Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We revealed the structural features of particular synaptic regions, nidi, and newly found neurons, tasseled cells, in the main olfactory bulb (MOB) of the laboratory musk shrew (Suncus murinus). Nidi were intensely immunoreactive for glutamic acid decarboxylase (GAD) and calbindin D28k (CB), were 30-80 microm in diameter, and were located beneath glomeruli, appearing to make glomerulus-nidus unit-like complexes. In contrast to glomeruli, they contained few or no olfactory nerves. Nidi were distributed throughout the whole MOB and made a distinctive layer, nidal layer. Tasseled cells were located in the mitral cell layer and in the middle of the external plexiform layer (EPL) and extended single primary dendrites to the nidus, where their small tuft-like complicated branches intermingled with processes of perinidal cells surrounding nidi. Primary dendrites of mitral/tufted cells also penetrated nidi but passed to glomeruli. In the outer half of the EPL, columnar structures were seen, where CB- and GAD-positive elements appeared to associate with bundles of cylindrical dendrites of presumed mitral/tufted and tasseled cells. By electron microscopic examinations, nidi were confirmed to be particular synaptic areas where GAD-positive processes made symmetrical synapses to GAD-negative presumed tasseled and mitral/tufted cell dendrites and received asymmetrical synapses from the latter. Retrograde tracings revealed that tasseled cells, in addition to mitral/tufted cells, projected their axons to the lateral olfactory tract, indicating that there were two parallel projection systems in the shrew MOB, which might interact with each other via various types of gamma-aminobutyric acid (GABA)ergic interneurons. The present study clearly showed that the neuronal organization of the shrew MOB was distinctly different from that in rodents.
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PMID:Nidus and tasseled cell: distinctive neuronal organization of the main olfactory bulb of the laboratory musk shrew (Suncus murinus). 1116 86

Intraglomerular dendritic tufts of Golgi-impregnated and biotinylated dextran amine (BDA)-labeled mitral cells in the rat main olfactory bulb were analyzed in detail. In particular, the relationships of BDA-labeled tufts with olfactory nerve (ON) terminals and processes of calbindin D-28K-immunoreactive (CB-IR) cells were investigated with confocal laser-scanning light microscopic (CLSM) and electron microscopic (EM) analyses. CB-IR cells were type 2 periglomerular cells that restricted their processes in the ON-free (non-ON) zone of the glomerulus and received few synapses from ON terminals. The mitral tufts varied in complexity, but individual branches were rather simple, smooth processes that bore some branchlets and spines and extended more or less in a straight line or a gentle curve rather than winding tortuously within glomeruli as though they did not consider the compartmental organization, which consisted of ON and non-ON zones that interdigitated in a complex manner with one another. Conventional EM analysis revealed that both thin and thick, presumed proximal branches of mitral/tufted cell dendritic tufts received asymmetrical synapses from ON terminals. Correlated CLSM-EM analysis confirmed direct contacts between the BDA- and CB-labeled processes detected in the CLSM examinations, and synapses were recognized at some of those sites. Furthermore, ON terminals and CB-IR processes were distributed on both proximal and distal dendritic branches in a more or less mosaic pattern. These findings revealed that, on the mitral dendritic tufts, ON terminals and processes of type 2 periglomerular neurons were not clearly segregated proximodistally but, rather, were arranged in a mosaic pattern, which may be important in fine tuning the output from individual glomeruli.
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PMID:Structure of intraglomerular dendritic tufts of mitral cells and their contacts with olfactory nerve terminals and calbindin-immunoreactive type 2 periglomerular neurons. 1174 19

A variety of immortalized cell lines have been proposed to exhibit sufficient phenotypic plasticity to allow them to replace primary embryonic neurons for restorative cell transplantation. In the present experiments we evaluate the functional viability of one particular cell line, the hNT cells developed by Layton Bioscience, to replace lost neurons and alleviate asymmetrical motor deficits in a unilateral excitotoxic lesion model of Huntington's disease. Because the grafts involved implantation of human-derived cells into a rat host environment, all animals were immunosuppressed. Cyclosporin A and FK-506 were similar in providing effective immunoprotection of the hNT xenografts, and whereas the lesions induced a marked inflammatory response in the host brain, this was not exacerbated by the presence of xenograft cells. The presence of grafted cells was determined with the human-specific antigen HuNu, and good graft survival was demonstrated in almost all animals up to the longest survival examined, 16 weeks posttransplantation. Although the cells exhibited progressively greater maturation and differentiation at 10-day, 4- and 16-week time points, staining for the mature neuronal marker NeuN was at best very weak, and we were unable to detect unequivocal staining with any markers of mature striatal phenotype, including DARPP-32, calbindin, parvalbumin, choline acetyl transferase, or NADPH diaphorase (with in all cases positive control provided by good staining on the intact contralateral side of the brain). Nor were we able to detect any differences between rats with lesions alone and rats with grafts in the contralateral motor deficits exhibited in a test of skilled paw reaching or cylinder placing. These results suggest that further and more extensive studies should be undertaken to assess whether hNT neurons can show more extensive and appropriate maturation and be associated with recovery in appropriate behavioral models, before they may be considered a suitable replacement for primary embryonic cells for clinical application in Huntington's disease.
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PMID:Transplanted hNT cells ("LBS neurons") in a rat model of huntington's disease: good survival, incomplete differentiation, and limited functional recovery. 1512 58

The interstitial nucleus of the spinal trigeminal tract (INV) contains many calbindin-D28k-containing neurons (CB-neurons) receiving convergence information from the somatic and visceral structures. The purpose of the present study was to confirm whether the primary afferent terminals from the inferior alveolar nerve (IAN) make close contact and synaptic connections with the same CB-neurons receiving visceral nociceptive signals in INV. Biotinylated dextran amine (BDA) and horseradish peroxidase (HRP) tracing combined with CB and Fos proteins immunohistochemistry were used. After injections of BDA and formalin into unilateral IAN and upper alimentary tract, respectively, the transganglionic labeled afferent fibers and terminals from IAN were observed in the ipsilateral INV, especially in its enlarged part. A large number of CB- and Fos-like immunoreactive (LI) neurons were found in bilateral INV. These CB- and Fos-LI neurons mostly overlapped with BDA-labeled terminals in the enlarged part of INV. About one half of the CB-LI neurons were double labeled with Fos-LI nuclei (74/153). The terminals from IAN were to made close contacts with many CB/Fos-double labeled or CB-single labeled neurons. After injection of HRP into IAN, HRP-labeled fibers and terminals in INV were similar to that labeled with BDA. Under the electron microscope, a large number of CB-LI dendrites and a few soma in the enlarged part of INV were found to form asymmetrical axo-dendritic and axo-somal synapses with the HRP-labeled axon terminals. These results indicate that the orofacial somatic inputs from IAN and the visceral nociceptive inputs from the upper alimentary tract converge onto the same CB-containing neurons in INV. These CB-containing neurons in INV probably play an important role in information integration as well as visceral and cardiovascular activity.
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PMID:Somatic and visceral nociceptive inputs from the orofacial area and the upper alimentary tract converge onto CB-containing neurons in interstitial nucleus of the spinal trigeminal tract in rats. 1549 38

Ten puppy dogs (82, 131 or 148 days-old) from a Pointer cross-colony, exhibiting a juvenile severe hearing loss transmitted as an autosomal recessive trait, were used for histopathological characterization of the inner ear lesion. Immunostaining with calbindin, Na,K-ATPase, cytokeratins, S100, S100A1 and S100A6 antisera were helpful in identifying the different cell types in the degenerated cochleae. Lesions, restricted to the Corti's organ and spiral ganglion, were bilateral but sometimes slightly asymmetrical. Mild to severe lesions of the Corti's organ were unevenly distributed among the different parts of the middle and basal cochlear turns while the apical turn remained unaffected at 148 days. In 82 day-old puppies (n = 2), severe lesions of the Corti's organ, meaning that it was replaced by a layer of unidentifiable cells, involved the lower middle and upper basal turns junction area, extending in the upper basal turn. Mild lesions of the Corti's organ, with both hair and supporting cells abnormalities, involved the lower middle turn and extended from the rest of upper basal turn into the lower basal turn. The outer hair cells (ohc) were more affected than the inner hair cell (ihc). The lesions extended towards the basal end of the cochlea in the 131 (n = 5) and 148 (n = 3) day-old puppies. Additionally, the number of spiral ganglion neurons was reduced in the 131 and 148 day-old puppies; it is earlier than observed in most other canine hereditary deafness. These lesions were interpreted as a degeneration of the neuroepithelial type. This possible animal model might provide information about progressive juvenile hereditary deafness and neuronal retrograde degeneration investigations in human.
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PMID:Inner ear histopathology in "nervous Pointer dogs" with severe hearing loss. 1566 38

Detailed neuropathological studies of the extent of hippocampal sclerosis (HS) in epilepsy along the longitudinal axis of the hippocampus are lacking. Neuroimaging studies of patients with temporal lobe epilepsy support that sclerosis is not always localised. The extent of HS is of relevance to surgical planning and poor outcomes may relate to residual HS in the posterior remnant. In 10 post mortems from patients with long histories of drug refractory epilepsy and 3 controls we systematically sampled the left and right hippocampus at seven coronal anatomical levels along the body to the tail. We quantified neuronal densities in CA1 and CA4 subfields at each level using Cresyl Violet (CV), calretinin (CR), calbindin (CB) and Neuropeptide Y (NPY) immunohistochemistry. In the dentate gyrus we graded the extent of granule cell dispersion, patterns of CB expression, and synaptic reorganisation with CR and NPY at each level. We identified four patterns of HS based on patterns of pyramidal and interneuronal loss and dentate gyrus reorganisation between sides and levels as follows: (1) symmetrical HS with anterior-posterior (AP) gradient, (2) symmetrical HS without AP gradient, (3) asymmetrical HS with AP gradient and (4) asymmetrical cases without AP gradient. We confirmed in this series that HS can extend into the tail. The patterns of sclerosis (classical versus atypical or none) were consistent between all levels in less than a third of cases. In conclusion, this series highlights the variability of HS along the longitudinal axis. Further studies are required to identify factors that lead to focal versus diffuse HS.
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PMID:Variability of sclerosis along the longitudinal hippocampal axis in epilepsy: a post mortem study. 2260 64


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