Microscopic anatomy of the subcommissural organ in the brain of the adult greater cane rat (Rodentia: Thryonomyidae).

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.

Tramadol and Codeine Stacking/Boosting Dose Exposure Induced Neurotoxic Behaviors, Oxidative Stress, Mitochondrial Dysfunction, and Neurotoxic Genes in Adolescent Mice.

In spite of the increasing epidemic of pharmaceutical opioids (codeine and tramadol) misuse and abuse among the adolescents, little is known about the neurotoxic consequences of the widespread practice of tramadol and codeine abuse involving increasing multiple doses across days, referred to as stacking and boosting. Hence, in this study, we replicated stacking and boosting doses of tramadol, codeine alone, or in combination on spontaneous motor activity and cognitive function in adolescent mice and adduced a plausible mechanism of possible neurotoxicity. Ninety-six adolescent mice were randomly distributed into 4 groups (n = 24 per group) and treated thrice daily for 9 days with vehicle, tramadol (20, 40, or 80 mg/kg), codeine (40, 80, or 160 mg/kg), or their combinations. Exposure of mice to tramadol induced hyperactivity and stereotypic behavior while codeine exposure caused hypoactivity and nootropic effect but tramadol-codeine cocktail led to marked reduction in spontaneous motor activity and cognitive function. In addition, tramadol, codeine, and their cocktail caused marked induction of nitroso-oxidative stress and inhibition of mitochondrial complex I activity in the prefrontal cortex (PFC) and midbrain (MB). Real-time PCR expression profiling of genes encoding neurotoxicity (RT) showed that tramadol exposure upregulate 57 and downregulate 16 neurotoxic genes, codeine upregulate 45 and downregulate 25 neurotoxic genes while tramadol-codeine cocktail upregulate 52 and downregulate 20 neurotoxic genes in the PFC. Findings from this study demonstrate that the exposure of adolescents mice to multiple and increasing doses of tramadol, codeine, or their cocktail lead to spontaneous motor coordination deficits indicative of neurotoxicity through induction of oxidative stress, inhibition of mitochondrial complex I activity and upregulation of neurotoxicity encoding genes in mice.

Some Aspects of Neuromorphology, and the Co-localization of Glial Related Markers in the Brains of Striped Owl (Asioclamator) from North East Nigeria.

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.

Novel NMDA-receptor antagonists ameliorate vanadium neurotoxicity.

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.

Changes in the brain antioxidant profile after chronic vanadium administration in mice.

Vanadium is known to induce reactive oxygen species (ROS) in biological systems. Exposure to vanadium has been linked to neurological defects affecting the central nervous system (CNS) early in life and culminates later to neurodegeneration. This study was designed to evaluate the effects of chronic vanadium exposure on antioxidant profile in mice, and progressive changes after withdrawal from treatment. A total of 85 male BALB/c mice (4 weeks old) were used for the experiment and were divided into three groups of vanadium exposed (3 mg/kg i.p at 3-18 months treatment), matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn. Vanadium exposure caused significant increases (p<0.05) in levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) generation and nitric oxide with a concomitant decrease (p<0.05) in the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase and a decline in the level of reduced glutathione (GSH) after 6 months of vanadium exposure in the brain. This trend continued in all vanadium-exposed groups (9, 12, 15 and 18 months) relative to the matched controls. Withdrawal after 3 months of vanadium exposure significantly reversed oxidative stress in intoxicated mice from 9 to 15 months after vanadium withdrawal. We have shown that chronic administration of vanadium led to oxidative stress in the brain which is reversible only after a long period of vanadium withdrawal.