diffusion was observed and further confirmed by electron microscopy imaging of QD-tagged receptors.

A first mammalian lysosomal transporter (LYAAT-1) was recently identified and functionally characterized. Preliminary immunocytochemical data revealed that LYAAT-1 localizes to lysosomes in some neurons. In order to determine whether it is expressed in specific neuron populations and other cell types, and to confirm whether it is localized at the membrane of lysosomes, we used in situ hybridization and immunohistochemistry methods in adult rat central nervous system (CNS). We found that LYAAT-1 is expressed in most areas of the CNS, specifically in neurons, but also in choroid plexus and ependymal epithelium cells. LYAAT-1-IR (immunoreactivity) levels varied among different neuroanatomical structures but were present in neurons independently of the neurotransmitter used (glutamate, GABA, acetylcholine, noradrenaline, serotonin, or glycine). Light and confocal microscopy demonstrated that LYAAT-1 and the lysosomal marker cathepsin D colocalized throughout the brain and electron microscopy showed that LYAAT-1-IR was associated with lysosomal membranes. In addition, LYAAT-1-IR was also found associated with other membranes belonging to the Golgi apparatus and lateral saccules and less frequently with multivesicular bodies, endoplasmic reticulum, and occasionally with the plasma membrane. The localization of LYAAT-1 at the lysosomal membrane is consistent with the view that it mediates amino acid efflux from lysosomes. Furthermore, its cell expression pattern suggests that it may contribute to specialized cellular function in the rat CNS such as neuronal metabolism, neurotransmission, and control of brain amino acid homeostasis.

The characterization of the Caenorhabditis elegans unc-47 gene recently allowed the identification of a mammalian (gamma)-amino butyric acid (GABA) transporter, presumed to be located in the synaptic vesicle membrane. In situ hybridization data in rat brain suggested that it might also take up glycine and thus represent a general Vesicular Inhibitory Amino Acid Transporter (VIAAT). In the present study, we have investigated the localization of VIAAT in neurons by using a polyclonal antibody raised against the hydrophilic N-terminal domain of the protein. Light microscopy and immunocytochemistry in primary cultures or tissue sections of the rat spinal cord revealed that VIAAT was localized in a subset (63-65%) of synaptophysin-immunoreactive terminal boutons; among the VIAAT-positive terminals around motoneuronal somata, 32.9% of them were also immunoreactive for GAD65, a marker of GABAergic presynaptic endings. Labelling was also found apposed to clusters positive for the glycine receptor or for its associated protein gephyrin. At the ultrastructural level, VIAAT immunoreactivity was restricted to presynaptic boutons exhibiting classical inhibitory features and, within the boutons, concentrated over synaptic vesicle clusters. Pre-embedding detection of VIAAT followed by post-embedding detection of GABA or glycine on serial sections of the spinal cord or cerebellar cortex indicated that VIAAT was present in glycine-, GABA- or GABA- and glycine-containing boutons. Taken together, these data further support the view of a common vesicular transporter for these two inhibitory transmitters, which would be responsible for their costorage in the same synaptic vesicle and subsequent corelease at mixed GABA-and-glycine synapses.

Aerial surveillance is an issue of key importance for warship protection. In addition to radar systems, infrared surveillance sensors represent an interesting alternative for remote observation. In this paper, we study such a system and an original approach to the tracking of complex cloudy patterns in noisy infrared image sequences is proposed. We have paid particular attention to robustness with regards to perturbations likely to occur (noise, 'lining effects' . . .). Our approach relies on robust parametric motion estimation and an original regularization scheme allows to handle with the appearance and the disappearance of objects in the scene. Numerous experiments performed on outdoor infrared image sequences underline the efficiency of the proposed method.© (1998) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

The distribution of glycine receptor (GlyR)-associated gephyrin has been investigated in rat spinal cord neurons maintained in vitro by means of immunocytochemical techniques. Gephyrin, which is crucial for the stabilization of postsynaptic GlyR microdomains, is present in mature neurons at postsynaptic differentiations. With immunofluorescence, discontinuous patches of gephyrin were detected within the neuronal soma of spinal cord neurons on the 1st day after plating. Subsequently, gephyrin was present at membrane areas that correspond to points of contact between cells or with the culture dish. By the 5th day, gephrin was mostly associated with the MAP2-positive somatodendritic compartment. With immunoelectron microscopy, gephyrin blobs detected at the earliest stages (1-3 days after plating) were found within the cytoplasm or associated with the plasma membrane. Asymmetrically immunostained intercellular contacts were only detected after 5 days, and gephyrin was found in association with clearly differentiated postsynaptic membranes at 7 days. At later stages, we observed gephyrin immunoreactivity only at some synapses. Our results suggest that gephyrin accumulates initially at the locus of cell-to-cell contacts involved in adhesion processes. These localizations may define hot spots for later accumulation of the GlyR and possibly other receptors.

International audience; Multiple-input multiple-output (MIMO) maxi-mum-SNR (max-SNR) system employs the maximum ratio combiner (MRC) at the receiver side and the maximum ratio transmitter (MRT) at the transmitter side. Its performances highly depend on MIMO channel characteristics, which vary according to both the number of antennas and their distribution between the transmitter and receiver sides. By using the decomposition of the ordered Wishart distribution in the uncorrelated Rayleigh case, we derived a closed-form expression of the largest eigenvalue probability density function (PDF). The final result yields to an expression form of the PDF where polynomials are multiplied by exponentials; it is worth underlining that, though this form had been previously observed for given couples of antennas, to date no formally-written closed-form was available in the literature for an arbitrary couple. Then, this new expression permits one to quickly and easily get the well known largest eigenvalue PDF and use it to determine the binary error probability (BEP) of the max-SNR.