Hippocampus Of Adult Wistar Rats Research Articles

Ameliorative effects of Aqueous Fruit Pulp Extracts of Adansonia digitata on the Hippocampus of Aluminium Chloride‐treated Adult Wistar Rats

AbstractBackgroundThis study evaluated the effects of aqueous extract of Adansonia digitata fruit pulp (AEAD) on the hippocampus of Aluminium chloride Alzheimer model Wistar rats.MethodThirty Wistar rats (110‐150g) were randomly divided into six groups (n = 5). The animals in Group 1 were administered 2ml/kg distilled water. Group 2 were administered 100mg/kg AlCl3. Groups 3 were administered 595mg/kg ascorbic acid. Group 4 and 5 were administered 100mg/kg AlCl3 + 500mg/kg AEAD and 100mg/kg AlCl3 + 1500mg/kg AEAD respectively. Group 6 were administered 100mg/kg AlCl3 + 595mg/kg ascorbic acid. Once daily, for four consecutive weeks, behavioral tests for spatial memory using the Morris water maze test were carried out. Experimentation lasted for 28 days after which the animals were humanely sacrificed.ResultAnimals treated with A. digitata and Ascorbic acid following Aluminium exposure showed significant decrease (11.67±1.74) in the time taken for the experimental rats to locate the escape platform. The result of the oxidative stress study showed a significant increase Malondialdehyde concentration and decrease in Superoxide dismutase (SOD) and reduced glutathione (GSH) in groups exposed to aluminium chloride, however, treatment with A. digitata and Ascorbic acid following Aluminium exposure did not show any significant difference when compared to the control group. Histopathological studies revealed degenerating pyramidal cells, Karyolysis, Pkynosis, were observed in the hippocampus of the aluminium treated group. Treatment with Adansonia digitata and Ascorbic acid ameliorated the changes observed in groups exposed to aluminium. The histoarchitecture of the aqueous extracts treated groups were preserved, particularly the 1500mg/kg doses.ConclusionA. digitata fruit pulp possess vital antioxidant properties that could ameliorate the toxic effects of aluminium on the Hippocampus of adult Wistar rats and as such could be used as a treatment of aluminium toxicity.

Separate and combined sub-acute effects of artesunate, amodiaquine on spatial memory and hippocampal morphology of adult Wistar rats

We evaluated the sub-acute effect of artesunate (AS), amodiaquine (AQ) and AS plus AQ on the structure and function of the hippocampus of adult Wistar rats. Forty adult male Wistar rats weighing between 110-215 g, were divided into 4 groups (n=10); group A-control (CT) rats administered distilled water, group B-4 mg/kg, AS, group C-10 mg/kg, AQ and group D- 4 mg/kg, AS + 10 mg/kg, AQ body weight. Drugs were administered orally for 3 days and neurobehavioral tests (Morris water maze) for spatial memory and cognition done from day 11 to 14. The rats were sacrificed on the day 15 and blood sample collected for full blood count. The rat brain of all groups was excised, and the hippocampus dissected out, fixed in 10% formol-saline and processed for histology and immunohistochemical (glial fibrillary acidic protein, GFAP (astrocytes) and inducible nitric oxide synthase, iNOS (oxidative stress)) studies. Data were analysed by one-way ANOVA at p<0.05. Subacute evaluation showed that the AQ-treated rats had significantly increased swimming time and distance, red blood cell (RBC), white blood cell (WBC), haemoglobin (Hb) and packed cell volume (PCV) compared with the CT and other groups. Histologically, there was decreased Cornus Ammonis 1 (CA 1) pyramidal neurons in the hippocampus of the AS and AQ-treated rats compared with the CT group. Increased astrocyte population was observed in the hippocampus of AS and AQ groups compared with the CT and AS+AQ groups, as well as increased iNOS expressions compared with the CT group. Subacute evaluation of the adult rat hippocampus indicated that amodiaquine decreased spatial memory and increased blood cell counts, while artesunate and amodiaquine induced oxidative stress resulting in pyknosis of and decreased pyramidal CA1 neurons and caused astrogliosis.

Preliminary Assessment of DNA Profile Patterns of Neuronal Differentiation Factor (NeuroD1) Gene in the Hippocampus of Wistar Rats (Rattus norvegicus) Ingested Hyoscyamine Fraction of Datura stramonium Seeds

The study was designed to find out how oral ingestion of hyoscyamine fraction of D. stramonium seeds affect the DNA profiles patterns and expression of NeuroD1 gene in the hippocampus of adult Wistar rats. Fresh D. stramonium seeds were procured, identified, macerated and fractionated. Thirty-two (32) male adult Wistar rats weighed 200-250 grams were procured and divided into four groups comprised of control and three treatment groups for the study. The control received an equivalent bodyweight of normal saline, while the treatment groups received 200, 400 and 800 mg/kgbwt of hyoscyamine fraction for three weeks respectively. The animals were sacrificed, tissues harvested for histology, gel electrophoresis and gene expression studies. The fold changes were calculated and DNA profiles were determined using LabImage bio-imaging software. One-way ANOVA followed by Fisher’s multiple comparisons post-hoc test was used to obtain the difference in the expression of the gene across the groups using Minitab 17 (LLC., U.K.) statistical package software. P < 0.05 was considered statistically significant. There was a statistically significant downregulation (p = 0.001) in the NeuroD1 expression, increased DNA fragment size, decreased DNA migration distance and band volume, and necrosis of the dentate gyrus (DG) region in the hippocampus of the treated animals. In conclusion, oral ingestion of hyoscyamine fraction of D. stramonium seeds is toxic to the DNA profile patterns and expression of the NeuroD1 gene in Wistar rats.

Evaluating the Effect of Chloroform Inhalation as a Method of Euthanasia on the Cerebellum and Hippocampus of Adult Wistar Rats

Chloroform inhalation is a common method of rodent euthanasia in Nigeria for research purposes. This work is designed to evaluate the consequence of this method of sacrifice on the cerebellum and hippocampus of Wistar rats. Twenty male Wistar rats weighing between 160 and 180 were divided into 4 groups of 5 rats each. Group A served as control and was sacrificed using cervical dislocation (a widely acceptable non-inhalation method of sacrifice). Groups B, C and D were exposed to chloroform for 5 minutes once a day (group B), once a day for 2 days and once a day for 3 days. The brains were removed; four from each group was processed for antioxidant assay while one from each group was fixed in Bouin’s fluid for histological studies. Our results show that chloroform inhalation adversely affected the results of the antioxidant parameters studied in a dose-dependent fashion. That means that the adverse effect worsened as the number of days increased. This was also the case with the histology results as there was evidence of cell necrosis in the cerebellar and hippocampal tissues. This also showed dose dependence. We therefore conclude from our results that when studying the brain tissues or carrying out brain related researches, chloroform inhalation is not the method of choice for rat euthanasia.

Quantitative characterization of proliferative cells subpopulations in the hilus of the hippocampus of adult Wistar rats: an integrative study.

The hilus plays an important role modulating the excitability of the hippocampal dentate gyrus (DG). It also harbors proliferative cells whose proliferation rate is modified during pathological events. However, the characterization of these cells, in terms of cellular identity, lineage, and fate, as well as the morphology and proportion of each cell subpopulation has been poorly studied. Therefore, a deeper investigation of hilar proliferative cells might expand the knowledge not only in the physiology, but in the pathophysiological processes related to the hippocampus too. The aim of this work was to perform an integrative study characterizing the identity of proliferative cells populations harbored in the hilus, along with morphology and proportion. In addition, this study provides comparative evidence of the subgranular zone (SGZ) of the DG. Quantified cells included proliferative, neural precursor, Type 1, oligodendrocyte progenitor (OPCs), neural progenitor (NPCs), and proliferative mature astrocytes in the hilus and SGZ of Wistar adult rats. Our results showed that 84% of the hilar proliferative cells correspond to neural precursor cells, OPCs and NPCs being the most abundant at 54 and 45%, respectively, unlike the SGZ, where OPCs represent only 11%. Proliferative mature astrocytes and Type 1-like cells were rarely observed in the hilus. Together, our results lay the basis for future studies focused on the lineage and fate of hilar proliferative cells and suggest that the hilus could be relevant to the formation of new cells that modulate multiple physiological processes governed by the hippocampus.

Histological and Anti-oxidative Effects of Eugenol on Aluminium Chloride-Induced Neurotoxicity in Wistar Rats

Accumulation of aluminium chloride results in damage to different brain regions, and has been used to model damage to the hippocampus which can be associated with various neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The aim of this study was to assess the protective effects of eugenol on aluminium induced neurotoxicity in the hippocampus of adult Wistar rats. 30 adult Wistar rats were procured and divided into six groups with five animals in each group, namely: EGH (300 mg/kg eugenol), EGL (150 mg/kg eugenol), EGH+AL (300 mg/kg eugenol and 100 mg/kg AlCl3), EGL+AL (150 mg/kg eugenol and 100 mg/kg AlCl3), AL (100 mg/kg AlCl3) and CTRL (2 mL/kg distilled water). All Groups were treated orally for 21 days after which they were humanely sacrificed under 0.8 mL/kg ketamine as an anaesthetizing agent. Thereafter, brain tissues were removed and processed for histological demonstration, while the frontal lobe was homogenized and the resultant homogenate obtained was used to assay the levels of superoxide dismutase (SOD) activity. Rat body weights were measured before and after treatment. Aluminium resulted in a significant (p<0.05) reduction in SOD activities. There was alteration in the histology of hippocampal neurons (CA1) and a significant (p<0.01) reduction in body weight of animals. However, the administration of Eugenol was able to restore the activity of SOD. The use of Eugenol offers a promising prospect in the management of neurodegenerative diseases associated with aluminium toxicity.

Behavioural and Microstructural Evaluation of the Hippocampus of Adult Wistar Rats Following Artequin Administration

Behavioural and Microstructural Evaluation of the Hippocampus of Adult Wistar Rats Following Artequin Administration

Effects of Kolaviron on Cuprizone-Induced Demyelination in the Hippocampus of Adult Wistar Rats

Effects of Kolaviron on Cuprizone-Induced Demyelination in the Hippocampus of Adult Wistar Rats

Protective role of adansonia digitata on lead-induced neurotoxicity in the hippocampus of adult wistar rats

Protective role of adansonia digitata on lead-induced neurotoxicity in the hippocampus of adult wistar rats

An evaluation of aversive memory and hippocampal oxidative status in streptozotocin-induced diabetic rats treated with resveratrol

The present study evaluated the effects of streptozotocin (STZ)-induced diabetes on aversive memory, free radical content and enzymatic antioxidant activity in the hippocampus of adult Wistar rats submitted to oral treatment with resveratrol. Animals were divided into eight groups: non-diabetic rats treated with saline (ND SAL), non-diabetic rats treated with resveratrol at a dose 5mg/kg (ND RSV 5), non-diabetic rats treated with resveratrol at a dose 10mg/kg (ND RSV 10), non-diabetic rats treated with resveratrol at a dose 20mg/kg (ND RSV 20), diabetic rats treated with saline (D SAL), diabetic rats treated with resveratrol at a dose 5mg/kg (D RSV 5), diabetic rats treated with resveratrol at a dose 10mg/kg (D RSV 10) and diabetic rats treated with resveratrol at a dose 20mg/kg (D RSV 20). The animals received oral gavage for 35days. The contextual fear conditioning task was performed to evaluate aversive-based learning and memory. The oxidative status was evaluated in the hippocampus, by measuring the free radical content – using a 2′,7′-dichlorofluorescein diacetate probe – and enzymatic antioxidant activities, such as superoxide dismutase and glutathione peroxidase. Our main behavioral results demonstrated that rats from the D RSV 10 and D RSV 20 groups showed an increase in freezing behavior when compared, respectively, to the ND RSV 10 (p<0.01) and ND RSV 20 (p<0.05). Oxidative stress parameters remained unchanged in the hippocampus of all the experimental groups. In contrast to previous experimental findings, our study was unable to detect either cognitive impairments or oxidative stress in the hippocampus of the diabetic rats. We suggest additional long-term investigations be conducted into the temporal pattern of STZ-induced diabetic disruption in memory and hippocampal oxidative status, as well as the effects of resveratrol on these parameters, in a time and dose-dependent manner.

Adult rat hippocampus soluble factors: A novel transplantation model mimicking intracranial microenvironment for tracing the induction and differentiation of adipose-derived stromal cells in vitro

Intracranial transplantation of ADSCs induces recovery of CNS diseases, but how they develop in host is poorly understood. The aim of this study is to observe induction and differentiation of ADSCs in the presence of hippocampus soluble factors (HiSF) extracted from the hippocampus of adult Wistar rats to mimic an intracranial microenvironment. To determine the optimal microenvironment, five conditions were tested: 0μg/ml (as control), 50μg/ml, 100μg/ml, 200μg/ml, and 400μg/ml of HiSF. The number of neurospheres was significantly higher in 200μg/ml group than in other groups on the sixth day. Immunofluorescence demonstrated that the neurospheres induced from ADSCs in 200μg/ml group expressed both nestin and CD133, which are more highly expressed in neurospheres than in ADSCs. This result was confirmed by Western blot analysis. Quantitative PCR revealed that the mRNA levels of nestin and CD133 in the neurospheres were 145- and 220-fold higher, respectively, than those in ADSCs. In the presence of 200μg/ml HiSF and 1% FBS, the neurospheres can further differentiate into Schwann-like cells which expressing characteristic markers GFAP, S100 and P75 NGFR. These data indicated that HiSF, mimicking a destination of ADSCs transplanted model in vitro, could effectively induce and differentiate neurospheres, representing a new method to obtain NSCs and Schwann-like cells from ADSCs.

Neuroprotective Effects of Kolaviron, a Biflavonoid Complex of &lt;i&gt;Garcinia kola&lt;/i&gt;, on Rats Hippocampus against Methamphetamine-Induced Neurotoxicity

Aim: To investigate the protective effects of kolaviron on brain weight and behavioural performance and the histology of the hippocampus of adult Wistar rats following methamphetamine challenge. Materials and Methods: Twenty four adult Wistar rats weighing between 150-200 g, randomly assigned into four groups of six each (Groups A, B, C, D) were used for this research. Group A served as control, while groups B and C were given single dose methamphetamine (10 mg/kg) intraperitoneally after group C was pre-treated with kolaviron (200 mg/kg) for 7 days and group D received cornoil (vehicle for kolaviron) only. Results: High level of methamphetamine-induced stereotypic movement was observed, and the onset was delayed by kolaviron administration. Animals administered methamphetamine only, showed significantly poor behavioural performance on the water maze after treatment when compared to the other groups (P<0.05). Histological analysis revealed neuronal destruction of the pyramidal layer of the hippocampus following methamphetamine administration. Kolaviron to some extent prevented destruction of pyramidal cells of the hippocampus in pre-treated rats. Conclusion: The present findings show the neuro-destructive effects of methamphetamine on hippocampal neurons and its ability to negatively affect behaviour and that kolaviron could prevent such behavioural deficit and also afford some protection to the hippocampus.

Vitamin C antioxidant effects in hippocampus of adult Wistar rats after seizures and status epilepticus induced by pilocarpine

Vitamin C (VIT C) is an exogenous antioxidant able to alter the brain oxidative stress. Antioxidant properties have been showed in seizures and status epilepticus (SE) induced by pilocarpine in adult rats. This present study was aimed at was investigating the VIT C effects on latency to first seizure, in percentage of seizures, mortality rate, as well as hippocampal lipid peroxidation levels and catalase activity after seizures and SE. The VIT C effects were investigated after the pretreatment with dose 250 mg/kg, i.p., 30 min before pilocarpine administration (400mg/kg, s.c., pilocarpine group (P400)). The VIT C increase the latency to first seizure and decrease the mortality rate and lipid peroxidation levels. In P400+VIT C and VIT C groups were observed an increase in hippocampal catalase activity. Our results suggests that the vitamin C can exert antioxidant and anticonvulsive effects in adult rats, suggesting that this vitamin can be able by reduction of lipid peroxidation content and increased of catalase enzymatic activity which cerebral compensatory mechanisms in free radical formation during SE.

Repeated Restraint Stress Induces Oxidative Damage in Rat Hippocampus

It has been shown that emotional stress may induce oxidative damage, and considerably change the balance between pro-oxidant and antioxidant factors in the brain. The aim of this study was to verify the effect of repeated restraint stress (RRS; 1 h/day during 40 days) on several parameters of oxidative stress in the hippocampus of adult Wistar rats. We evaluated the lipid peroxide levels (assessed by TBARS levels), the production of free radicals (evaluated by the DCF test), the total radical-trapping potential (TRAP) and the total antioxidant reactivity (TAR) levels, and antioxidant enzyme activities (SOD, GPx and CAT) in hippocampus of rats. The results showed that RRS induced an increase in TBARS levels and in GPx activity, while TAR was reduced. We concluded that RRS induces oxidative stress in the rat hippocampus, and that these alterations may contribute to the deleterious effects observed after prolonged stress.