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Related Concept Videos

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
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Adaptive Mossy Cell Circuit Plasticity after Status Epilepticus.

Corwin R Butler1, Gary L Westbrook2, Eric Schnell3,4

  • 1Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, Oregon 97239.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|February 19, 2022
PubMed
Summary

Surviving mossy cells in epilepsy reorganize to increase inhibition in the hippocampus. This adaptive plasticity in parvalbumin-positive interneurons may offer therapeutic targets for epilepsy treatment.

Keywords:
epilepsymossy cellsoptogeneticsplasticity

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Area of Science:

  • Neuroscience
  • Epilepsy Research
  • Hippocampal Circuitry

Background:

  • Hilar mossy cells are crucial for hippocampal network function, mediating both excitation and inhibition of dentate granule cells (DGCs).
  • Epilepsy is characterized by significant mossy cell loss and altered hippocampal circuit function, contributing to hyperexcitability.

Purpose of the Study:

  • To investigate the functional contribution of surviving mossy cells to network activity in the reorganized dentate gyrus following pilocarpine-induced status epilepticus (SE).
  • To elucidate adaptive plasticity in mossy cell outputs and their impact on the excitation/inhibition balance in the epileptic hippocampus.

Main Methods:

  • Utilized optogenetics to stimulate mossy cells in acute hippocampal slices from control and pilocarpine-treated mice.
  • Examined monosynaptic excitatory and di-synaptic inhibitory currents in DGCs and excitation of parvalbumin-positive (PV+) basket cells.
  • Employed transgenic mice, translational mouse modeling, and viral vectors for selective functional circuit analysis.

Main Results:

  • Mossy cell density and their excitatory drive onto DGCs were reduced post-SE.
  • Mossy cell-driven excitation of PV+ basket cells, key mediators of feedforward inhibition, was preserved.
  • The overall effect of surviving mossy cells shifted towards increased net inhibition of DGCs due to maintained feedforward inhibition.

Conclusions:

  • Mossy cell outputs undergo adaptive reorganization following seizures, enhancing their inhibitory influence on the hippocampal network.
  • The preserved mossy cell-driven excitation of PV+ interneurons suggests a homeostatic mechanism to counteract hyperexcitability.
  • These findings highlight potential therapeutic strategies targeting the reorganized mossy cell-interneuron microcircuit in epilepsy.