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Related Experiment Videos

Activity-dependent ionic changes and neuronal plasticity in rat hippocampus.

U Heinemann1, J Stabel, G Rausche

  • 1Institut für Neurophysiologie, Zentrum Physiologie und Pathophysiologie, Universität zu Köln, F.R.G.

Progress in Brain Research
|January 1, 1990
PubMed
Summary

Repetitive brain stimulation causes ionic shifts, including reduced calcium, that are crucial for long-term potentiation (LTP) and kindling plasticity. These changes facilitate N-methyl-D-aspartate (NMDA) receptor activation, impacting neuronal excitability and epilepsy progression.

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Area of Science:

  • Neuroscience
  • Cellular Physiology
  • Neuroplasticity

Background:

  • Repetitive neuronal stimulation induces ionic microenvironment changes.
  • These ionic shifts are implicated in long-term potentiation (LTP) and kindling plasticity.
  • N-methyl-D-aspartate (NMDA) receptor activation is critical for LTP induction.

Purpose of the Study:

  • To investigate the ionic changes during repetitive stimulation that induces plasticity.
  • To elucidate the role of extracellular calcium ([Ca2+]o) reduction in NMDA receptor activation.
  • To understand the mechanisms underlying stimulus-induced neuronal plasticity and temporal lobe epilepsy progression.

Main Methods:

  • Analysis of ionic changes, specifically [Ca2+]o, during repetitive stimulation.

Related Experiment Videos

  • Investigating the contribution of NMDA-operated channels to [Ca2+]o reduction.
  • Examining the effects of extracellular potassium ([K+]o), [Ca2+]o, and magnesium ([Mg2+]o) on NMDA receptor activation.
  • Analyzing quisqualate and NMDA-induced [Ca2+]o changes.

    • Main Results:

    • Only a fraction of [Ca2+]o decrease is mediated by NMDA channels.
    • Increases in [K+]o and reductions in [Ca2+]o and [Mg2+]o, along with K(+)-dependent reduction of slow inhibitory postsynaptic potential (IPSP), promote NMDA receptor activation.
    • NMDA receptor activation appears to slow calcium extrusion from cells, potentially aiding long-term changes.
    • [Ca2+]o changes are linked to stimulus and excitatory amino acid (EAA)-induced neuronal excitability alterations.

    Conclusions:

    • Ionic shifts, including [K+]o increase and [Ca2+]o/[Mg2+]o reduction, facilitate NMDA receptor activation during stimulation trains.
    • This ionic modulation helps overcome hyperpolarization-induced blockade of NMDA receptors.
    • Slower calcium extrusion post-NMDA activation may contribute to long-term plasticity.
    • Alterations in the ionic microenvironment are key to stimulus-induced plasticity and possibly temporal lobe epilepsy progression.