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1.
Anat Histol Embryol ; 53(1): e12990, 2024 Jan.
Article in English | MEDLINE | ID: mdl-37874623

ABSTRACT

The subcommissural organ (SCO) is a well-developed gland present in the brain of vertebrates. The SCO secretes glycoproteins into the circulating cerebrospinal fluid and these assemble to form Reissner's fibre. It also plays an important function in neurogenesis and axonal guidance during embryogenesis. This study delves into the microscopic anatomy of the SCO in the adult greater cane rat (GCR), shedding light on its histoarchitectural characteristics. By utilizing histological techniques and microscopic analysis, we investigated the SCO's location and cellular composition within the brain of adult GCR. Our findings showed that the SCO in this species is located ventrally to the posterior commissure (PC) and dorsally to the third ventricle. The SCO consists of specialized ependymal or nuclear cell layer and apical processes lining the third ventricle. Moreover, the SCO's proximity to the PC and the third ventricle highlights its strategic position within the brain's ventricular system. With immunohistochemical analyses, the SCO cells expressed glial fibrillary protein when immunolabelled with Glial fibrillary acid protein (GFAP) antibody, a marker for astrocytes/astrocytic-like cells. Few microglia-like cells were immuno-positive for Ionized calcium-binding adapter molecule 1 (Iba1) antibody, that are existing within the SCO. However, the SCO in the GCR showed a negative immunostaining to NeuN antibody. This study contributes to our understanding of the microscopic anatomy of the SCO in a lesser-studied mammalian species. Further research into the SCO's functional significance especially during development in the GCR, may hold promise for more insights into neurological health and pathology.


Subject(s)
Rodentia , Subcommissural Organ , Rats , Animals , Subcommissural Organ/metabolism , Subcommissural Organ/ultrastructure , Canes
2.
Niger J Physiol Sci ; 35(1): 109-114, 2020 Jun 30.
Article in English | MEDLINE | ID: mdl-33084626

ABSTRACT

The striped owl (Asioclamator) is unique with its brownish white facial disc and they are found in the north eastern part of Nigeria. Little is known in the literature on the basic neuroanatomy of this species. This study focuses on the histology and glial expression of some brain regions of the striped owl. Five owls were obtained in the wild, and their brains were routinely prepared for Haematoxylin and Eosin, and Cresyl violet staining. Immunostaining was done with anti-Calbindin, anti MBP, anti-GFAP, and anti-Iba-1 antibodies; for the expression of cerebellar Purkinje cells and white matter, cerebral astrocytes and microglia cells respectively. These were qualitatively described. We found that the hippocampal formation of the striped owl, though unique, is very similar to what is seen in mammals. The cerebellar cortex is convoluted, has a single layer of Purkinje cells with profuse dendritic arborization, a distinct external granular cell layer, and a prominent stem of white matter were seen in this study. The astrocytic population in cerebral gray is similar, though lacking in many processes as is typical in protoplasmic astrocytes, while the microglia were not strongly stained. The few stained microglia cells did not, however, show any features of activation. The striped owl's brain reveals some conserved aspects of cellular neuroanatomy in both the avian and mammals that are typical in these species. More work is however needed particularly in age related differences in these structures. This is perhaps the first report of Calbindin immunostaining in the brain of the striped owl.


Subject(s)
Astrocytes/metabolism , Brain/metabolism , Strigiformes/metabolism , Animals , Glial Fibrillary Acidic Protein/immunology , Glial Fibrillary Acidic Protein/metabolism , Nigeria , Purkinje Cells/metabolism
3.
Naunyn Schmiedebergs Arch Pharmacol ; 393(9): 1729-1738, 2020 09.
Article in English | MEDLINE | ID: mdl-32388602

ABSTRACT

Various NMDA-receptor antagonists have been investigated for their therapeutic potential in Alzheimer's disease with memantine shown to be safe and with relative efficacy. There is, however, need to develop novel drugs to counter tolerance and with better efficacy in ameliorating neurodegeneration. We have shown neurodegeneration in different models of vanadium-exposed mice. This study was designed to evaluate and ascertain the potency of three novel NMDA-receptor antagonists (Compounds A, B and C) to ameliorate neurodegeneration in vanadium-exposed mice. One-month-old mice (n = 6) received sterile water (control) and another group (n = 6) was treated with vanadium (3 mg/kg sodium metavanadate) intraperitoneally for 1 month. Three other groups (n = 6) received vanadium and compounds A, B and C (4.35 mg/kg, 30 mg/kg and 100 mg/kg, respectively) simultaneously for the same period. Assessment of pathologies and neurodegeneration in different brain regions was done to test the ameliorative effects of the 3 antagonists using different immunohistochemical markers. Vanadium exposure resulted in reduced calbindin expression and pyknosis of Purkinje cells, cell loss and destruction of apical dendrites with greater percentage of cytoplasmic vacuolations, morphological alterations characterized by cell clustering and multiple layering patterns in the Purkinje cell layer. In addition, the observed degeneration included demyelination, increased GFAP-immunoreactive cells and microgliosis. Simultaneous administration of the compounds to vanadium-exposed mice resulted in the preservation of cellular integrity in the same anatomical regions and restoration of the cells' vitality with reduced astroglial and microglial activation.


Subject(s)
Excitatory Amino Acid Antagonists/pharmacology , Nerve Degeneration , Neurotoxicity Syndromes/prevention & control , Purkinje Cells/drug effects , Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors , Animals , Astrocytes/drug effects , Astrocytes/metabolism , Astrocytes/pathology , Calbindins/metabolism , Cell Death/drug effects , Disease Models, Animal , Glial Fibrillary Acidic Protein/metabolism , Mice , Microglia/drug effects , Microglia/metabolism , Microglia/pathology , Neurotoxicity Syndromes/etiology , Neurotoxicity Syndromes/metabolism , Neurotoxicity Syndromes/pathology , Purkinje Cells/metabolism , Purkinje Cells/pathology , Receptors, N-Methyl-D-Aspartate/metabolism , Vanadates
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