scholarly journals Impaired Short-Term Plasticity in Mossy Fiber Synapses Caused by Mitochondrial Dysfunction of Dentate Granule Cells Is the Earliest Synaptic Deficit in a Mouse Model of Alzheimer's Disease

2012 ◽  
Vol 32 (17) ◽  
pp. 5953-5963 ◽  
Author(s):  
S. H. Lee ◽  
K.-R. Kim ◽  
S.-Y. Ryu ◽  
S. Son ◽  
H. S. Hong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Mitochondrial Dysfunction ◽  
Granule Cells ◽  
Mossy Fiber ◽  
Short Term ◽  
Short Term Plasticity ◽  
Dentate Granule Cells ◽  
Model Of Alzheimer’S Disease

Impairment of PGC-1α-mediated mitochondrial biogenesis precedes mitochondrial dysfunction and Alzheimer's pathology in the 3xTg mouse model of Alzheimer's disease

2020 ◽  
Vol 133 ◽  
pp. 110882 ◽  
Author(s):  
Monique Patricio Singulani ◽  
Carolina Parga Martins Pereira ◽  
Ana Flávia Fernandes Ferreira ◽  
Priscila Crespo Garcia ◽  
Gustavo Duarte Ferrari ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Biogenesis ◽  
Model Of Alzheimer’S Disease ◽  
Alzheimer’S Pathology

scholarly journals Synaptosomal Mitochondrial Dysfunction in 5xFAD Mouse Model of Alzheimer's Disease

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150441 ◽  
Author(s):  
Lu Wang ◽  
Lan Guo ◽  
Lin Lu ◽  
Huili Sun ◽  
Muming Shao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Mitochondrial Dysfunction ◽  
Model Of Alzheimer’S Disease ◽  
5Xfad Mouse

scholarly journals Retrograde suppression of post-tetanic potentiation at the mossy fiber-CA3 pyramidal cell synapse

2020 ◽  
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo
Keyword(s):  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Mossy Fiber ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Short Term ◽  
Short Term Plasticity ◽  
Dentate Granule Cells ◽  
Post Tetanic Potentiation ◽  
Frequency Facilitation

ABSTRACTIn the hippocampus, the excitatory synapse between dentate granule cell axons – or mossy fibers (MF) – and CA3 pyramidal cells (MF-CA3) expresses robust forms of short-term plasticity, such as frequency facilitation and post-tetanic potentiation (PTP). These forms of plasticity are due to increases in neurotransmitter release, and can be engaged when dentate granule cells fire in bursts (e.g. during exploratory behaviors) and bring CA3 pyramidal neurons above threshold. While frequency facilitation at this synapse is limited by endogenous activation of presynaptic metabotropic glutamate receptors, whether MF-PTP can be regulated in an activity-dependent manner is unknown. Here, using physiologically relevant patterns of mossy fiber stimulation in acute mouse hippocampal slices, we found that disrupting postsynaptic Ca2+ dynamics increases MF-PTP, strongly suggesting a form of Ca2+-dependent retrograde suppression of this form of plasticity. PTP suppression requires a few seconds of MF bursting activity and Ca2+ release from internal stores. Our findings raise the possibility that the powerful MF-CA3 synapse can negatively regulate its own strength not only during PTP-inducing activity typical of normal exploratory behaviors, but also during epileptic activity.SIGNIFICANCE STATEMENTThe powerful mossy fiber-CA3 synapse exhibits strong forms of plasticity that are engaged during location-specific exploration, when dentate granule cells fire in bursts. While this synapse is well-known for its presynaptically-expressed LTP and LTD, much less is known about the robust changes that occur on a shorter time scale. How such short-term plasticity is regulated, in particular, remains poorly understood. Unexpectedly, an in vivo-like pattern of presynaptic activity induced robust post-tetanic potentiation (PTP) only when the postsynaptic cell was loaded with a high concentration of Ca2+ buffer, indicating a form of Ca2+–dependent retrograde suppression of PTP. Such suppression may have profound implications for how environmental cues are encoded into neural assemblies, and for limiting network hyperexcitability during seizures.

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