Network synchronization across the longitudinal axis of the developing rat hippocampus

Abstract

Epilepsy is a neurological disorder characterized by recurrent seizures. Researching epilepsy requires animal models, as the brain manipulation required to understand epileptogenic activity is not possible in humans. Extracellular recordings measure network level activation in slice models of epilepsy. A magnesium-free solution is often used in slice physiology to increase excitation, through enhanced glutamate receptor activity. Magnesium blocks the activation of glutamate receptors via binding near the pore region. Magnesium also lowers calcium’s ability to initiate presynaptic neurotransmitter release. We aim to elucidate the mechanisms of a dorsal neuro-protective system, which reduces the excitability of dorsal hippocampal tissue with age. While the mechanisms underlying the magnesium-free model are well established, the effects of this model across the longitudinal axis of the hippocampus and throughout development have not been clearly characterized. We studied the effects of the magnesium-free model through extracellular field recordings of CA1 pyramidal neurons from dorsal and ventral hippocampal slices throughout development, and found young, dorsal hippocampal tissue to be the most excitable. Additionally, our data suggests the effect of no magnesium is minimal in ventral slices. These data support the theory of the dorsal protection system being critical in the reduction of excitability seen with age.