Related Experiment Videos
NMDA receptor-mediated synapses between CA1 neurones: activation by ischaemia
T Tsintsadze1, N Lozovaya, A Klishin
1Department of Cellular Membranology, Bogomoletz Institute of Physiology, Kiev, Ukraine.
Neuroreport
|November 4, 1996
Summary
Transient ischemia potentiates excitatory postsynaptic currents (EPSC) in hippocampal CA1 neurons. This potentiation involves a stimulus-dependent slowing of EPSC decay, suggesting recruitment of previously inactive synapses.
Area of Science:
- Neuroscience
- Cellular Physiology
- Ischemia Research
Background:
- Excitatory postsynaptic currents (EPSC) are crucial for neuronal communication in the hippocampus.
- Understanding synaptic plasticity after ischemic events is vital for brain injury research.
Purpose of the Study:
- To investigate the long-term effects of transient ischemia on synaptic transmission in hippocampal CA1 neurons.
- To characterize changes in excitatory postsynaptic current (EPSC) kinetics and stimulus-dependence following anoxic/aglycemic episodes.
Main Methods:
- In situ patch clamp recordings were performed on hippocampal CA1 mini-slices.
- Stimulus strength applied to CA3 neuronal axons was varied to measure excitatory postsynaptic currents (EPSC).
- Effects of N-methyl-D-aspartate (NMDA) and non-NMDA receptor blockers were assessed.
Main Results:
- Post-ischemic potentiation of EPSC was observed 60-80 minutes after 10 minutes of anoxia/aglycaemia.
- EPSC decay slowed significantly in most neurons post-ischemia.
- In a majority of cells, EPSC kinetics became stimulus-strength dependent, with slower decay at higher stimulus strengths.
Conclusions:
- Transient ischemia induces long-term potentiation of synaptic transmission in hippocampal CA1 neurons.
- The observed stimulus-dependent EPSC kinetics suggest the recruitment of previously inactive synapses.
- This recruitment is likely polysynaptic and involves NMDA receptors, indicating a potential mechanism for altered neuronal excitability after ischemia.