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.

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.

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Epilepsy is a life-threatening brain disorder that affects about 1-2 % of the world's population. Various mechanisms facilitating epilepsy development and seizure propagation have been identified. Nevertheless, an improved understanding of the cellular mechanisms that underlie epilepsy development is necessary for designing better therapeutic strategies for epilepsy treatment. Cellular senescence, a cellular mechanism wherein cell growth is permanently halted and causes cells to exit the proliferative pool, has been associated with neurological disorders such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and epilepsy. How the various mechanisms that drive a cell towards senescence and the phenotypes that characterize senescent cells are associated with the development and progression of epilepsy might be necessary in improving our understanding of epilepsy. Therefore, this review discusses the mechanisms and pathways associated with cellular senescence and how senescence-associated secretory phenotype (SASP) promotes inflammation and tissue dysfunction. We then explained how different types of cells, including brain cells, become senescent, the inter-relationship between cellular senescence and epilepsy, and potential biomarkers common to epilepsy and cellular senescence. Finally, we reviewed the use of senolytics and senomorphics for epilepsy treatment. Further research can, therefore, be directed towards a thorough understanding of cellular senescence in epilepsy development, and this can open new frontiers for epilepsy treatment.