Faculty Opinions recommendation of Dendritic sodium spikes are required for long-term potentiation at distal synapses on hippocampal pyramidal neurons.

2016 ◽  
Author(s):  
Johannes Hell
Keyword(s):  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Hippocampal Pyramidal Neurons ◽  
Term Potentiation

scholarly journals Excitatory synapses are stronger in the hippocampus of Rett syndrome mice due to altered synaptic trafficking of AMPA-type glutamate receptors

2016 ◽  
Vol 113 (11) ◽  
pp. E1575-E1584 ◽  
Author(s):  
Wei Li ◽  
Xin Xu ◽  
Lucas Pozzo-Miller
Keyword(s):  
Rett Syndrome ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Afferent Stimulation ◽  
Altered Expression ◽  
Hippocampal Pyramidal Neurons ◽  
Term Potentiation ◽  
Theta Burst

Deficits in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cognitive impairments in neurodevelopmental disorders associated with intellectual disability and autism. Using the methyl-CpG-binding protein 2 (Mecp2) knockout (KO) mouse model of Rett syndrome, we show that naïve excitatory synapses onto hippocampal pyramidal neurons of symptomatic mice have all of the hallmarks of potentiated synapses. Stronger Mecp2 KO synapses failed to undergo LTP after either theta-burst afferent stimulation or pairing afferent stimulation with postsynaptic depolarization. On the other hand, basal synaptic strength and LTP were not affected in slices from younger presymptomatic Mecp2 KO mice. Furthermore, spine synapses in pyramidal neurons from symptomatic Mecp2 KO are larger and do not grow in size or incorporate GluA1 subunits after electrical or chemical LTP. Our data suggest that LTP is occluded in Mecp2 KO mice by already potentiated synapses. The higher surface levels of GluA1-containing receptors are consistent with altered expression levels of proteins involved in AMPA receptor trafficking, suggesting previously unidentified targets for therapeutic intervention for Rett syndrome and other MECP2-related disorders.

scholarly journals Dendritic sodium spikes are required for long-term potentiation at distal synapses on hippocampal pyramidal neurons

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Yujin Kim ◽  
Ching-Lung Hsu ◽  
Mark S Cembrowski ◽  
Brett D Mensh ◽  
Nelson Spruston
Keyword(s):  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Long Term Effects ◽  
Hippocampal Pyramidal Neurons ◽  
Term Potentiation ◽  
Nav Channels ◽  
Processing And Storage ◽  
And Storage ◽  
Apical Dendrites

Dendritic integration of synaptic inputs mediates rapid neural computation as well as longer-lasting plasticity. Several channel types can mediate dendritically initiated spikes (dSpikes), which may impact information processing and storage across multiple timescales; however, the roles of different channels in the rapid vs long-term effects of dSpikes are unknown. We show here that dSpikes mediated by Nav channels (blocked by a low concentration of TTX) are required for long-term potentiation (LTP) in the distal apical dendrites of hippocampal pyramidal neurons. Furthermore, imaging, simulations, and buffering experiments all support a model whereby fast Nav channel-mediated dSpikes (Na-dSpikes) contribute to LTP induction by promoting large, transient, localized increases in intracellular calcium concentration near the calcium-conducting pores of NMDAR and L-type Cav channels. Thus, in addition to contributing to rapid neural processing, Na-dSpikes are likely to contribute to memory formation via their role in long-lasting synaptic plasticity.

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