292. THE ROLE OF ANT IN MODULATING HIPPOCAMPAL OSCILLATIONS IN ANIMAL MODELS OF EPILEPSY

Abstract Background Epilepsy is a complex neurological disorder characterized by recurrent seizures, which are caused by abnormal neural synchrony in the brain. The anterior nucleus of the thalamus (ANT) and the hippocampus are two critical brain structures involved in the pathophysiology of epilepsy. The ANT plays a significant role in modulating seizure activity, and its GABAergic interneurons are possibly involved in generating low-frequency delta oscillations. Aims & Objectives This study aims to investigate whether the ANT influences the severity of seizures by modulating the neural oscillations in hippocampus and to elucidate the underlying neurophysiological mechanisms. The hypothesis posits that delta oscillations in the ANT, enhanced by GABAergic interneurons, influence local field potentials (LFPs) in the hippocampus through thalamo-hippocampal circuits. Method The experimental design involved inducing seizures in rats via kainic acid (KA) injection into the CA3 region of the hippocampus. Local field potentials (LFPs) were recorded from the CA1 region to assess neural excitability. Analyzing changes in LFPs during seizures between the ANT and hippocampus; validating the neural circuitry connecting these two regions and identifying specific cell types within the ANT that affect hippocampal oscillations. Expected outcomes of this research will reveal the neuronal populations in the ANT responsible for generating delta oscillations and provide insights into the dynamics and neural circuits between the ANT and hippocampus. Results KA injection significantly increased the number of epileptiform spikes in the CA1 region compared to saline controls, indicating heightened neural excitability. Following tDCS treatment, a notable reduction in spike numbers was observed in comparison to the sham group. Applying tDCS to the dorsal hippocampus enhances LFPs delta power of the CA1 and ANT, and trends towards increased delta coherence between ANT and CA1. This result suggests that delta oscillations at CA1 and ANT were enhanced as well as the coherence between both areas by weak current stimulations. This finding supports our hypothesis that tDCS can enhance hippocampal delta power and facilitate low-frequency oscillations through neural circuits, thereby promoting low-frequency synchrony between ANT and CA1. Discussion & Conclusions By understanding how thalamic activity influences hippocampal excitability through delta oscillation, this study will contribute significantly to our knowledge of epilepsy's mechanisms and potentially facilitate the development of novel therapeutic strategies.