Complexity of contacts between synaptic boutons and dendritic spines in adult rat hippocampus: Three-dimensional reconstructions from serial ultrathin sections in vivo

Synapse ◽  
2009 ◽  
Vol 63 (5) ◽  
pp. 369-377 ◽  
Author(s):  
Victor I. Popov ◽  
Michael G. Stewart
Keyword(s):  
Dendritic Spines ◽  
Three Dimensional ◽  
Rat Hippocampus ◽  
Adult Rat ◽  
Ultrathin Sections ◽  
Synaptic Boutons ◽  
Serial Ultrathin Sections

scholarly journals The in vivo Three-dimensional Form of a Plant Mycoplasma-like Organism by the Analysis of Serial Ultrathin Sections

Microbiology ◽  
1980 ◽  
Vol 116 (1) ◽  
pp. 111-131
Author(s):  
H. Waters ◽  
P. Hunt
Keyword(s):  
Three Dimensional ◽  
Ultrathin Sections ◽  
Serial Ultrathin Sections

Bidirectional redistribution of AMPA but not NMDA receptors after perforant path simulation in the adult rat hippocampus in vivo

Hippocampus ◽  
2006 ◽  
Vol 16 (11) ◽  
pp. 990-1003 ◽  
Author(s):  
D.E. Moga ◽  
M.L. Shapiro ◽  
J.H. Morrison
Keyword(s):  
Nmda Receptors ◽  
Rat Hippocampus ◽  
Perforant Path ◽  
Adult Rat

Localization of EphA4 in axon terminals and dendritic spines of adult rat hippocampus

2007 ◽  
Vol 501 (5) ◽  
pp. 691-702 ◽  
Author(s):  
Marie-ève Tremblay ◽  
Mustapha Riad ◽  
David Bouvier ◽  
Keith K. Murai ◽  
Elena B. Pasquale ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Rat Hippocampus ◽  
Axon Terminals ◽  
Adult Rat

scholarly journals Neuronal hibernation following hippocampal demyelination

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Selva Baltan ◽  
Safdar S. Jawaid ◽  
Anthony M. Chomyk ◽  
Grahame J. Kidd ◽  
Jacqueline Chen ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Three Dimensional ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Mammalian Brain ◽  
Gene Transcript ◽  
Ca1 Neurons

AbstractCognitive dysfunction occurs in greater than 50% of individuals with multiple sclerosis (MS). Hippocampal demyelination is a prominent feature of postmortem MS brains and hippocampal atrophy correlates with cognitive decline in MS patients. Cellular and molecular mechanisms responsible for neuronal dysfunction in demyelinated hippocampi are not fully understood. Here we investigate a mouse model of hippocampal demyelination where twelve weeks of treatment with the oligodendrocyte toxin, cuprizone, demyelinates over 90% of the hippocampus and causes decreased memory/learning. Long-term potentiation (LTP) of hippocampal CA1 pyramidal neurons is considered to be a major cellular readout of learning and memory in the mammalian brain. In acute slices, we establish that hippocampal demyelination abolishes LTP and excitatory post-synaptic potentials of CA1 neurons, while pre-synaptic function of Schaeffer collateral fibers is preserved. Demyelination also reduced Ca2+-mediated firing of hippocampal neurons in vivo. Using three-dimensional electron microscopy, we investigated the number, shape (mushroom, stubby, thin), and post-synaptic densities (PSDs) of dendritic spines that facilitate LTP. Hippocampal demyelination did not alter the number of dendritic spines. Surprisingly, dendritic spines appeared to be more mature in demyelinated hippocampi, with a significant increase in mushroom-shaped spines, more perforated PSDs, and more astrocyte participation in the tripartite synapse. RNA sequencing experiments identified 400 altered transcripts in demyelinated hippocampi. Gene transcripts that regulate myelination, synaptic signaling, astrocyte function, and innate immunity were altered in demyelinated hippocampi. Hippocampal remyelination rescued synaptic transmission, LTP, and the majority of gene transcript changes. We establish that CA1 neurons projecting demyelinated axons silence their dendritic spines and hibernate in a state that may protect the demyelinated axon and facilitates functional recovery following remyelination.

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