Author/Authors :
Hu, Yue Chongqing University of Medical Sciences - Children’s Hospital, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders - Department of Neurology, Key Laboratory of Child Development and Disorders, China , Jiang, Li Chongqing University of Medical Sciences - Children’s Hospital, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders - Department of Neurology, Key Laboratory of Child Development and Disorders, China , Chen, Hengsheng Chongqing University of Medical Sciences - Children’s Hospital, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders - Key Laboratory of Child Development and Disorders, China
Abstract :
Infants and children are at a higher risk for seizures compared with adults. Increasing experimental animal data strongly suggest young animals are less vulnerable than mature animals to cell loss in the hippocampus with more neurogenesis after status convulsion (SC). Earlylife seizures cause permanent functional alterations in neuronal networks and render the brain susceptible to later epilepsy and cognitive deficits. Such seizures may intervene with developmental programs, and lead to inadequate construction of cortical networks rather than induction of neuronal cell loss. The developing brain has a greater capacity in long-term synaptic plasticity than the adult brain, but the molecular mechanism is not well understood. Long-term synaptic plasticity involves both functional and morphological changes of synapses. In the CNS, postsynaptic silent synapses have been identified as showing only N-Methyl-D-aspartate (NMDA), but not alpha-amino-3-hydroxy-5-methyl- 4-isoxazole-propionic acid (AMPA) receptors, and activation of these postsynaptically silent synapses has been demonstrated to contribute significantly to longterm synaptic plasticity. Presynaptic silent synapses have also been reported, which are possibly caused by a very low probability of synaptic vesicle release or the small quanta. The influence of SC on activation of presynaptic silent synapses and their contribution to long-term synaptic plasticity is widely unknown. The current study aims to observe the dynamic changes and age-related differences of vesicle pool organization at hippocampal synapses by monitoring vesicle recycling, and to explore the influences of SC on hippocampal synaptic transmission in immature and adult rats through a presynaptic mechanism.
