Peripheral Nerve Injury Alters Excitatory and Inhibitory Synaptic Transmission in Rat Spinal Cord Substantia Gelatinosa.
- Author:
Dong Ho YOUN
1
Author Information
1. Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Korea. dyoun@mail.knu.ac.kr
- Publication Type:Original Article
- Keywords:
Spinal substantia gelatinosa;
Synaptic transmission;
Neuropathic pain;
Spared nerve injury
- MeSH:
Animals;
Depression;
Excitatory Postsynaptic Potentials;
Glutamic Acid;
Horns;
Inhibitory Postsynaptic Potentials;
Models, Animal;
Neuralgia;
Neurons;
Patch-Clamp Techniques;
Peripheral Nerve Injuries*;
Peripheral Nerves*;
Rats*;
Spinal Cord*;
Substantia Gelatinosa*;
Synaptic Transmission*
- From:The Korean Journal of Physiology and Pharmacology
2005;9(3):143-147
- CountryRepublic of Korea
- Language:English
-
Abstract:
Following peripheral nerve injury, excessive nociceptive inputs result in diverse physiological alterations in the spinal cord substantia gelatinosa (SG), lamina II of the dorsal horn. Here, I report the alterations of excitatory or inhibitory transmission in the SG of a rat model for neuropathic pain ("spared nerve injury"). Results from whole-cell recordings of SG neurons show that the number of distinct primary afferent fibers, identified by graded intensity of stimulation, is increased at 2 weeks after spared nerve injury. In addition, short-term depression, recognized by paired-pulse ratio of excitatory postsynaptic currents, is significantly increased, indicating the increase of glutamate release probability at primary afferent terminals. The peripheral nerve injury also increases the amplitude, but not the frequency, of spontaneous inhibitory postsynaptic currents. These data support the hypothesis that peripheral nerve injury modifies spinal pain conduction and modulation systems to develop neuropathic pain.
