A comparison of the effects of serotonin, substance P and thyrotropin-releasing hormone on excitability of rat spinal motoneurons in vivo.
Lumbar spinal motoneurons of urethane-anesthetized rats were driven at stable low firing rates by automatically cycled iontophoretic applications of glutamate or aspartate. The effects of iontophoretically applied serotonin, substance P or thyrotropin-releasing hormone (TRH) on glutamate or aspartate-evoked activity were then tested. All 3 substances were found to enhance both glutamate- and aspartate-induced excitation of the motoneurons. This enhancement of excitability was usually preceded by a brief period of inhibition at current onset. Although the effects of serotonin and substance P were qualitatively remarkably similar, TRH differed in that TRH occasionally inhibited motoneuron excitability without subsequent facilitation, and tachyphylaxis developed for the facilitatory effects of TRH. After TRH desensitization, serotonin could still enhance spinal motoneuron excitability.
S R
SR
White
D000818:Animals; D000870:Anterior Horn Cells / Q000187:drug effects*; D001224:Aspartic Acid / Q000494:pharmacology; D004357:Drug Synergism; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D008297:Male; D009046:Motor Neurons / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000494:pharmacology*; D013373:Substance P / Q000494:pharmacology*; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D005971:Glutamates; D001224:Aspartic Acid; D012701:Serotonin; D013373:Substance P; D018698:Glutamic Acid; D013973:Thyrotropin-Releasing Hormone