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Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices
Published on: November 26, 2012
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Activity-dependent changes in transporter and potassium currents in hippocampal astrocytes
Albina Lebedeva1, Alex Plata1, Olga Nosova1
1UNN Institute of Neuroscience, University of Nizhny Novgorod, Nizhny Novgorod, Russia.
Brain Research Bulletin
|September 12, 2017
Summary
Astrocytes regulate synaptic function through glutamate and potassium ion (K+) transport. Blocking K+ channels with barium chloride (BaCl2) prevents activity-dependent changes in glutamate transporter currents, revealing K+ accumulation
Area of Science:
- Neuroscience
- Cellular Physiology
- Astrocyte Biology
Background:
- Astrocytes maintain synaptic homeostasis via glutamate uptake and K+ clearance.
- These processes involve ion currents, specifically glutamate transporter (IGluT) and K+ (IK) currents.
- Previous studies indicated BaCl2 blockade of IK enhances IGluT.
Purpose of the Study:
- To investigate the role of extracellular K+ accumulation in activity-dependent modulation of astrocytic glutamate transporter currents.
- To elucidate the interplay between K+ and glutamate transport in astrocytes.
- To understand astrocytic contributions to synaptic function and neurological disorders.
Main Methods:
- Electrophysiological recordings of astrocytic currents.
- Pharmacological manipulation using BaCl2 (K+ channel blocker) and TBOA (glutamate transporter blocker).
- Activity-dependent stimulation protocols (5 stimuli at 50Hz) to induce ion accumulation.
Main Results:
- BaCl2 abolished activity-dependent prolongation of IGluT decay time, suggesting extracellular K+ accumulation causes astrocytic depolarization.
- Blockade of inward rectifying K+ channels (Kir) with BaCl2 rendered astrocytic membrane potential insensitive to elevated extracellular K+.
- TBOA decreased IK decay time but enhanced its activity-dependent facilitation, suggesting glutamate accumulation enhances K+ release.
Conclusions:
- Activity-dependent extracellular K+ accumulation leads to astrocytic depolarization, influencing glutamate transporter current kinetics.
- Astrocytic K+ homeostasis is crucial for regulating synaptic glutamate levels.
- Bidirectional interactions between K+ and glutamate dynamics in astrocytes impact synaptic transmission and neuronal excitability, relevant to conditions like stroke, migraine, and epilepsy.
