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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Published on: November 19, 2012
Ca(2+)-dependent non-NMDA receptor-mediated synaptic currents in ischemic CA1 hippocampal neurons
H Tsubokawa1, K Oguro, T Masuzawa
1Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.
Journal of Neurophysiology
|March 1, 1994
Summary
Transient cerebral ischemia in gerbils significantly slows excitatory postsynaptic currents (EPSCs) in CA1 neurons, primarily due to altered non-N-methyl-D-aspartate receptor activity and calcium influx.
Area of Science:
- Neuroscience
- Cellular Physiology
- Ischemic Stroke Research
Background:
- Transient cerebral ischemia is a major cause of neuronal damage.
- Understanding the alterations in synaptic transmission post-ischemia is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the changes in excitatory postsynaptic currents (EPSCs) in CA1 pyramidal neurons of gerbils following transient cerebral ischemia.
- To elucidate the underlying mechanisms responsible for these synaptic alterations.
Main Methods:
- Whole-cell patch-clamp recordings were performed on CA1 pyramidal neurons in gerbils 1.5-3 days after ischemia.
- Pharmacological agents, including N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists, were used to characterize the EPSC components.
- Experiments involving manipulation of extracellular calcium concentration and the use of a calcium chelator (BAPTA-AM) were conducted.
Main Results:
- A significant slowing of the EPSC time course was observed in 64% of ischemic neurons compared to controls.
- The slowed EPSCs were primarily mediated by non-NMDA receptor currents and were unaffected by NMDA receptor blockade.
- The prolonged decay of these currents was dependent on extracellular calcium concentration and intracellular calcium buffering.
Conclusions:
- Transient cerebral ischemia induces a persistent alteration in non-NMDA receptor-mediated synaptic transmission in CA1 neurons.
- Calcium influx plays a critical role in prolonging the decay of EPSCs following ischemic events.
- These findings provide insights into the synaptic dysfunction occurring after cerebral ischemia.
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