Involvement of nitric oxide in 3-nitropropionic acid-induced depression of spinal reflexes in neonatal rat spinal cord in vitro

The objective of the present investigation is to study the involvement of nitric oxide (NO) in 3-nitropropionic acid (3-NPA)-induced depression of spinal reflexes. Experiments were conducted on preparations of hemisected spinal cord isolated from 4 to 8 day old rats. Stimulation of a dorsal root evoked reflex potentials (monosynaptic, MSR; polysynaptic, PSR) in the corresponding segmental ventral root. Superfusion of 3-NPA (3.4 mM) depressed the spinal reflexes in a time-dependent manner and the reflexes were abolished after 35 min. The time required to produce 50% depression of the reflexes (T-50) was 17.8 ± 5.3 min for MSR and 17.5 ± 2.1 min for PSR. L-NAME (Nω-nitro-l-arginine methyl ester; 100 µM), a nitric oxide synthase inhibitor, antagonized the 3-NPA (3.4 mM)-induced depression of reflexes and increased the T-50 values (34 and 30 min for MSR and PSR, respectively) significantly (P < 0.05). In addition, hemoglobin (Hb, 100 µM), a NO scavenger, blocked the 3-NPA-induced depression of reflexes significantly (P < 0.05). T-50 values in Hb pretreated cords were 57 and 45 min for MSR and PSR, respectively which were greater than the cords pretreated with L-NAME. The nitrite (NO2−) content of the 3-NPA exposed cords was 84 µM/g of tissue which was significantly greater than the control (13 µM/g; P < 0.05). Pretreatment of cords with L-NAME or Hb antagonized the 3-NPA-induced increase in NO2−. The results indicate that NO produced by 3-NPA is involved in the 3-NPA-induced depression of spinal reflexes.