Stephen Temitayo Bello

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Objective: Several studies have attributed epileptic activities in temporal lobe epilepsy (TLE) to the hippocampus; however, the participation of nonhippocampal neuronal networks in the development of TLE is often neglected. Here, we sought to understand how these nonhippocampal networks are involved in the pathology that is associated with TLE disease.Methods: A kainic acid (KA) model of temporal lobe epilepsy was induced by injecting KA into dorsal hippocampus of C57BL/6J mice. Network activation after spontaneous seizure was assessed using c‐Fos expression. Protocols to induce seizure using visual or auditory stimulation were developed, and seizure onset zone (SOZ) and frequency of epileptic spikes were evaluated using electrophysiology. The hippocampus was removed to assess seizure recurrence in the absence of hippocampus.Results: Our results showed that cortical and hippocampal epileptic networks are activated during spontaneous seizures. Perturbation of these networks using visual or auditory stimulation readily precipitates seizures in TLE mice; the frequency of the light‐induced or noise‐induced seizures depends on the induction modality adopted during the induction period. Localization of SOZ revealed the existence of cortical and hippocampal SOZ in light‐induced and noise‐induced seizures, and the development of local and remote epileptic spikes in TLE occurs during the early stage of the disease. Importantly, we further discovered that removal of the hippocampi does not stop seizure activities in TLE mice, revealing that seizures in TLE mice can occur independent of the hippocampus.Significance: This study has shown that the network pathology that evolves in TLE is not localized to the hippocampus; rather, remote brain areas are also recruited. The occurrence of light‐induced or noise‐induced seizures and epileptic discharges in epileptic mice is a consequence of the activation of nonhippocampal brain areas. This work therefore demonstrates the fundamental role of nonhippocampal epileptic networks in generating epileptic activities with or without the hippocampus in TLE disease.

Understanding neuronal firing patterns and long-term potentiation (LTP) induction in studying learning, memory, and neurological diseases is critical. However, recently, despite the rapid advancement in neuroscience, we are still constrained by the experimental design, detection tools for exploring the mechanisms and pathways involved in LTP induction, and detection ability of neuronal action potentiation signals. This review will reiterate LTP-related electrophysiological recordings in the mammalian brain for nearly 50 years and explain how excitatory and inhibitory neural LTP results have been detected and described by field- and single-cell potentials, respectively. Furthermore, we focus on describing the classic model of LTP of inhibition and discuss the inhibitory neuron activity when excitatory neurons are activated to induce LTP. Finally, we propose recording excitatory and inhibitory neurons under the same experimental conditions by combining various electrophysiological technologies and novel design suggestions for future research. We discussed different types of synaptic plasticity, and the potential of astrocytes to induce LTP also deserves to be explored in the future.

Environmental pollution with vanadium may pose neurotoxicity threats to known unique neural attributes (cognition and olfaction) of the African giant rat (AGR). This rodent lives within the same ecological zones as the human populace. Thus, experimental investigations on the effect of vanadium on this rodent may mirror latent epidemiological scenarios in the human populace. This work was designed to evaluate the neurotoxic effect of vanadium on the hippocampal neuronal infrastructure and circuitry and provide cellular correlates to its significant pathologies in the AGR. Twelve adult male AGRs were assigned into two groups (n = 6/group; vanadium and control). They were dosed daily with 3 mg/kg body sodium metavanadate and sterile water for 14 days, respectively, and harvested brains were processed for histology. Using Nissl and Golgi staining techniques with stereological analysis, we demonstrated the effect of vanadium on AGR neuronal architecture of the hippocampal trisynaptic loop as a probable cellular mechanism of vanadium-induced memory deficits. Specifically, the most significant pathologies were seen in the dentate gyrus and CA3, with significantly decreased neuronal density disrupted cytoarchitecture and loss of dendritic arborisations and axonal extensions. At the same time, hippocampal subfields CA2 and CA4 showed region-specific resistance to vanadium-induced neurotoxicity. Furthermore, the selective vulnerability to vanadium-induced neurotoxicity is adduced. This work has demonstrated the neurotoxic effect of vanadium on the hippocampal subfields and circuitry in the AGR and highlighted its probable impact on their translational purposes. This rodent may be a suitable model for evaluating memory pathologies in neurotoxicological studies

Environmental pollution with vanadium may pose neurotoxicity threats to known unique neural attributes (cognition and olfaction) of the African giant rat (AGR). This rodent lives within the same ecological zones with the human populace thus, experimental investigations on the effect of vanadium on this rodent may mirror latent epidemiological scenario on the human populace. This work was designed to evaluate the neurotoxic effect of vanadium on the hippocampal neuronal infrastructure and circuitry, and provide cellular correlates to its notable pathologies in the AGR. Adult male AGRs were dosed daily with 3mg/kg body sodium metavanadate for 14days and harvested brains were processed for histology Using Nissl and Golgi staining techniques with stereological analysis. we demonstrated the effect of vanadium on AGR neuronal architecture of the hippocampal trisynaptic loop as a probable cellular mechanism of vanadium-induced memory deficits. Specifically, the most notable pathologies were seen in the dentate gyrus and CA3 with significant decrease in neuronal density, disruption of the cytoarchitecture, and loss of dendritic arborizations and axonal extensions. while hippocampal subfields CA2 and CA4 show region-specific resistance to the vanadium-induced neurotoxicity. The selective vulnerability to the vanadium-induced neurotoxicity is adduced. Given the unique neural attributes of the AGR and their translational benefits, as sniff rats it then becomes expedient to note the impact of environmental pollution (in this case vanadium) on their performance index. It is also proposed that this indigenous rodent may be a suitable model for evaluating memory pathologies in ecological studies of neurotoxicities.

Ependymal cells line the interface between the ventricular surfaces and the brain parenchyma. These cells, in addition to the choroid plexus, form the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) and serve important functions in the protection and regulation of brain metabolism. The African giant rat (AGR) has been used as sentinels to detect potential neuropathology arising from ecotoxicological pollutions. This study examined the lateral ventricular lining by using histology, immunohistochemistry and electron microscopy. Marked variations were observed in some regions of the ventricles which showed multi-layering of ependymal cells that differed from the typical single layered ependymal cells at the apical surface, while subependymal structures revealed indistinctive neuropil and glia following histological examinations. The ependymal cells which form the epithelial lining of the ventricles were comprised of cuboidal or low columnar cells, with the plasmalemma of abutting cells forming intercellular bridge appearing links by: tight junctions ( zonula occludens ), intermediate junctions ( zonula adherens ), desmosomes ( macula adherens ) and infrequent gap junctions. The choroid plexus revealed cells of Kolmer with several cilia and microvilli. The possible functional components of the ependyma and choroid plexus morphology of the AGR are discussed and thus provide a baseline for further research on the AGR brain.

Processing rodent brain tissues: review of basic anatomical techniques for scientists with minimal knowledge of neuroanatomy