The pharmacology of dorsal root potentials recorded from the isolated spinal cord of the neonate rat

Abstract

1. 1. Dorsal root potentials (DRP) evoked by stimulating an adjacent dorsal root or the dorsal columns were recorded from the hemisected cord of 5–10 day old rats. 2. 2. GABA (10 −4 M) evoked a depolarization of the primary afferents and at concentrations of 10 −6, 10 −5 and 10 −4 M reduced DRP amplitude by 14, 39 and 45%, respectively. 3. 3. Bicuculline and picrotoxin (10 −5 M) reduced DRP amplitude by 62 and 52%, respectively. 4. 4. 5-HT (10 −6, 10 −5) and 10 −4 M) reduced DRP amplitude by 19, 40 and 44%, respectively. 5. 5. Phentolamine (10 −6 M) did not alter this action of 5-HT significantly, but quipazine (10 −6 M) almost entirely blocked it. 6. 6. Noradrenaline (NA) (10 −6 M) enhanced the amplitude of the DRP in some preparations and reduced it in others. Both actions were blocked by phentolamine (10 −6 M). Quipazine did not alter the effects produced by this concentration of NA. 7. 7. At higher concentrations (10 −5, 10 −4 M NA) only depressions of DRP amplitude were observed, but these effects were insensitive to phentolamine (10 −6 M). Quipazine potentiated the depressant action of NA (10 −5 M). 8. 8. DRPs were also reduced in amplitude by changes in [K +] 0. An increase to 6 or 4.5 mM reduced amplitude by 39 or 13%, respectively, while a decrease to 1.5 mM reduced it by 15%. Alteration in [K +] 0 produced changes in primary afferent resting potential. DRPs were abolished when [Cl −] 0 was reduced by 94%. 9. 9. The results are consistent with a dependence of the DRP on interneurones releasing GABA. 10. 10. Some part of the neural mechanism generating the DRP appears to possess distinct 5-HT receptors, capable of being blocked by quipazine, and α adrenoceptors; the neural mechanism is also sensitive to changes in [Cl −] 0 and [K +] 0.