Inward Currents Induced by Ischemia in Rat Spinal Cord Neurons
Author Information
Author(s): Chen Meng, Tao Yuan-Xiang, Gu Jianguo
Primary Institution: Department of Oral and Maxillofacial Surgery, McKnight Brain Institute and College of Dentistry, University of Florida; Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine
Hypothesis
Ischemic conditions result in the reversal operation of the glutamate transport system to cause glutamate release and subsequent excitation of sensory neurons in the spinal cord dorsal horn.
Conclusion
Ischemia induces significant inward currents in dorsal horn neurons of the spinal cord, which can be blocked by glutamate receptor and transporter inhibitors.
Supporting Evidence
- The ischemia-simulating medium induced large inward currents in dorsal horn neurons.
- The onset of ischemia-induced inward currents was age-dependent, being shorter in older animals.
- Electrical stimulation of afferent fibers significantly shortened the onset time of ischemia-induced inward currents.
- Glutamate receptor antagonists CNQX and APV abolished the ischemia-induced inward currents.
- The glutamate transporter inhibitor TBOA substantially inhibited the ischemia-induced inward currents.
Takeaway
When the spinal cord doesn't get enough blood, it can cause nerve cells to become overactive and hurt. This study shows how this happens and how certain drugs can help.
Methodology
Spinal cord slice preparations and patch-clamp recordings were used to investigate the effects of an ischemia-simulating medium on dorsal horn neurons.
Limitations
The study did not examine animals older than 20 days, which may limit the understanding of age-dependence beyond this range.
Participant Demographics
Sprague Dawley rats aged 4 to 21 days were used in the experiments.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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