NMDA receptors mediate background and excessive activity of gamma-motoneurones in the spinal cord.
The effects of 3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), a selective and potent antagonist of N-methyl-D-aspartic acid (NMDA) receptors, were studied on gamma-motoneurone activity in the spinal cord of unanaesthetized spinal cats. CPP (1-10 mg/kg i.v.) dose dependently reduced the spontaneous activity of gamma-motoneurones. The kainic acid (1 mg/kg i.v.)-induced bursting firing pattern of gamma-motoneurones was unaffected or enhanced by CPP. In contrast, CPP suppressed the increase of gamma-motoneuronal excitability caused by NMDA (3 mg/kg i.v.), suggesting that both the background and the exaggerated activity of gamma-motoneurones are mediated by an amino acid that activates NMDA receptors.
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Pharmaceutical Research Department, F. Hoffmann-La Roche & Co. Ltd., Basel, Switzerland.
D000818:Animals; D002415:Cats; D007608:Kainic Acid / Q000494:pharmacology; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D010879:Piperazines / Q000494:pharmacology*; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology*
D010879:Piperazines; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; D007608:Kainic Acid