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Modulation of plateau properties in dorsal horn neurones in a slice preparation of the turtle spinal cord.
Author(s) -
Russo R E,
Nagy F,
Hounsgaard J
Publication year - 1997
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.1997.sp021941
Subject(s) - depolarization , bicuculline , acpd , cnqx , chemistry , biophysics , neuroscience , kainate receptor , agonist , metabotropic glutamate receptor , glutamate receptor , gabaa receptor , biology , ampa receptor , receptor , biochemistry
1. Modulation of plateau properties in dorsal horn neurones was studied in a transverse slice preparation of the spinal cord of the turtle. In plateau‐generating neurones high frequency stimulation of the ipsilateral dorsal root (10‐20 Hz, 0.5‐2 min) produced a slow depolarization (2.9 +/‐ 0.6 mV, mean +/‐ S.E.M.; n = 6) and enhanced the properties mediated by dihydropyridine‐sensitive Ca2+ channels. The tetanic stimulus facilitated wind‐up and after‐discharges even when fast synaptic transmission was blocked by 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX, 10‐20 microM), (+/‐)‐2‐amino‐5‐phosphonopentanoic acid (AP5, 100 microM), bicuculline (10‐20 microM) and strychnine (5‐20 microM). 2. Application of cis‐(+/‐)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (ACPD, 10‐50 microM) produced a slow depolarization (5.9 +/‐ 0.5 mV, n = 21) accompanied by an increase in input resistance (28.8 +/‐ 5.1%, n = 12). 3. ACPD increased the excitability by facilitating the plateau properties. In the presence of tetrodotoxin (TTX, 1 microM) a lower threshold and a slower decay of the plateau potential were observed. These effects resulted in facilitation of wind‐up and prolonged after‐discharges. 4. All ACPD‐induced effects were blocked by alpha‐methyl‐4‐carboxyphenylglycine (MCPG, 0.5‐1 mM), a selective antagonist of metabotropic glutamate receptors. The selective agonist for the type I metabotropic glutamate receptor ((RS)‐3,5‐dihydrophenylglycine (DHPG, 50 microM)) reproduced all the effects of ACPD. 5. Application of a supposed neuromodulator, substance P (1‐2 microM) produced a transient depolarization (4 +/‐ 0.6 mV) lasting 4‐6 min during continued application of substance P. Variable effects on the input resistance were observed, a slight increase (12 +/‐ 2%) being the most frequent. In 61% of the cells, substance P induced a clear increase in excitability with no detectable change in input resistance or membrane potential. 6. The effects of substance P on plateau properties were indistinguishable from those produced by ACPD. Unlike the transient depolarization, the facilitation of the plateau properties persisted in the presence of the agonist. 7. The substance P‐induced facilitation of the plateau potential was blocked by GR 82334 (5‐10 microM), a selective NK‐1 tachykinin‐receptor antagonist, and was not affected by MEN 10376 (2 microM), a selective NK‐2 antagonist. 8. The facilitation of plateau properties produced by dorsal root stimulation was also reduced by antagonists of metabotropic glutamate receptors and NK‐1 tachykinin receptors. 9. We propose that modulation of postsynaptic plateau properties in dorsal horn neurones by activation of type I metabotropic glutamate receptors and NK‐1 tachykinin receptors is involved in processing nociceptive information.