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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.
West Afr J Med ; Vol. 38(11): 1042-1049, 2021 Nov 30.
Article in English | MEDLINE | ID: mdl-34919360

ABSTRACT

BACKGROUND: The hippocampus is the brain's centre for the consolidation of short-term and spatial memory that enables navigation. Hippocampal injury occurs in hydrocephalus and is associated with loss of memory. OBJECTIVE: We assessed pyknotic changes in kaolin-induced chronic hydrocephalus in adult rats using qualitative and quantitative means, and related these to memory deficits in the rats. METHODS: Adult rats were randomly divided into control and experimental groups. Hydrocephalus was induced by intracisternal injection of 0.1ml sterile kaolin suspension for 6weeks. Control rats received sham injections. Spatial memory was assessed with the Morris water maze test. Coronal sections of the brains were grouped into either mild or moderate hydrocephalus and then stained with H&E and cresyl violet stains. Thus, there were three groups: control, mild hydrocephalus and moderate hydrocephalus (n=10), respectively. RESULTS: Shrinking and thinning of the hippocampal tissue, distortion of the pyramidal layer and pyknotic cells were observed in the CA1 and CA3 regions of the hydrocephalic rats. The pyknotic indices in the mild hydrocephalic rat (Cornus Ammonis, CA) CA1, CA2, CA3 (54.30±1.38; 27.62±0.83; 57.61±0.74) and moderate hydrocephalic rat CA1, CA2, CA3 (48.18±0.67; 32.00±0.84; 42.41±1.19) regions were significantly increased compared to the controls' CA1, CA2, CA3 (12.14±0.56; 9.21±0.36; 13.04±0.59). CONCLUSION: Chronic hydrocephalus in adult rats was associated with cell death in all the regions of the hippocampus, irrespective of the degree of ventricular enlargement. The extent of cell death corresponded with the severity of learning and memory deficits. CONTEXTE: L'hippocampe est le centre du cerveau pour la consolidation de la mémoire à court terme et de la mémoire spatiale qui permet la navigation. Une lésion de l'hippocampe se produit dans l'hydrocéphalie et est associée à la perte de mémoire. OBJECTIF: Nous avons évalué les changements pyknotiques dans l'hydrocéphalie chronique induite par le kaolin chez des rats adultes en utilisant des moyens qualitatifs et quantitatifs, et nous les avons reliés aux déficits de mémoire chez les rats. MÉTHODES: Des rats adultes ont été répartis au hasard en groupes témoins et expérimentaux. L'hydrocéphalie a été induite par injection intracisternale de 0,1 ml de suspension stérile de kaolin pendant 6 semaines. Les rats témoins ont reçu des injections simulées. La mémoire spatiale a été évaluée par le test du labyrinthe aquatique de Morris. Les sections coronales des cerveaux ont été regroupées en hydrocéphalie légère ou modérée, puis colorées au H&E et au crésyl violet. Il y avait donc trois groupes : contrôle, hydrocéphalie légère et hydrocéphalie modérée (n=10), respectivement. RÉSULTATS: Un rétrécissement et un amincissement du tissu hippocampique, une distorsion de la couche pyramidale et des cellules pyknotiques ont été observés dans les régions CA1 et CA3 des rats hydrocéphales. Les indices pyknotiques dans les régions CA1, CA2 et CA3 des rats hydrocéphales légers (Cornus Ammonis, CA) (54,30±1,38 ; 27,62±0,83 ; 57,61±0,74) et des rats hydrocéphales modérés CA1, CA2 et CA3 (48. 18±0.67 ; 32.00±0.84 ; 42.41±1.19) ont été significativement augmentées par rapport aux régions CA1, CA2, CA3 des témoins (12.14±0.56 ; 9.21±0.36 ; 13.04±0.59). CONCLUSION: L'hydrocéphalie chronique chez les rats adultes était associée à la mort cellulaire dans toutes les régions de l'hippocampe, quel que soit le degré d'élargissement ventriculaire. L'étendue de la mort cellulaire correspondait à la sévérité des déficits d'apprentissage et de mémoire. MOTS CLÉS: Hydrocéphalie chronique, hippocampe, rats adultes, mémoire, cellules pyknotiques.


Subject(s)
Hydrocephalus , Spatial Memory , Animals , Hippocampus , Humans , Hydrocephalus/chemically induced , Pyramidal Cells , Rats
3.
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
4.
Int J Vet Sci Med ; 8(1): 56-58, 2020 Aug 19.
Article in English | MEDLINE | ID: mdl-32953876

ABSTRACT

We report a possible spontaneous case of oxalate nephrosis in an African fruit bat (Epomops franqueti), incidentally observed in Ibadan, South-West Nigeria, in an anatomical and serological survey of the species. Wild caught bats underwent sedation, intracardial perfusion, necropsy and histopathology. All 15 wild-caught African fruit bats were apparently healthy. However, light microscopy revealed mild oligofocal tubulonephrosis with intraluminal deposition of polarizing crystals interpreted as subclinical oxalate nephrosis in one case. In summary, we suggest a dietary aetiology, based on seasonal availability of high ascorbic acid or oxalate containing fruits. However, exposure to anthropogenic contaminants cannot be completely ruled out.

5.
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
6.
Niger. j. paediatr ; 47(4): 298-304, 2020. ilus
Article in English | AIM (Africa) | ID: biblio-1267473

ABSTRACT

Background: Hippocampus is a neural structure in the temporal lobe that plays a crucial role in learning and memory. Cognitive impairment with learning disabilities is a common feature in hydrocephalus and is more prominent in adult-onset hydrocephalus. The aim of this study is to describe the morphological alterations in the pyramidal cells of the hippocampus of adult hydrocephalic mice. Method: Hydrocephalus was induced in adult albino mice by intra-cisternal injection of kaolin suspension (250 mg/ml in sterile water). They were sacrificed 7, 14 and 21 days post-induction. Morphological analysis was carried out on hematoxylin and eosin stained coronal sections of the hippocampus: the pyramidal neurons (normal and pyknotic) in the CA1 and CA3 subregions were counted and the pyknotic index (PI) was calculated. The somatic and dendritic features of Golgi stained pyramidal neurons were examined by light microscopy in both hydrocephalic and control mice. Result: The PI was significantly greater in the CA1 region of the hippocampus in the hydrocephalic groups compared to the age matched controls. The dendritic processes of pyramidal neurons in the CA1 region were fewer with shorter terminal branches in the hydrocephalic mice than in controls; this was pronounced at 7 days post-induction. In the CA3 region, there was no difference in dendritic arborization between hydrocephalic and control mice. Conclusion: Acute adult-onset hydrocephalus was associated with increased pyknosis and reduced dendritic arborization in hippocampal pyramidal cells in the CA1 but not CA3 region


Subject(s)
Golgi Apparatus , Hydrocephalus , Pyramidal Cells
7.
Anat Histol Embryol ; 47(3): 231-238, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29492996

ABSTRACT

Oligodendrocyte and myelin-related studies have been pivotal in understanding disruption of central nervous system (CNS) myelin through injury, toxicological, pathological degeneration or genetic intervention. The African giant rat (AGR) has been postulated as an indigenous wild-type model within the African context. This work thus describes oligodendrocyte morphologies and myelin components of the developing African giant rat brain using histological, immunohistochemical and ultrastructural techniques. Five types, precursor-progenitor oligodendrocytes, pre-oligodendrocytes, immature oligodendrocytes, mature non-myelinating oligodendrocytes and mature myelinating oligodendrocytes, were identified. The first four types were observed in neonates while juvenile and adult AGR had predominantly mature myelinating oligodendrocytes with evidence of myelin sheath deposition. All cell types identified showed positive CNPase-positive immunosignalling across all age groups. This suggests CNPase as a suitable, sensitive and reliable biomarker for studying CNS neurodegenerative/demyelinating disorders in the AGR. This baseline study has given detailed insight into the morphology of oligodendrocytes and myelin in the AGR. It may be useful for anatomical studies and detection of alterations in neurocellular profile of oligodendrocytes and myelin in the AGR in real-life or in experimental models.


Subject(s)
Brain/cytology , Brain/growth & development , Oligodendroglia/ultrastructure , Rodentia/anatomy & histology , Rodentia/growth & development , Aging , Animals , Immunohistochemistry , Male , Microscopy, Electron, Transmission , Oligodendroglia/physiology
8.
Niger J Physiol Sci ; 31(2): 105-113, 2017 Mar 06.
Article in English | MEDLINE | ID: mdl-28262845

ABSTRACT

Hydrocephalus is usually associated with functional deficits which can be assessed by neurobehavioral tests. This study characterizes the neurobehavioral deficits occurring with increasing duration and severity of ventriculomegaly in an experimental neonatal hydrocephalic rat model. Hydrocephalus was induced in three weeks old albino rats by intracisternal injection of kaolin while controls received sterile water injection. They were sacrificed in batches at one, four and eight weeks post-injection after neurobehavioral tests (forelimb grip strength, open field and Morris water maze tests) were performed. The hydrocephalic rats were also categorized into mild, moderate and severe hydrocephalus based on ventricular size. The indices of muscular strength and vertical movements in severely hydrocephalic rats were 28.05 ± 5.19 seconds and 7.29 ± 2.71 rearings respectively, compared to controls (75.68 ± 8.58 seconds and 17.09 ± 1.25 rearings respectively). At eight weeks, vertical movements were significantly reduced in hydrocephalic rats compared to controls (3.14 ± 1.3 vs 13 ± 4.11 rearings). At one week, indices of learning and memory were significantly reduced in hydrocephalic rats, compared to controls (0.89±0.31 vs 3.88±1.01 crossings), but at 8 weeks, the indices were similar (2.56 ± 0.41 vs 3.33 ± 0.71 crossings). Untreated hydrocephalus is accompanied by decline in motor functions which increase with duration and severity of ventriculomegaly. However, cognitive deficits appear to partially recover.


Subject(s)
Behavior, Animal , Hydrocephalus/physiopathology , Hydrocephalus/psychology , Nervous System/physiopathology , Animals , Animals, Newborn , Cognition , Disease Models, Animal , Disease Progression , Female , Hydrocephalus/chemically induced , Kaolin , Male , Maze Learning , Memory , Motor Activity , Muscle Strength , Rats, Wistar , Recovery of Function , Severity of Illness Index , Time Factors
9.
Niger J Physiol Sci ; 26(1): 55-60, 2011 Nov 23.
Article in English | MEDLINE | ID: mdl-22314988

ABSTRACT

The work investigated the protective role of vitamin E on vanadium induced neurotoxicity. Three adult female rats were divided into three groups, A-C with each dam and her pups forming a group. Group A served as control. The dam in Group B was given 3mg/kg b.w./day of vanadium from PND 1 while the Group C dam were given 3mg/kg b.w./day of vanadium, for 14 days and 500mg/kg b.w. of vitamin E 72 hourly in the same time frame. The results showed that pups from Group B, exhibited behavioural deficits in most tests, a significant reduction in body weight gain and absolute brain weight; in addition immunohistochemistry showed reactive astrogliosis induced by vanadium exposure. All these findings were however attenuated in pups whose dam was exposed to vanadium and vitamin E depicting the significant protective effects of this antioxidant against vanadium. This study is novel in that both vanadium and vitamin E were introduced through the lactation route. We conclude that though caution remains essential in the posology of vitamin E, the management of lactating mothers who have been exposed to vanadium occupationally, environmentally or therapeutically with supplementation of this antioxidant may be beneficial at least in the short term to both mother and offspring.


Subject(s)
Behavior, Animal/drug effects , Brain/drug effects , Lactation , Milk/metabolism , Neuroprotective Agents/pharmacology , Neurotoxicity Syndromes/prevention & control , Vanadates/toxicity , Vitamin E/pharmacology , Animals , Astrocytes/drug effects , Astrocytes/metabolism , Astrocytes/pathology , Biomarkers/metabolism , Body Weight/drug effects , Brain/metabolism , Brain/pathology , Brain/physiopathology , Female , Glial Fibrillary Acidic Protein/metabolism , Immunohistochemistry , Injections, Intraperitoneal , Maternal Exposure/adverse effects , Motor Activity/drug effects , Neurotoxicity Syndromes/etiology , Neurotoxicity Syndromes/metabolism , Neurotoxicity Syndromes/pathology , Neurotoxicity Syndromes/physiopathology , Neurotoxicity Syndromes/psychology , Rats , Time Factors , Vanadates/administration & dosage , Vanadates/metabolism
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