抄録
Activity-dependent long-term potentiation (LTP) in the spinal cord is believed to underlie hyperalgesia after inflammation or nerve injury. We report a presynaptic form of LTP in the rat spinal cord slices by visualizing pre- and postsynaptic excitation. To record presynaptic excitation, we stained primary afferent fibers anterogradely from the dorsal root. A single-pulse test stimulation of C fiber-activating strength to the dorsal root (TS) elicited action potential (AP)- or compound AP-like optical signals. After conditioning stimulation (CS, at 2 Hz for 2 min), the presynaptic excitation was augmented. Furthermore, new excitation was elicited in previously silent areas. For postsynaptic recording, projection neurons in spinal lamina I were stained retrogradely from the brain stem. TS elicited AP-like or EPSP-like optical signals in the stained neurons. After CS, the EPSP-like responses were augmented, and previously silent neurons were converted to active ones. The facilitation and generation of new excitation in pre- and postsynaptic excitation were inhibited by nitric oxide (NO) synthase inhibitors and a glial metabolism inhibitor. Application of a NO donor with shorter CS, that normally did not induce facilitation, augmented the excitation and elicited new excitation. Furthermore, the augmentation of presynaptic excitation was inhibited by metabotropic glutamate receptor (mGluR) antagonist, and mGluR agonist without CS augmented presynaptic excitation. This NO-, glia- and mGluR-mediated presynaptic LTP may contribute to the induction of hyperalgesia. [Jpn J Physiol 55 Suppl:S11 (2005)]
