title: Decreased Na(+) influx lowers hippocampal neuronal excitability in a mouse model of neonatal influenza infection.
abstract: Influenza virus infection is one of common infectious diseases occurring worldwide. The human influenza virus can infect the central nervous system and cause brain dysfunctions affecting cognition and spatial memory. It has been previously shown that infection with the influenza viral protein within the hippocampus decreases Ca(2+) influx and reduces excitatory postsynaptic currents. However, the neuronal properties of animals surviving neonatal infection have not been investigated. Using a mouse model of neonatal influenza infection, we performed thorough electrophysiological analyses of hippocampal neurotransmission. We found that animals surviving the infection exhibited reduced spontaneous transmission with no significant defects in evoked neurotransmission. Interestingly, the hippocampus of the infected group conducted synaptic transmission with less fidelity upon repeated stimulations and failed to generate action potentials faithfully upon step current injections primarily due to reduced Na(+) influx. The reversal potential for the Na(+) current was hyperpolarized and the activation of Na(+) channels was slower in the infected group while the inactivation process was minimally disturbed. Taken together, our observations suggest that neonatally infected offsprings exhibit noticeable deficits at rest and severe failures when higher activity is required. This study provides insight into understanding the cellular mechanisms of influenza infection-associated functional changes in the brain.
authors: Department of Biological Sciences, College of Bioscience and Biotechnology, Konkuk University, Seoul, 143-701, South Korea.
authors: Hoyong
authors: H
authors: Park
authors: Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, 143-701, South Korea.
authors: Ji Eun
authors: JE
authors: Yu
authors: Department of Biological Sciences, College of Bioscience and Biotechnology, Konkuk University, Seoul, 143-701, South Korea.
authors: Sungmin
authors: S
authors: Kim
authors: Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, 143-701, South Korea.
authors: Sang-Soep
authors: SS
authors: Nahm
authors: Department of Biological Sciences, College of Bioscience and Biotechnology, Konkuk University, Seoul, 143-701, South Korea.
authors: ChiHye
authors: C
authors: Chung
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology*; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels / Q000378:metabolism; D015640:Ion Channel Gating; D007700:Kinetics; D008297:Male; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000378:metabolism*; D009976:Orthomyxoviridae Infections / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism*; D009435:Synaptic Transmission
chemical_list: D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D012964:Sodium