Lateral Connectivity in the Olfactory Bulb is Sparse and Segregated

Kim, David H.; Phillips, Matthew E.; Chang, Andrew Y.; Patel, Hetal K.; Nguyen, Katherine T.; Willhite, David C.

doi:10.3389/fncir.2011.00005

Cited by 43 publications

(53 citation statements)

References 49 publications

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“…If we model a double injection in two of the mitral cells of the same glomerulus (red and green in Fig. 1E, Middle), we observe that they form connections with different sets of GCs (red and green dots below the glomerulus), as suggested by experiments (7). Finally, as shown in Fig.…”

Section: Significancesupporting

confidence: 54%

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Synaptic clusters function as odor operators in the olfactory bulb

Migliore

Cavarretta

Marasco

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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How the olfactory bulb organizes and processes odor inputs through fundamental operations of its microcircuits is largely unknown. To gain new insight we focus on odor-activated synaptic clusters related to individual glomeruli, which we call glomerular units. Using a 3D model of mitral and granule cell interactions supported by experimental findings, combined with a matrix-based representation of glomerular operations, we identify the mechanisms for forming one or more glomerular units in response to a given odor, how and to what extent the glomerular units interfere or interact with each other during learning, their computational role within the olfactory bulb microcircuit, and how their actions can be formalized into a theoretical framework in which the olfactory bulb can be considered to contain "odor operators" unique to each individual. The results provide new and specific theoretical and experimentally testable predictions. T he organization of olfactory bulb network elements and their synaptic connectivity has evolved to subserve special computational functions needed for odor detection and recognition (1-5). Key to this organization are the olfactory glomeruli, collecting input from olfactory receptor neuron subsets. These connect to the dendrites of mitral, tufted, and periglomerular cells, and the mitral and tufted cells in turn connect to granule cells. We term these interconnected cells a cluster, and a cluster related to a given glomerulus is a glomerular unit (GU), often visualized as a column of granule cell bodies located below a glomerulus (6, 7). The existence of such GUs has also been suggested from 2-deoxyglucose (8) and voltage-sensitive dye studies (9).Understanding the neural basis of odor processing therefore requires understanding the computational functions and role of GUs. These issues, which are difficult or impossible in experiments, can be conveniently explored using realistic computational models, provided they are able to explain and reproduce crucial experimental findings on glomerular clusters or units.Analyzing synaptic interactions between cells with overlapping dendrites requires modeling in real 3D space. Scaling up to the network level further requires scaling up realistic structural and functional properties to many thousands of cells (10). Building on this unique approach, we show that this model generates columnar clusters of cells related to individual glomeruli, as in the experiments, and further demonstrates mechanisms of odor processing within and between the GUs. Finally, interpreting this network activity requires a theoretical framework, incorporating distributed activated glomeruli within the global network, for which we introduce the concept of the odor operator. The results provide a basis for extension to the glomerular level on the one hand and interactions with olfactory cortex on the other.

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Section: Significancesupporting

confidence: 54%

“…1B, adapted from ref. 7), that mitral cells belonging to the same glomerulus form connections with different sets of GCs and make connections through their lateral dendrites with granule cells belonging to different GUs (yellow spots within columns in Fig. 1B).…”

Section: Resultsmentioning

confidence: 99%

Synaptic clusters function as odor operators in the olfactory bulb

Migliore

Cavarretta

Marasco

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Propagated spikes in granule cells also mediate lateral inhibition to other mitral/tufted cells [63]. However, connectivity between mitral/tufted cells and granule cells are very sparse [25,64]. Indeed, a sparse, rather than dense, receptive field better explains odor response profiles of mitral/tufted cells in vivo [65,66].…”

Section: Lateral Inhibitions By Granule Cellsmentioning

confidence: 94%

“…Furthermore, patterns of lateral dendrites are diverse among sister cells [10]. Because lateral connectivity among mitral/tufted cells does not seem to be center-surround [24,25], they are likely to be independent in odor information processing. Consistent with this notion, it is known that their post-synaptic neurons in the piriform cortex are not shared among sister neurons [26,27].…”

Section: Odor Coding By 'Sister' Mitral/tufted Cellsmentioning

confidence: 97%

Construction of functional neuronal circuitry in the olfactory bulb

Imai

2014

Seminars in Cell & Developmental Biology

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Recent studies using molecular genetics, electrophysiology, in vivo imaging, and behavioral analyses have elucidated detailed connectivity and function of the mammalian olfactory circuits. The olfactory bulb is the first relay station of olfactory perception in the brain, but it is more than a simple relay: olfactory information is dynamically tuned by local olfactory bulb circuits and converted to spatiotemporal neural code for higher-order information processing. Because the olfactory bulb processes ∼1000 discrete input channels from different odorant receptors, it serves as a good model to study neuronal wiring specificity, from both functional and developmental aspects. This review summarizes our current understanding of the olfactory bulb circuitry from functional standpoint and discusses important future studies with particular focus on its development and plasticity.

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“…After blocking, another washing was performed, and then the brain sections were incubated overnight with rabbit polyclonal antibody against amino acids 2732–2750 of rat IP3R1 (1:350, #2435031, AB5882, Millipore, USA)[16] or rabbit monoclonal antibody against residues subsequent to Ser29 of human Caspase-3 (1:250, #2365527, AB4-439, Millipore, USA)[17,18] in solutions containing 5% NDS and 0.5% Triton-X 100 in PBS 0.1M at room temperature. Then, the brain sections were washed and incubated with rabbit IgG tagged to Alexa 488 (1:500, A2120-6, Life Technologies, EUA), containing phosphate buffer + 0.3% Triton X-100 + DAPI, for 2 h at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Functional Role of Intracellular Calcium Receptor Inositol 1,4,5-Trisphosphate Type 1 in Rat Hippocampus after Neonatal Anoxia

et al. 2017

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Anoxia is one of the most prevalent causes of neonatal morbidity and mortality, especially in preterm neonates, constituting an important public health problem due to permanent neurological sequelae observed in patients. Oxygen deprivation triggers a series of simultaneous cascades, culminating in cell death mainly located in more vulnerable metabolic brain regions, such as the hippocampus. In the process of cell death by oxygen deprivation, cytosolic calcium plays crucial roles. Intracellular inositol 1,4,5-trisphosphate receptors (IP3Rs) are important regulators of cytosolic calcium levels, although the role of these receptors in neonatal anoxia is completely unknown. This study focused on the functional role of inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) in rat hippocampus after neonatal anoxia. Quantitative real-time PCR revealed a decrease of IP3R1 gene expression 24 hours after neonatal anoxia. We detected that IP3R1 accumulates specially in CA1, and this spatial pattern did not change after neonatal anoxia. Interestingly, we observed that anoxia triggers translocation of IP3R1 to nucleus in hippocampal cells. We were able to observe that anoxia changes distribution of IP3R1 immunofluorescence signals, as revealed by cluster size analysis. We next examined the role of IP3R1 in the neuronal cell loss triggered by neonatal anoxia. Intrahippocampal injection of non-specific IP3R1 blocker 2-APB clearly reduced the number of Fluoro-Jade C and Tunel positive cells, revealing that activation of IP3R1 increases cell death after neonatal anoxia. Finally, we aimed to disclose mechanistics of IP3R1 in cell death. We were able to determine that blockade of IP3R1 did not reduced the distribution and pixel density of activated caspase 3-positive cells, indicating that the participation of IP3R1 in neuronal cell loss is not related to classical caspase-mediated apoptosis. In summary, this study may contribute to new perspectives in the investigation of neurodegenerative mechanisms triggered by oxygen deprivation.

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Lateral Connectivity in the Olfactory Bulb is Sparse and Segregated

Cited by 43 publications

References 49 publications

Synaptic clusters function as odor operators in the olfactory bulb

Synaptic clusters function as odor operators in the olfactory bulb

Construction of functional neuronal circuitry in the olfactory bulb

Functional Role of Intracellular Calcium Receptor Inositol 1,4,5-Trisphosphate Type 1 in Rat Hippocampus after Neonatal Anoxia

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