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Articles by A.J. Ajibade
Total Records ( 3 ) for A.J. Ajibade
  A.J. Ajibade , P.B. Fakunle and P.D. Shallie
  Several neurological disorders following abuse of artesunate used in chloroquine resistant malarial cases have been reported but little attention has been given the effects of this drug on histology of cerebellar cortex and Nissl substances. Twenty-four adult wistar rats of both sexes weighing between 150 and 230 g were randomly separated into four groups, N = 6. Rats in group D (control), received distilled water throughout exposure period while groups A, B and C (experimental groups) received 4 mg kg-1 b.wt. of artesunate orally on treatment day 1. Group A continued with (4 mg kg-1 b.wt.) for the next 3 days while group B and C received 2 mg kg-1 b.wt. of artesunate orally for the next 6 and 13 days, respectively. Groups A, B and C rats were sacrificed respectively on 5th, 8th and 15th day of treatment while Group D rats were sacrificed on the 15th day. Cerebellum of each rat was carefully dissected out and fixed in 10% formal saline for routine histological techniques. Histological findings showed normal cortical layers in control rats compared with degenerated and loss of purkinje cells, cellular hypertrophy with intercellular vacuolation appearing in the stroma of cerebellar cortex of treated rats. Nissl substances in cerebellar cortex of treated rats stained less intensely and appeared degenerated compared to more intensely stained and distinctly distributed Nissl substances in control rats. The observed vacuolation and neuronal loss in the cortical layers of the treated rats may adversely affect cerebellar functions while less intensely stained and degenerative changes in the Nissl substances in the cerebellar cortex of the treated rats may adversely affect protein synthesis in relation to neuronal functions.
  P.B. Fakunle , A.J. Ajibade , E.B. Oyewo , O.A. Alamu and A.K. Daramola
  Hippocampal formation is involved in learning and memory and has also been reported to be sensitive to neurotoxic insults. However, little has been reported on the chronic simultaneous intake of ethanol and acetaminophen despite their degrees of abuse and misuse as regards hippocampus. In this study, forty adult wistar rats of average weight 150±20.2 g were randomly distributed into four groups of treatments T1, T2, T3 and control C (N = 10). For a period of six weeks, animals in group T1 received 100 mg kg-1 b.wt. acetaminophen and 25% ethanol in 2% sucrose solution while group T2 animals received 25% ethanol in 2% sucrose solution. T3 animals were given 100 mg kg-1 b.wt. acetaminophen and group C animals were given only distilled water. The animals were sacrificed by whole body intracardiac perfusion fixation and the regions of hippocampus were dissected out using Paxinos stereotaxic coordinate method. Brain specimens were processed for routine histological techniques, sectioned at 6 μ and stained for nissl’s substance. Significantly reduced neuronal density (p>0.05) of 44 and 38% neuronal loss in CA3 subfield, respectively in treatment groups T1 and T2 compared to control group was recorded. Also, marked degeneration of pyramidal neurons in the regions of CA1 and CA3 of treatment groups that received 100 mg kg-1 b.wt. acetaminophen and 25% ethanol in 2% sucrose solution as well as animals that received 25% ethanol in 2% sucrose solution, respectively with mild degenerative effects in the group that took 100 mg kg-1 b.wt. acetaminophen compared to the control group was also observed. These alterations observed following exposure to chronic simultaneous administration of ethanol and acetaminophen point to possibilities of higher memory impairments and learning deficits which are of very strong public health concern.
  P.B. Fakunle , A.J. Ajibade , L.O. Ehigie , O.A. Alamu and E.A. Ashamu
  Alcohol abuse and misuse has been widely reported to impair vision with majority of information available implicating the retina but with very scanty literature laying emphasis on the visual relay centers. Hence, some effects of chronic administration of ethanol was studied on the neuronal cells population in the visual relay centers Lateral Geniculate Body (LGB) and Superior Colliculus (SC) of 40 adult Wistar rats of both sexes grouped into treatments T1 and T2 and controls C1 and C2. The treatment groups received 25% ethanol in 2% sucrose (ad libitum) for 6 weeks except T2 animals that were made to undergo an additional 2 weeks of ethanol withdrawal period while the control groups C1 and C2 received tap water and 2% sucrose solution, respectively for 6 weeks. At the end of administration, the animals were sacrificed and process for routine histological techniques and stained for nissl substances. Body weight loss was significantly (p<0.05) observed as well as significantly (p<0.05) reduced neuronal cells population of 47 and 40% for LGB and 42 and 38% for SC neuronal loss, respectively in treatment groups T1 and T2 compared to control group. Hence, these alterations may again underline visual imbalance associated with the malfunctioning of the visual relay center most especially in the maintenance of saccade and recoding of visual signals which are postretinal related functions.
 
 
 
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