Philip Adeyemi Adeniyi

Cerebrovascular changes in the rat brain in two models of ischemia

BACKGROUND Vascular occlusion and cyanide neurotoxicity induces oxidative stress and degeneration in the brain. This oxidant induced stress changes the vascular dynamics of cerebral blood vessels, and participates in homeostatic response mechanisms which balance oxygen supply to hypoxic stress-sensitive neurons. The associated changes in vascular morphology include remodeling of the microvasculature and endothelial changes, alterations in regional circulation and variations in the blood brain barrier (BBB). This study compares alterations in physiology of the cerebral artery after a short-term oxidative stress induced by cyanide toxicity and vascular occlusion. METHOD Adult Wistar rats (N=30) were divided into three groups; vascular occlusion (VO) (n=12), potassium cyanide administration (CN) (n=12) and Control-CO (n=6). The CN rates were treated with 30mg/kg of orally administered KCN while the VO was subjected to global vascular occlusion, both for a duration of 10 days, described as the treatment phase. Control animals were fed on normal rat chow and water for 10 days. At the end of the treatment phase, n=6 animals in each of the VO, CN and VO groups were anesthetized with sodium pentobarbital (50IP) and the CCA exposed, after which pin electrodes were implanted to record the spikes form the tunica media of the CCA. After day 10, treatment was discontinued for these animals, each remaining in the VO and CN groups (VO-I and CN-I) until day 20 (withdrawal phase) following which the spikes were recorded using the procedure described above. RESULTS/DISCUSSION Vascular occlusion and cyanide toxicity increased vascular resistance in the MCA (reduced lumen thickness ratio) and increased the diameter of the CCA after the treatment phase of 10 days. After 10 days of withdrawal, the VO group showed a reduction in resistance and an increase in the lumen width/wall thickness ratio (LWR) while the CN group showed increased resistance and a reduction in LWR. CONCLUSION Cyanide toxicity increased vascular resistance by inducing degenerative changes in the wall of the artery while vascular occlusion increased resistance through mechanical stress and increased thickness of arterial wall. After the withdrawal phase, vascular resistance diminished in the VO to a significantly greater extent than the CN.

The malleable brain: plasticity of neural circuits and behavior - a review from students to students

One of the most intriguing features of the brain is its ability to be malleable, allowing it to adapt continually to changes in the environment. Specific neuronal activity patterns drive long‐lasting increases or decreases in the strength of synaptic connections, referred to as long‐term potentiation and long‐term depression, respectively. Such phenomena have been described in a variety of model organisms, which are used to study molecular, structural, and functional aspects of synaptic plasticity. This review originated from the first International Society for Neurochemistry (ISN) and Journal of Neurochemistry (JNC) Flagship School held in Alpbach, Austria (Sep 2016), and will use its curriculum and discussions as a framework to review some of the current knowledge in the field of synaptic plasticity. First, we describe the role of plasticity during development and the persistent changes of neural circuitry occurring when sensory input is altered during critical developmental stages. We then outline the signaling cascades resulting in the synthesis of new plasticity‐related proteins, which ultimately enable sustained changes in synaptic strength. Going beyond the traditional understanding of synaptic plasticity conceptualized by long‐term potentiation and long‐term depression, we discuss system‐wide modifications and recently unveiled homeostatic mechanisms, such as synaptic scaling. Finally, we describe the neural circuits and synaptic plasticity mechanisms driving associative memory and motor learning. Evidence summarized in this review provides a current view of synaptic plasticity in its various forms, offers new insights into the underlying mechanisms and behavioral relevance, and provides directions for future research in the field of synaptic plasticity.

Motor and memory function in rat models of cyanide toxicity and vascular occlusion induced ischemic injury

Although oxidative stress is characteristic of global vascular occlusion and cyanide toxicity, the pattern of cerebral metabolism reconditioning and rate of progression or reversal of neural tissue damage differ for both forms of ischemia. Thus, it is important to compare cognitive and motor functions in both models of ischemia involving cyanide treatment (CN) and vascular occlusion (VO). Adult Wistar rats (N=30) were divided into three groups; VO (n=12), CN (n=12) and Control-CO (n=6). The CN was treated with 30mg/Kg of potassium cyanide (KCN); VO was subjected to global vascular occlusion-both for duration of 10 days. The control (CO) was fed on normal rat chow and water for the same duration. At day 10, the test and control groups (CN, VO and CO) were subjected to motor function tests (Table edge tests and Open Field Test) and memory function tests (Y-Maze and Novel object recognition) while the withdrawal groups CN-I and VO-I were subjected to the same set of tests at day 20 (the withdrawal phase). The results show that both cyanide toxicity and vascular occlusion caused a decline in motor and memory function when compared with the control. Also, the cyanide treatment produced a more rapid decline in these behavioral parameters when compared with the vascular occlusion during the treatment phase. After the withdrawal phase, cyanide treatment (CN-I) showed either an improvement or restoration of motor and memory function when compared to the CN and control. Withdrawal of vascular occlusion caused no improvement, and in some cases a decline in motor and memory function. In conclusion, cyanide toxicity caused a decline in motor and memory function after the treatment while vascular occlusion caused no significant decline in cognition and motor function at this time. After the withdrawal phase, the effect of cyanide toxicity was reduced and significant improvements were observed in the behavioral tests (motor and cognitive), while a decline in these functions were seen in the vascular occlusion group after this phase.

Retarded hippocampal development following prenatal exposure to ethanolic leaves extract of Datura metel in wistar rats.

Background: Datura metel contains atropine alkaloids and has been used to treat complication like asthma and, bronchitis, because of its anticholinergic properties. Aim: This study aimed to determine the prenatal effects of ethanolic extract of D. metel leaves exposure on the development of hippocampus. Materials and Methods: Twenty rats (12 females and 8 males) were purchased. The females were grouped into four groups (A_D). Group A were given 500 mg/kg body weight of the extract on the first day of fertilization to the end of gestation period, Group B were given 500 mg/kg body weight on the 8th day of fertilization to the end of gestation period, Group C were given 500 mg/kg body weight on 15th day of fertilization to the end of gestation period and Group D were given normal saline throughout the gestation period. Results: Rats in Group A showed no implantation, rats in Group B had abortion on the 7th day after administration, and rats in Group C gave birth with their litters showing retarded hippocampus development and neural degeneration and rats in Group D (control) showed normal development. Conclusion: Ethanolic extract of D. metel leaf is teratogenic in the late stage of pregnancy, is abortificient and can serve as a contraceptive.

Tetracarpidium conophorum Müll. Arg modulates sexual behaviour and biochemical parameters relevant to sexual function in male Wistar rats

Walnut (Tetracarpidium conophorum Müll. Arg) has been reported to be an essential ingredient in folklore medicine for sexual enhancement with little scientific validation. Hence, this study investigated the effects of walnut supplemented diet on sexual behaviour and biochemical parameters relevant to erection in male Wistar rats. Forty animals used in this study were divided into five groups (n = 8); Group 1 - normal control rats fed with basal diet, Group II - rats fed diet supplemented with 10% processed walnut, Group III - rats fed diet supplemented with 10% raw walnut, Group IV - rats fed diet supplemented with 20% processed walnut and Group V - rats fed diet supplemented with 20% raw walnut. Behavioural studies (copulation tendency and anxiety) associated with sexual function, measurement of nitric oxide (NO) levels, adenosine deaminase (ADA), arginase and acetylcholinesterase (AChE) activities in the Corpus cavernosum as well as characterization of bioactive components of the nut were evaluated. Marked reductions in ADA and arginase activities and a concomitant increase (% inclusion dependent) in the level of NO as well as enhanced sexual behaviours were observed in rat fed supplemented walnut when compared to the control. Furthermore, analysis of the walnut using high performance liquid chromatography indicated the presence of some polyphenols. From our findings, it showed that walnut improves sexual behaviour and modulates activities of key enzymes relevant to erection in male rats which may justify its used in traditional medicine.

Nicotine-Cadmium Interaction Alters Exploratory Motor Function and Increased Anxiety in Adult Male Mice

In this study we evaluated the time dependence in cadmium-nicotine interaction and its effect on motor function, anxiety linked behavioural changes, serum electrolytes, and weight after acute and chronic treatment in adult male mice. Animals were separated randomly into four groups of n = 6 animals each. Treatment was done with nicotine, cadmium, or nicotine-cadmium for 21 days. A fourth group received normal saline for the same duration (control). Average weight was determined at 7-day interval for the acute (D1-D7) and chronic (D7-D21) treatment phases. Similarly, the behavioural tests for exploratory motor function (open field test) and anxiety were evaluated. Serum electrolytes were measured after the chronic phase. Nicotine, cadmium, and nicotine-cadmium treatments caused no significant change in body weight after the acute phase while cadmium-nicotine and cadmium caused a decline in weight after the chronic phase. This suggests the role of cadmium in the weight loss observed in tobacco smoke users. Both nicotine and cadmium raised serum Ca2+ concentration and had no significant effect on K+ ion when compared with the control. In addition, nicotine-cadmium treatment increased bioaccumulation of Cd2+ in the serum which corresponded to a decrease in body weight, motor function, and an increase in anxiety.In this study we evaluated the time dependence in cadmium-nicotine interaction and its effect on motor function, anxiety linked behavioural changes, serum electrolytes, and weight after acute and chronic treatment in adult male mice. Animals were separated randomly into four groups of n = 6 animals each. Treatment was done with nicotine, cadmium, or nicotine-cadmium for 21 days. A fourth group received normal saline for the same duration (control). Average weight was determined at 7-day interval for the acute (D1-D7) and chronic (D7-D21) treatment phases. Similarly, the behavioural tests for exploratory motor function (open field test) and anxiety were evaluated. Serum electrolytes were measured after the chronic phase. Nicotine, cadmium, and nicotine-cadmium treatments caused no significant change in body weight after the acute phase while cadmium-nicotine and cadmium caused a decline in weight after the chronic phase. This suggests the role of cadmium in the weight loss observed in tobacco smoke users. Both nicotine and cadmium raised serum Ca2+ concentration and had no significant effect on K+ ion when compared with the control. In addition, nicotine-cadmium treatment increased bioaccumulation of Cd2+ in the serum which corresponded to a decrease in body weight, motor function, and an increase in anxiety.

Smoke and ethanolic extract of nicotiana tabacum altered hippocampal histology and behaviour in mice

The effects of tobacco use on human health are well known and are documented in scientific reports. When tobacco is smoked or chewed, nicotine is absorbed by the lungs and oral cavity and quickly moved into the bloodstream where it is distributed rapidly through the circulatory system to reach the brain and peripheral nervous system. Male and female adult mice (N=32) were used for this study. The animals were randomly divided in to four (4) groups, A, B, C and D, of eight (n=8) animals each. Group A animals were treated by oral administration of 10.72 mg of the extract, B 10.72 mg of the tobacco smoke exposure for 3 min (in a controlled air chamber), C were given 0.2 ml of normal saline and D were expose to equal weight (0.02 g) of cotton wool for 3 min, for 21 experimental days. The mice were sacrificed 4 h after the last administration and the brains excised, blotted, weighed and fixed in formol calcium for histological analysis, using Haematoxylin and Eosin. There was a significant decrease in the body weight, brain weight and relative brain weight in the treatment groups. The pyramidal and granular cell layers showed changes in cell count scores; significant at p<0.05 when compared with the control. The results suggested that the consumption of Nicotiana tabacum leaves; either smoking or chewing may lead to alterations in cell count, brain weight and neurobehavioral patterns. Weight loss was also observed in the treatment and was found to be dependent on the route of administration. Key words: Nicotine tobacco, hippocampus, memory, cell death.

Cadmium increases the sensitivity of adolescent female mice to nicotine-related behavioral deficits.

This study investigates spatial and nonspatial working memory, anxiety related behavior, and motor activities in cadmium and/or nicotine exposed female adolescent mice. P28 female adolescent mice (albino strain) were divided into four groups of five (n = 5) mice each. A set of mice (Nic) received subcutaneous nicotine (2.0 mg/kg) while a separate set (Cd) was treated with 2.0 mg/kg cadmium (subcutaneous). For the combined treatments of cadmium and nicotine, we administered 2.0 mg/kg Nicotine and 2.0 mg/kg of Cd. Subsequently, a separate group of animals (n = 5; control) received normal saline. The total duration of treatment for all groups was 28 days (P28–P56). At P56, the treatment was discontinued, after which the animals were examined in behavioural tests. Nicotine and cadmium increased the metabolism and food intake in the female adolescent mice. This also corresponded to an increase in weight when compared with the control. However, a combined nicotine-cadmium treatment induced a decline in weight of the animals versus the control. Also, nicotine administration increased the motor function, while cadmium and nicotine-cadmium treatment caused a decline in motor activity. Both nicotine and cadmium induced a reduction in memory index; however, nicotine-cadmium treatment induced the most significant decrease in nonspatial working memory.