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Presynaptic modulation by neuromedin U of sensory synaptic transmission in rat spinal dorsal horn neurones
Author(s) -
Moriyama Maiko,
Furue Hidemasa,
Katafuchi Toshihiko,
Teranishi Hitoshi,
Sato Takahiro,
Kano Tatsuhiko,
Kojima Masayasu,
Yoshimura Megumu
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.070110
Subject(s) - neuroscience , excitatory postsynaptic potential , spinal cord , postsynaptic potential , tetrodotoxin , dorsal root ganglion , neurotransmission , inhibitory postsynaptic potential , sensory system , chemistry , axon , anatomy , sensory neuron , biology , endocrinology , receptor , biochemistry
Neuromedin U (NMU) is a brain–gut peptide first isolated from the spinal cord. Recent studies on NMU and its receptors have suggested a role of NMU in sensory transmission. Here we report on the localization of NMU in sensory neurones, and the actions of NMU in the substantia gelatinosa (SG) and the deep layer of the dorsal horn (laminae III–V) in adult rat spinal cord slices using the patch‐clamp technique. An immunohistochemical study revealed that NMU peptide was present in most of the dorsal root ganglion neurones. In the spinal cord, NMU‐immunoreactive neurones were located in the deep layer (laminae III–V), but not in the SG. However, NMU‐positive axon terminals were observed in the SG as well as the deep layer. Bath‐applied NMU (10 μ m ) increased the frequency, but not amplitude, of miniature excitatory postsynaptic currents (mEPSCs) in the SG and deep layer neurones by 146 ± 14% ( P < 0.01, n = 17) and 174 ± 21% ( P < 0.01, n = 6), respectively, without inducing any postsynaptic membrane currents recorded in tetrodotoxin. On the other hand, NMU did not affect miniature inhibitory postsynaptic currents recorded in tetrodotoxin. These findings, taken together, suggest that NMU acts on the presynaptic terminals of the primary afferent fibres working as an autocrine/paracrine neuromodulator to increase mEPSC frequency of the SG and deep layer neurones. This may account for the spinal mechanisms of the NMU‐induced hyperalgesia reported previously.