NMDA receptors mediate background and excessive activity of γ-motoneurones in the spinal cord

Abstract

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 γ-motoneurone activity in the spinal cord of unanaesthetized spinal cats. CPP (1–10 mg/kg i.v.) dose dependently reduced the spontaneous activity of γ-motoneurones. The kainic acid (11 mg/kg i.v.)-induced bursting firing pattern of γ-motoneurones was unaffected or enhanced by CPP. In contrast, CPP suppressed the increase of γ-motoneuronal excitability caused by NMDA (3 mg/kg i.v.), suggesting that both the background and the exaggerated activity of γ-motoneurones are mediated by an amino acid that activates NMDA receptors.