The study was designed to determine whether lactational exposure to hyoscyamine fraction of Datura stramonium L. (D. stramonium) seeds affect the cognitive, spatial learning and memory functions of the hippocampus in Wistar rats at adulthood. Fresh seeds of D. stramonium L. were procured, macerated and fractionated using high-performance liquid chromatography (HPLC). Eight (8) Wistar rats weighed 150-250 grams of equal gender were used for the study. The rats were mated and divided into control and treatment groups. Equivalent body weight of normal saline and 400 mg/kgbwt of hyoscyamine fraction were orally administered to the breastfeeding rats respectively on lactational days (LD) 1-21. At adulthood, the rats were subjected to neurobehavioural tests using novel objects recognition (NORT) and Morris water maze (MWM) respectively. The data obtained were expressed as mean ± SEM, independent two samples t-test and General Linear Model (GLM) repeatedmeasures ANOVA with Fisher’s multiple comparisons post-hoc tests were used to show the mean differences using Minitab 17 (LLC., U.K.) statistical package software. P < 0.05 was considered statistically significant. A significant increase in the meantime of exploration between the groups (p = 0.049) was observed during the NORT. No statistically significant increase (p = 0.626) in the meantime to locate the escape platform between the groups during the MWM test. The CA1 region of the treated group showed mild nuclear hyperchromasia, cytoplasmic vacuolations and pyknosis. In conclusion, exposure to hyoscyamine fraction of D. stramonium L. seeds at lactation caused histologic changes in the CA1 region, loss in short-term memory but not spatial learning and memory functions of the hippocampus of Wistar rats at adulthood.

Aim: Several reports have shown environmental neuron toxins such as aluminium to accumulate in the brain, potentially triggering neurodegenerative disorders. Adansonia digitata (Baobab) has been reported to possess beneficial properties. This study, assessed the neuroprotective properties of aqueous fruit pulp extract of Adansonia digitata (AEAD) on aluminum chloride (AlCl3) – induced memory dysfunctions and hippocampal changes in Wistar rats. The neuroprotective effects of AEAD were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione (GSH), superoxide dismutase (SOD), and Malondialdehyde (MDA), and histopathological changes on the hippocampal CA3 region using histological techniques. Materials and Methods: Thirty male Wistar rats (110 and 150 g) were divided into six groups at random (n=5). The Control group, the animals in Group 1 received 2 ml/ kg distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the AEAD (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform in the Morris water maze test was observed with remarkable (P<0.05) improvement in the AEAD treatments compared with the AlCl3- treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the AEAD-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neurodegenerative changes, whereas, administration of AEAD ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Aqueous fruit pulp extract of Adansonia digitata demonstrated a possible neuroprotection against aluminium chloride-induced memory deficit and CA3 hippocampal neurotoxicity.

Background: Lead acetate (Pb) exposure during frontal cortex development is associated with developmental
toxicity later in life, causing both morphological and functional alterations. Curcuma longa,
however, has been suggested to possess neuroprotective qualities that could lessen these adverse effects.
Objective: Assessed the frontal cortex following treatment with Curcuma longa. Materials and Methods:
Twenty adult female Wistar rats and ten adult male Wistar rats were matched during the proestrous phase
of the estrous cycle in order to mate and create five groups of six (n=6) in a 4:2 (4 females to 2 males)
ratio. Gestational day 0 was marked as the confirmation of pregnancy based on if sperm is present and a
vaginal plug in the vaginal smear. Four (n=4) pregnant Wistar rats were put together. Group 1 (control) rats
were given 2 milliliters per kilogram of distilled water. Pb was given at a dose of 120 mg/kg to Group 2.
Group 3 rats were given 120 mg/kg of lead and 100 mg/kg of vitamin C. The animals in Group 4 received
750 mg/kg of Curcuma longa and 120 mg/kg of Pb. The animals in Group 5 rats were given 1500 mg/kg
of Curcuma longa and 120 mg/kg of Pb. From gestational day 7 to day 21 (14 days), the medication was
administered orally. The animals were allowed to litter naturally. At postnatal day (PND) 1, some pups
were euthanized using chloroform inhalation and their brains were harvested for Oxidative stress markers,
histology, histochemical assessments. While some pups were kept for Cliff avoidance test at PND 4-7.
Results: The study found that lead acetate (Pb) exposure during gestation significantly decreased the mean
turning latency in the cliff avoidance test and increased lipid peroxidation (MDA) levels, while decreasing
antioxidant enzyme levels (SOD, CAT, GSH) compared to the control group. These neurological and oxidative
changes were mitigated by co-administration of Curcuma longa, with a notable improvement in the
cliff avoidance test performance and restoration of the altered histological and histochemical markers. The
results suggest that Curcuma longa, a natural antioxidant, has neuroprotective properties that can counteract
the adverse effects of lead toxicity during gestational development. Conclusion: N-Butanol Fraction
of Curcuma Longa ameliorated lead-induced neurotoxicity in rat pups.