Dr Mohammad Reza Balali, Dr Mohaddeseh Hosseini, Dr Maryam Khanboloki, Dr Mohammad Mohammadi, Dr Amir Mohammad Khorshidvand, Dr Mohammad Taghi Joghataei,
Volume 0, Issue 0 (3-2018)
Abstract
Objective: Despite injury to area V1 resulting in visual impairment, some patients maintain visual capabilities in an unconscious manner, a phenomenon called blindsight. This systematic review critically evaluates the role of neural pathways that facilitate blindsight.
Methods: The review comprehensively assesses research from online databases. Following the screening process, we employed the JBI critical appraisal checklist and the SYRCLE tool for the assessment of risks in human and animal studies. Two authors conducted separate evaluations of each study. Every disagreement was effectively settled by mutual agreement. We selected 25 articles focusing on the mediating pathways of blindsight.
Results: In humans, the pathways from the Lateral Geniculate Nucleus (LGN) to V5, from the Superior Colliculus (SC) to higher brain areas, and to the remaining segments of V1 are crucial. The pathway that connects the SC, pulvinar, and amygdala is essential for processing emotional visual information. Studies conducted on animals emphasize how important the SC-Pulvinar pathway and the connections between the LGN and extrastriate areas are for developing blindsight.
Conclusion: Individual differences in neuroplasticity, the precise site and timing of the damage, and the amount of time that has passed since the injury all play a major role in the activation of pathways that enable blindsight. This demonstrates a complicated system that successfully lessens the loss of the primary visual cortex, highlighting the necessity of developing rehabilitation plans that are specific to each individual with visual impairments.
Grace Akingbade, Omamuyovwi Ijomone, Sunday Adelakun, Bernard Enaibe,
Volume 12, Issue 6 (11-2021)
Abstract
Introduction: Prenatal exposure to Marijuana (MJN) has been associated with various brain deficits. The main activity in marijuana, Δ9-Tetrahydrocannabinol (THC), crosses the placenta and affects fetal brain development. Despite this, marijuana remains a commonly abused substance among pregnant women. The current study examined the histological and biochemical changes in the Superior Colliculus (SC) and Lateral Geniculate Nucleus (LGN) in rat brains prenatally exposed to marijuana.
Methods: Four groups of pregnant rats (n=5 rats/group) were exposed to the smoke of 10 g/kg marijuana at various days during their gestational period, with a group (control), i.e., not exposed. After parturition, the litters from each group were sacrificed by cervical dislocation on postnatal days 7, 14, and 21; the superior colliculi and lateral geniculate nuclei were excised. Tissue sections were prepared for histological studies using Haematoxylin and Eosin stains. Biochemical studies were performed on alkaline phosphatase, acid phosphatase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase activity levels. The histological and biochemical analyses of tissues were performed.
Results: Prenatal exposure to marijuana resulted in spontaneous abortion and affected neuronal morphology in the SC and LGN of the progeny. Furthermore, the levels of enzyme activities were altered following maternal exposure to MJN.
Conclusion: These data suggested that histological changes in the SC and LGN were associated with oxidative damage.
