Fast Violet Research Articles

Microstructure of the dentate gyrus and spontaneous alternation behaviour of male Wistar rats following Rauvolfia vomitoria and Gongronema latifolium extracts administration

Rauvolfia vomitoria (RV) and Gongronema latifolium (GL) are medicinal plants used for the local treatment of various health issues. Their activities on the brain motivated this investigation on the histology and immunohistochemistry of the dentate gyrus and spontaneous alternation behaviour (SAB) of adult Wistar rats following RV root bark and GL leaf extract administrations. Twenty young adult Wistar rats (130–160 g) were assigned into four groups: Group 1 served as the control (5 mL/kg of distilled water placebo), while the test groups 2–4 were, respectively, singly administered 200 of mg/kg of RV, 200 of mg/kg of GL, and their combination. The administrations were oral and lasted for seven days. A T-maze SAB test was carried out, and the animals were sacrificed immediately after ketamine hydrochloride intraperitoneal anaesthesia. Serial sections of the hippocampal region from perfused rat brains were stained with Cresyl fast violet and immunolabelled with neuronal nuclei (NeuN) for neurons and glial fibrillary acidic protein (GFAP) for astrocytes. Results indicated that SAB was significantly (p < 0.05) lower in the test groups. Histologically, Nissl was less distributed in the RV and GL-only groups but not in the combined group, while there was less NeuN positivity in the RV group, with the GL and RV + GL groups not affected. There was less positive GFAP expression in individual RV and GL groups, but not in the RV + GL combined group, all compared with the control. In conclusion, the combination of RV and GL did not improve SAB but modulated Nissl, NeuN, and GFAP expression in the dentate gyrus.

Neem Leaf Supplement Ameliorates Depressive Like Behaviour in Alzheimer’s Disease Model in Adult Male Wistar Rats

Aim of the Study: Currently, reports linked neuropathological changes in Alzheimer’s Disease (AD) to be a risk factor in depression. There is a need to develop natural therapeutics, with strong antioxidant property like Neem leaf, to avert AD’s neuropathological and behavioural changes using animal model induced by neurotoxin aluminium chloride. This study is aimed at ascertaining depressive like disorders in AD model while evaluating mechanism through which Neem averts AD neurodegeneration in the fronto-cerebellar cortex and possible depressive like behaviour. Methodology: Twenty (20) adult male Wistar rats used were grouped (n=5) viz: control group (A), neurodegenerative model given aluminium (B), 200mg/kg Neem leaf supplement (C) and 200mg/kg Neem leaf treated AD model (D). Neurobehavioural changes for reward memory and depressive like behaviour were evaluated using Y-maze (open arm reward test) and the tail suspension test (TST). The frontal and cerebellar cortices were excised, fixed and processed for Haematoxylin and Eosin stain (H and E), Cresyl fast violet (CFV) stain for Nissl bodies and astrocytes immunohistochemistry using glial fibrillary acidic protein (GFAP). Behavioural test data were analyzed using ANOVA and test for significance done @ p<0.05. Results: Aluminum induced neurodegeneration similar to AD pathology characterized by loss of neurons, chromatolysis, proliferation of astrocytes and decline in cognitive function in addition to exhibiting depressive like behaviour seen in a decrease number of reward arm entries, increase in time spent to reach reward arm and immobility time in the TST attributed to loss of cognitive function relative to loss of neurons integrity in the fronto-cerebellar cortex. However, neem leaf supplementation mitigates against AD model neuropathological and neurobehavioural presentations resulting in an improved neurocognition, neuron survival or repair, decline in astrocytes proliferation and decline in depressive like behavior as compared to Aluminum induced AD model. Conclusion: Neem leaf alleviates depressive like behaviour associated with neurocognitive impairment through the interaction between neuron-astrocytes to protect neurons against aluminum induced neuroinflamamation and strengthens neural circuit for cognitive function.

Structural and spectroscopic insights into the performance of K3Tb(PO4)2 green phosphor.

A narrow-band green emitting K3Tb(PO4)2 phosphor has been synthesized by a novel single-crystal growth approach involving the application of an inert flux. Its structural and spectroscopic peculiarities have been systematically studied by means of single-crystal X-ray diffraction, scanning electron microscopy, energy-dispersive X-ray spectroscopy analysis, and diffuse reflectance, infrared and photoluminescence spectroscopy. The layered framework of the title compound is organized by linking together slightly distorted phosphate tetrahedra with non-condensed TbO7 polyhedra into [Tb(PO4)2]3- sheets interconnected by potassium cations. K3Tb(PO4)2 reveals an intense slow green photoluminescence (PL) (decay time constant τ is near 2.6 ms) under excitation in the range from VUV (100 nm) up to blue light (484 nm). Intensive narrow lines of the 5D4 → 7F6-0 (4f8 → 4f8) radiative transitions in Tb3+ ions form the PL spectra. Besides, fast violet PL (time constant τ < 20 ns) occurs under PL excitations in a narrow range from 250 to 325 nm. Dependencies of the PL quantum yield, and the green and violet PL decays on the excitation wavelength have been analyzed taking into account the multi-phonons, cross-relaxation processes and exciting light absorption by the inherent defects in the K3Tb(PO4)2 crystal lattice. The dependency of the complex characteristics of PL quantum yield on the excitation wavelength and violet photoluminescence is ascribed to the formation of Tb4+ ions. The color coordinates and color purity of the emission were estimated for the cases of PL excitation in the 160-371 nm spectral range. It has been shown that these characteristics are similar to or even better than those reported for conventional commercial green phosphors. The high values of correlated color temperature (T> 4863 K) of the emission indicates the potential use of K3Tb(PO4)2 for enhancing cold-light emitting devices.

Efficient photodegradation of fast sulphon black and crystal violet dyes from water systems using locust bean gum (LBG)-encapsulated zirconium-based nanoparticles and antibacterial activity

Efficient photodegradation of fast sulphon black and crystal violet dyes from water systems using locust bean gum (LBG)-encapsulated zirconium-based nanoparticles and antibacterial activity

Neuro-protective and Neuro-curative effect of Vernonia Amygdalina in rat model of neurodegenerative disease

BackgroundIn this study, we assessed the protective potential of Vernonia amygdalina methanolic extract on aluminum chloride- induced neurotoxicity damage in Wistar rats. MethodologyForty Adult female Wistar rats weighing (109 ± 16 g) were randomly divided into four (4) groups (A-D, of 10 rats respectively). Group A rats served as the normal control (treated with 5 mL/kg normal saline) for 28 days, Group B rats received 0.43 mL/kg Aluminum chloride (AlCL3) via oropharyngeal cannula for 14 days and 1.31 mL of Vernonia amygdalina extract after AlCL3 treatment for 14days, Group C rats received 1.31 mL of Vernonia amygdalina (VA) extract for 14 days and 0.43 mL/kg AlCL3 after VA treatment for 14 days, D rats received only 0.43 mL/kg Aluminum chloride (AlCL3) via oropharyngeal cannula for 14 days. The rats were sacrificed, and the hippocampus processed using Haematoxylin and Eosin (H&E) and Cresyl fast violet. ResultsResults showed a significant (P ≤ 0.05) increase in body weight of groups B-D rats when compared to group A rats. Histological examinations showed clumpy of cell neurons, condensed pyramidal cells, necrotic and vascular edema and scanty neurofibrillary tangle which was an indication of neurodegeneration in the other groups when compared to the control group. Conclusionthat the oral administration of aluminum chloride could induce brain damage which may impair memory and learning as seen in Alzheimer disease and can be ameliorated with Vernonia Amygdalina leaf extract.

High consumption of Garcinia Kola may impair hippocampal morphology, memory and learning in albino mice model

The use of various psychoactive substances can easily alter and modified the subtle chemical and electrical processes of the brain. Hence this study analyzed the effect of varying doses and duration of kolanut extract (KNE) on hippocampal morphology, learning and memory. Fifty albino mice were divided into five groups of ten mice each. Group 1 received 3.3 mg/kg of extract for 10days, Group 2 received 2.84 mg/kg of extract for 7days, Group 3 received 2.45 mg/kg of extract for 5days, Group 4 received 2.73 mg/kg of extract for 3days, Group 5 were treated with 5 ml/kg of distilled water for 10days. Memory and navigation skills were assessed with Radial Arm Maze and T Maze. The hippocampus was fixed after cervical dislocation for H&E and Cresyl Fast Violet Stain. The pyknotic index (PI) was calculated for each hippocampal subarea.Results revealed a significant (p<0.05) increase in time of group 1 and 2 mice with regards Radial Arm Maze and T Maze assessments. Group 2 rats, group 3 and group 4 mice showed no significant changes (p<0.05) in body weight. There was a significant (p<0.05) increase in Pyknotic index in group 1 and 2 rats both at the CA1 and CA3 subarea of hippocampus when compared to the other treatment groups (group 3–4) whose Pykonotic index appear to be similar to that of the control. The sections from groups 1–4 had distorted arrangement of the pyramidal cells with several of them being pyknotic with dark shrunken nuclei and abnormal clumping of cellular formation were observed. In conclusion, the present study showed that high dose and long-term consumption of KNE can inhibit hippocampal neurogenesis and hippocampus-dependent learning and memory. We recommend that the fundamental mechanism that explains the degeneration and inhibition of neurogenesis by KNE be fully elucidated in future studies.

Evaluation of the antioxidant potential of Neem (Azadirachta indica) leaf supplement in alleviating Alzheimer’s Disease like behaviour induced by Aluminum neurotoxicity

AbstractBackgroundTo evaluate the antioxidant potential of Neem (Azadirachta indica) leaf supplement in attenuating Alzheimer’s disease (AD) pathology induced by aluminum neurotoxicity (Animal model of AD). Y‐ maze test, neuro‐morphology and astrocytic proliferation will be study in the fronto‐hippocampal and cerebellar cortices to elucidates the therapeutic role of neem leaf in AD pathology.MethodsTwenty (20) adult male Wistar rats were grouped (4 groups, n = 5); Control group (A), Aluminum treated group for 7 days (B), 200mg/kg body weight Neem leaf supplement for 7 days (C), and the AD model post‐treated with 200mg/kg Neem leaf supplement for 7 days (D). Study was done for 14 days via oral administration of study materials. Neurobehavioral test for memory and learning done using Y‐maze test. Excised brain was fixed in 10% formol calcium, processed for Cresyl fast violet (CFV) stain for Nissl (chromatophilic) bodies and astrocytes immunohistochemistry using glial fibrillary acidic protein (GFAP) monoclonal primary antibodies in biotinylated secondary antibodies. Behavioural test data were analyzed using ANOVA, post hoc test and significance set at p&lt;0.05.ResultsAluminum treated group cortical area was characterized by necrosis, chromatolysis, neuropil vacuolations and astrocytes proliferation with impaired memory demonstrated by a reduction in the number of arm entries and spontaneous alternations as compared with the control and neem treated groups. However, these pathological changes were reversed by neem leaf supplementation seen in AD model neem leaf post‐treated group (D) showing an increased number of arm entries and spontaneous alternations, regeneration of neurons and a reduced reactive astrocytes (astro‐gliosis) proliferation.ConclusionNeem leaf supplement neuroprotective and repair role in AD pathological is proposed to be via ameliorating astrocytes mediated neuroinflammatory response via the neuron‐astrocytes interaction and antioxidant role during neuroinflammation induced by aluminum in the fronto‐hippocampal and cerebellar cortices

Calcium Supplementation Ameliorates Cerebellar Oxidative Stress in Lactational Aluminum-induced Neurotoxicity in Rats.

The neurotoxic effects of aluminum exposure during the critical period of neurodevelopment have been well documented. This study investigated the known protective effects of calcium supplementation on the cerebellum of juvenile Wistar rats following aluminum-induced neurotoxicity during lactation. Four groups of juvenile rats were exposed via lactation to distilled water (control group), aluminum (40 mg/kg/d), calcium supplement (50 mg/kg/d), and a combination of both aluminum and calcium from postnatal day 4 to day 28. The cerebella of the animals were excised to access the levels of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPx]), lipid peroxidation (malondialdehyde), histomorphological alterations (hematoxylin and eosin staining), Nissl profile (cresyl fast violet staining), and glial activation (glial fibrillary acidic protein immunohistochemistry). Lactational aluminum significantly decreased the activities of superoxide dismutase and glutathione peroxidase while exacerbating lipid peroxidation and reactive astrocyte in cerebellar lysates. Lactational calcium supplementation normalized the activities of SOD and GPx, thereby preventing excessive lipid peroxidation and glial activation. Despite no apparent changes in the general histology of the cerebellum, aluminum-induced chromatolysis changes in the Purkinje cell layer, which was counteracted by the antioxidant propensities of calcium supplementation. These findings support that calcium supplementation significantly protects the cerebellum against aluminum-induced oxidative stress, chromatolysis, and neuroinflammation.

The Combined Psychoactive Effects of Caffeine, Nicotine and MDMA on the Prefrontal Cortex of Juvenile Male Wistar Rats

The juvenile is vulnerable to psychoactive agents and environmental influences. Caffeine, nicotine, and 3,4-Methylenedioxymethamphetamine (MDMA) could influence the developing brain with potential consequences on mental attributes including memory, cognition, behaviour, and learning. This research studied the structural and functional changes attributable to the combined use of caffeine, nicotine and MDMA on the prefrontal cortex. Thirty-two juvenile male Wistar rats were grouped into four (n=8) and administered water-dissolved caffeine, nicotine and MDMA by oral gavages. An untreated group served as control. The second group received caffeine (100mg/kg bw) and nicotine (50mg/kg bw), the third group received caffeine (100mg/kg bw) and MDMA (10mg/kg bw) and the last group received nicotine (50mg/kg bw) and MDMA (10mg/kg bw). Treatments lasted thirty days, after which animals were sacrificed. The prefrontal cortices were fixed in formal saline, processed, and demonstrated using eosin and haematoxylin (H&amp;E), Cresyl fast violet, and Luxol fast blue histological methods as well as glial-acidic fibrillary protein (GFAP) immunohistochemistry. Representative photomicrographs were obtained and analysed. Combined ingestion of caffeine, nicotine and MDMA affected the brain causing neuronal morphological aberrations, aberrations in Nissl expression, and astrocyte reactions especially with the combination of caffeine + nicotine as well as caffeine + MDMA with mild aberrations in myelin integrity. Effects also included significant elevations in GABA and serotonin activities with the combination of nicotine and MDMA (p&lt; 0.05). Results showed that the combined use of psychoactive agents could elicit peculiar effects

MO11 and MS06 ameliorated cadmium chloride-induced neuro-inflammation, hyperplasia and apoptosis via NF-kB/ Caspase-3/p53 pathway and down-regulated sVEGFR in rats

Cadmium is a neurotoxin, carcinogen and a suspected agent in aetiology of Parkinson’s disease and Alzheimer’s disease (AD). Furthermore, upregulations of Caspase-3 and p53 were reported in brains of AD patients. This study evaluated the neuroprotective potentials of MO11 (isolated from Moringa oleifera leaves) and MS06 (isolated from Musa sapientum suckers) in Cadmium Chloride (CdCl)-induced neurotoxicity in the cerebrum of rats. Twenty-eight adult male wistar rats (average weight of 155 g) were randomly divided into 7 groups (n = 4). Group 1 received physiological saline. Groups 2-4 and 7 received single 1.5 mg/Kg bodyweight of CdCl (i.p.) (Day 1). Groups 3-4 and 7 were post-treated with 15 mg/Kg bodyweight of MO11, 15 mg/Kg bodyweight of MO11 + 7 mg/Kg bodyweight of MSF1 and 3.35 mg/Kg bodyweight of Doxorubicin respectively (Days 1-17). Groups 5-6 received only MO11 and Vegetable Oil (vehicle) respectively (Days 1-17). Cerebral histopathology (Cresyl Fast Violet method) was evaluated in rats. ELISA evaluations of biomarkers of pro-inflammation (IL-1β, IL-6, IL-8 and NF-kB), anti-inflammation (IL-4 and IL- 10), apoptosis (Caspase-3 and p53), proliferation (Ki67) and angiogenesis (sVEGFR) in cerebral homogenates of rats were also conducted. Histopathological evaluations showed a high number of chromatolytic cells in Group 2, compared with Groups 1 and 3-7. Post-treatments of CdCl-induced neurotoxicity with MO11 and MS06 resulted in decreased levels of IL-1β, IL-6, IL-8, NF-kB, Caspase-3, Ki67, p53 and sVEGFR, but increased levels of IL-4 and IL-10 in Groups 3-4, compared with Group 2. Therefore, MO11 and MS06 possess neuroprotective, neuroregenerative, anti-AD, anti-inflammatory and anticancer potentials. Key words: Cadmium – Neurotoxicity – Alzheimer’s disease – Moringa oleifera – Musa sapientum – Neuroprotection – Neuroregeneration

Caffeic Acid Phenethyl Ester With Mesenchymal Stem Cells Improves Behavioral and Histopathological Changes in the Rat Model of Parkinson Disease.

Parkinson disease (PD) results from the destruction of dopaminergic neurons in the brain. This study aimed to investigate the protective effects of natural antioxidants such as caffeic acid phenethyl ester (CAPE) to maintain these neurons. CAPE is one of the main ingredients of propolis. Intranasal administration of 1-methyl-4-phenyl-2;3;4;6-tetrahydropyridine (MPTP) was used to generate a PD model in rats. A total of 2×bone marrow stem cells (BMSCs) were injected from the tail vein. Behavioral tests, immunohistochemistry, DiI, cresyl fast violet, and TUNEL staining were used to evaluate the rats 2 weeks after treatment. In all treatment groups with stem cells, the DiI staining method revealed that the cells migrated to the substantia nigra pars compacta after injection. Treatment with CAPE significantly protects dopaminergic neurons from MPTP. The highest number of tyrosine hydroxylase (TH) positive neurons was seen in the pre-CAPE+PD+stem cell (administration of CAPE, then the creation of PD, finally injection of stem cells) group. The number of TH+cells in all groups that received CAPE was significant compared to groups that received the stem cells only (P<0.001). Intranasal administration of MPTP significantly increases the number of apoptotic cells. The lowest number of apoptotic cells was in the CAPE+PD+stem cell group. The results showed that the use of CAPE and stem cells in Parkinson rats caused a significant reduction in the apoptotic cells.

Alpha lipoic acid reverses scopolamine-induced spatial memory loss and pyramidal cell neurodegeneration in the prefrontal cortex of Wistar rats.

Neurodegenerative disorders are linked to oxidative tissue damage characterized by gradual loss of cognitive functions and neuronal cells. Alpha-lipoic acid (AHA) has a strong antioxidant property. Scopolamine is an anti-muscarinic agent used to study the mechanism of memory loss in an animal model. This study is aimed at evaluating the antioxidant role of alpha lipoic acid in reversing scopolamine induced memory loss and neurodegenerative process in the prefrontal cortex of Wistar rats. Twenty adult male Wistar rats used were divided into four groups (n = 5): Group 1 received vehicle (Control), Group 2 had scopolamine (1 mg/kg, i.p) for 4 days, Group 3 received AHA (200 mg/kg, p.o) for 10 days while Group 4 were pretreated with scopolamine (1 mg/kg, i.p) for 4 days followed by oral administration of 200 mg/kg of AHA for 10 days. The rats were subjected to Y-maze test to assess their spatial memory. The rats were euthanized, the prefrontal area was excised and fixed in 10% formol-calcium and processed for Haematoxylin and Eosin, Cresyl fast violet for Nissl Bodies (Ribosome), and Glial Fibrillary Acidic Protein (GFAP) stains. Scopolamine caused a significant decline in spatial working memory, prefrontal neuron cell loss, and increased proliferation of reactive astrocytes (astrogliosis) when compared with the control and AHA treated group. AHA process of reversing scopolamine-induced memory deficit, prefrontal neuron cell loss, and generation of reactive astrocytes (astrogliosis) is mediated by its antioxidant mediated positive modulation of astrocyte-neuronal interaction during neuroinflammation in response to oxidative tissue damage.

Ascorbic acid modulates prefrontal cortex cellular changes in androgen deprived rats

Background: Testosterone deficiency has been implicated in numerous neurodegenerative diseases such as Alzheimer's, Parkinson and Huntington's disease. We used a model of androgen deprived rats to determine the effects of ascorbic acid on prefrontal cortex (PFC) cellular changes associated with a subset population of androgen deprived patients.Methodology: Chemical castration (using testosterone antagonist) as well as orchiectomy can induce androgen deprivation. Twenty-one (21) adult male Wistar rats with an average weight of 170g±10g were randomly assigned into three groups with each group containing seven (7) rats. Group A was control group, Group B= Orchiectomy + Flutamide (11 mg/kg body weight), and group C= Orchiectomy + Flutamide (11 mg/kg body weight)+Ascorbic acid (100 mg/kg body weight). Treatment lasted for 30 days. Nitric oxide and Malondialdehyde levels were assessed; while serum testosterone level was assayed. Histological, Histochemical, and immunohistochemical investigations were performed using Hematoxylin &amp; Eosin, Cresyl fast violet, and Bielschowsky stains respectively.Result: Our results showed increased expression of Nitric Oxide (NO), and increased lipid peroxidation (MDA) in the PFC of orchiectomized animals with altered cytoarchitectural morphology evidenced by decreased Nissl staining polarity in neuronal axons and aggregation of neurofibrillary tangles. Oxidative and nitrosative stress were well modulated in animals treated with ascorbic acid with unaltered prefrontal cortex morphology.Conclusion: The results indicated that decline in brain androgen activities caused nitrosative and oxidative stress-driven pathology in the prefrontal cortex while supplementing endogenous ascorbic acid offered therapeutic value by scavenging free radicals in the prefrontal cortex

Neuropharmacological effects of honey in lipopolysaccharide-induced neuroinflammation, cognitive impairment, anxiety and motor impairment

ABSTRACT Objectives: Honey contains phenolic acids and flavonoids, which are significant in developing drugs against neuroinflammation. The study was designed to evaluate the ameliorative potential of honey in lipopolysaccharides-induced neuroinflammation. Methods: Thirty male Wistar rats were divided into six groups, namely: the control group (10 mL/kg vehicle), the LPS only group (250 µg/kg), the honey (0.26, 0.31 and 0.36 g/kg) and the ibuprofen (100 mg/kg). LPS (250 µg/kg i.p) was administered for 7days followed by the treatment with honey and Ibuprofen for another 7days. Animals were assessed for memory impairment and anxiety levels using a Novel object recognition test (NORT), elevated plus maze (EPM), and open field test (OFT). Brain levels of pro-inflammatory cytokine level, acetylcholinesterase activity, and oxidative stress were determined. The neuronal alteration was assessed histologically using cresyl fast violet staining of the hippocampus, prefrontal cortex, and striatum. Results: Honey (0.31 and 0.36 g/kg) significantly ameliorated LPS-induced memory impairment on NORT and increased time spent in the open arm and increased the locomotor activity in the OFT. Honey significantly (p < 0.05) reduced LPS-induced elevation of tumor necrosis factor (TNF-α) and interleukin-6 (IL-6). It significantly reduced malondialdehyde and nitrite levels in mice brains and reversed depletion of reduced glutathione levels. Honey attenuated LPS-induced elevation of acetylcholinesterase activity in rat brains. Cresyl violet staining showed the restoration of neuronal organization and Nissl body distribution in the hippocampus, prefrontal cortex and striatum compared to the LPS only group. Discussion: Honey effectively ameliorated LPS-induced poor cognitive performance, anxiety, motor coordination responses to neuroinflammation, and oxidative stress.

Stepwise pesudopolyrotaxane nanostructure formation from supramolecular self-assembly by inclusion complexation of fast violet B with α- and β-cyclodextrins

The current work deals with fast violet B (FVB) and cyclodextrins (α-CD and β-CD) inclusion complex into pesudopolyrotaxane nanorod by supramolecular self-assembly. FVB/α-CD forms 2:2 from 1:1 and FVB/β-CD forms 1:2 from 1:1 inclusion complexes, which further self assembled to form nanorod and nano cluster structures. The nanorods formed through step-by-step process after FVB encapsulation into cyclodextrins nano cavities. Wide angle powder X-ray diffraction exposed the crystallinity of the materials, thermal analysis, Fourier Transform Infrared Spectroscopy (FTIR) and Proton Nuclear Magnetic Resonance spectroscopy (1H NMR and 2D ROESY) confirmed FVB encapsulation into the CDs cavities. Amido functionality of FVB molecule is twisted when it is encapsulated within α-CD and β-CD cavities. Computational studies further divulge that the complex formation is an enthalpy-entropy driven process.

Brain antioxidants and hippocampal microanatomical alterations following the administration of Efavirenz/Lamivudine/Tenofovir disoproxil fumarate and Lamivudine/Nevirapine/Zidovudine in adult male Wistar rats.

Highly active antiretroviral therapies (HAARTs) are used for the management of human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS). The present study was designed to characterize the neurotoxicity profile of two popular HAARTs on the brains’ antioxidants and hippocampal microanatomical alterations in an in vivo model. Fifteen adults male Wistar rats, were assigned to three groups (n = 5); group I the normal control (NC) received distilled water (5 mL/kg b.wt), groups II administered with oral therapeutic doses of Efavirenz/ Lamivudine/ Tenofovir disproxil fumerate (TLE 17.14 mg/kg b.wt), and group III with Lamivudine/ Nevirapine/ Zidovudine (LNZ 9.28 mg/kg b.wt), respectively which were available for use in University of Uyo Teaching Hospital Nigeria at the time of this experiment. After a 30-day administration, biochemical parameters (catalase, superoxide dismutase, reduced glutathione, glutathione S-transferase, malondialdehyde, glutathione peroxidase, vitamins A, C and E) were determined via serum from blood of ketamine (100 mg/kg, i.p) anesthetized rats. Brains were carefully removed and post-fixed for tissue processing employing hematoxylin and eosin (H&E), cresyl fast violet (CFV) stains, and glial fibrillary acidic protein (GFAP) antibody expression. Results revealed significantly (p < 0.05) decreased antioxidant concentrations and increase in oxidative markers in HAART-administered groups. Normal histoarchitecture was shown in NC, but TLE-administered group demonstrated some neuronal atrophy, and degeneration of pyramidal neurons, with milder distortions in LNZ. TLE-administered group demonstrated intense Nissl substances with chromatolysis compared to LNZ and NC, while GFAP was strongly expressed in TLE-administered group compared to LNZ. In conclusion, TLE is more neurotoxic compared with LNZ.

Cytoarchitecture of the medial nucleus of trapezoid body of three neotropical species of bats (Noctilio leporinus, Phyllostomus hastatus, and Carollia perspicillata) with different foraging behavior

Abstract The present study was taken to test the hypothesis that the medial nucleus of the trapezoid body (MNTB) of echolocating neotropical bats with different foraging behavior will exhibit morphological variations in relative size, degree of complexity and spatial distribution. The brains were collected from six male adult bats of each species: Noctilio leporinus (fish-eating), Phyllostomus hastatus (carnivorous/ omnivorous) and Carollia perspicillata (fruit-eating) and were double-embedded and transverse serial sections were cut and stained with cresyl fast violet. The results showed that the MNTB is well developed in all the bats in general and the mean length of the MNTB was 1160 ± 124 µm in N. leporinus, 400 ± 59 µm in P. hastatus and 320 ± 25µm in C. perspicillata. The body and brain weight do not reflect proportionately on the size of the MNTB in the present study. The hearing frequency spectrum did not covary with the size of the MNTB among the bats studied. The MNTB is clearly demarcated from the ventral nucleus of the trapezoid body (VNTB) only in P. hastatus. The MNTB comprised mainly three types of cells in all three bats: dense-staining multipolar cells (12.5 µm and 25.0 µm diameter); light-staining multipolar cells measuring (12.5 µm and 25.0 µm diameter) and light-staining round cells (5.0 µm diameter). The large sized MNTB was observed in N. leporinus, which suggests that it relies heavily on echolocation whereas P. hastatus and C. perspicillata use echolocation as well but also rely on hearing, smell and vision.

An investigative study to demonstrate the link between combined intake of marijuana and codeine in Alzheimer’s disease pathology

AbstractBackgroundAssessment of the contributory role of combined ingestion of codeine and Marijuana to the pathogenesis of Alzheimer’s disease which is the most common cause of dementia among older adults; by studying changes in spatial memory, astrocytic proliferation, Nissl bodies, lipid peroxidation and antioxidant enzyme status.MethodTwenty (20) adult male Wistar rats used for this study were divided into four groups (n=5): the control, codeine, marijuana and a group given both codeine and marijuana. The animals were exposed to the drug treatment for ten (10) days. Behavioral tests for memory using Y maze was conducted. The animals were euthanized and brain tissues fixed in 4% PFA and processed for Cresyl fast Violet stain for Nissl bodies, glial fibrillary acidic protein (GFAP) immunohistochemistry for astrocytes with focus on prefronto‐hippocampus cortex. Serum antioxidant activity of superoxide dismutase (SOD), glucose‐6‐phosphodehydrogenase (G6PDH), Lactate dehydrogenase (LDH) activity and lipid peroxidation enzyme marker –Malondialdehyde (MDA) were accessed.ResultThe prefronto‐hippocampal cortex of rats exposed to Codeine, Marijuana (B and C) and those give both drugs (D) were characterized with loss of neurons, necrosis, chromatolysis and proliferation of astrocytes as compared with the control. However, combined drug use has more severity in the loss of loss of spatial memory, reduced number of arm entries and increased immobility time as compared with the control, codeine and Marijuana only groups. Group D, had severe decline in SOD and G6PDH serum activity and an elevation in lipid peroxidation as compared with B and C.Conclusionthe combine use of codeine and marijuana has more deleterious effects on neuron cell integrity, memory, cognition and antioxidant enzymes because it induces severe oxidative stress that predisposes to the development of Alzheimer’s disease in an individual.

Correlation of Histomorphometric Changes with Diffusion Tensor Imaging for Evaluation of Blast-Induced Auditory Neurodegeneration in Chinchilla.

In the present study, we have evaluated the blast-induced auditory neurodegeneration in chinchilla by correlating the histomorphometric changes with diffusion tensor imaging. The chinchillas were exposed to single unilateral blast-overpressure (BOP) at ∼172dB peak sound pressure level (SPL) and the pathological changes were compared at 1 week and 1 month after BOP. The functional integrity of the auditory system was assessed by auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE). The axonal integrity was assessed using diffusion tensor imaging at regions of interests (ROIs) of the central auditory neuraxis (CAN) including the cochlear nucleus (CN), inferior colliculus (IC), and auditory cortex (AC). Post-BOP, cyto-architecture metrics such as viable cells, degenerating neurons, and apoptotic cells were quantified at the CAN ROIs using light microscopic studies using cresyl fast violet, hematoxylin and eosin, and modified Crossmon's trichrome stains. We observed mean ABR threshold shifts of 30- and 10-dB SPL at 1 week and 1 month after BOP, respectively. A similar pattern was observed in DPAOE amplitudes shift. In the CAN ROIs, diffusion tensor imaging studies showed a decreased axial diffusivity in CN 1 month after BOP and a decreased mean diffusivity and radial diffusivity at 1 week after BOP. However, morphometric measures such as decreased viable cells and increased degenerating neurons and apoptotic cells were observed at CN, IC, and AC. Specifically, increased degenerating neurons and reduced viable cells were high on the ipsilateral side when compared with the contralateral side. These results indicate that a single blast significantly damages structural and functional integrity at all levels of CAN ROIs.

Cnidoscolus aconitifolius-supplemented diet enhanced neurocognition, endogenous antioxidants and cholinergic system and maintains hippocampal neuronal integrity in male Wistar rats.

Cnidoscolus aconitifolius have been investigated to have abundant phytochemicals. However, study on the effect of Cnidoscolus aconitifolius on neurobehavioral performance when supplemented with diet is lacking. The study is aimed at investigating the memory-enhancing effect of Cnidoscolus aconitifolius-supplemented diet (CAD) using Morris water maze and Novel object recognition test. Ninety male Wistar rats (80-100g) were fed with CAD (1, 2.5, 5 and 10%) continuously for a period of 4, 8 and 12weeks respectively. Six animals per group were used for assessment of memory performance (Morris water maze [MWM] and Novel object recognition test [NORT]); afterwards the brain tissues were harvested for malondialdehyde (MDA), glutathione (GSH) and catalase (CAT) estimation. Acetylcholinesterase (AChE) concentration was also determined. Hippocampal architectural change in the neuron was examined using hematoxylin and eosin (H&E) and cresyl fast violet (Nissl) stain. Higher percentage of CAD significantly (p<0.05) improve memory performance with time-dependent effects in rats fed with CAD on MMW and NORT. MDA significantly (p<0.05) reduce in 1 and 2.5% CAD groups at 4th weeks and in 2.5 and 5% CAD groups at 8th weeks while GSH concentration significantly (p<0.05) increase at 12th weeks in 2.5 and 10% CAD groups. However, CAT concentration significantly (p<0.05) increase in 2.5, and 5%, CAD groups, 1, 5, and 10% CAD groups and in 5, and 10% CAD groups at 4th, 8th and 12th weeks. AChE significantly (p<0.05) reduce at 4th and 12th weeks. Histological assessment reveals no neuronal and pyramidal degeneration (chromatolysis) at the hippocampal Cornu Ammonis 3 (CA3) region. The results suggest that CAD boost memory performance in rats through positive modulation of oxidative stress, cholinergic system and degeneration of hippocampal neurons.