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INTEGRATIVE |
1 King's College London, Hodgkin Building, Guy's Hospital Campus, London SE1 1UL, UK
Two types of dorsal root potential (DRP) were found in the spinal cord of urethane-anaesthetized rats. Local DRPs with short latency-to-onset were evoked on roots close to the point of entry of an afferent volley. Diffuse DRPs with a longer latency-to-onset were seen on more distant roots up to 17 segments from the volley entry zone. The switch to long latency-to-onset occurred abruptly as a function of distance along the cord and could not be explained by conduction delays within the dorsal columns. Long-latency DRPs were also present and superimposed on the short-latency DRPs on nearby roots. Both local and diffuse DRPs were evoked by light mechanical stimuli: von Frey hair thresholds were 
1 gram force Changes in excitability of the terminals of sural nerve afferents were used to confirm that both local and diffuse DRPs were associated with primary afferent depolarization (PAD). These effects were potent: the area of the antidromic volley evoked in the sural nerve by intraspinal microstimulation in the L4/5 spinal segment was increased by 109 ± 50% (mean ±
S.D.; n
= 5) by nearby conditioning stimuli, and by 52 ± 12% (n
= 6) with stimuli applied 9–13 mm (5–8 segments) away. The time course of the changes in terminal excitability closely matched those of the DRPs. Reduction of the field potentials evoked in the dorsal horn by stimulation of dorsal roots was also shown to accompany both local and diffuse DRPs. The area of the monosynaptically evoked field potential was reduced by 48 ± 19% (n
= 7) with nearby conditioning stimulation and 16 ± 9% (n
= 10) with stimulation 9–12 mm distant. Evidence is presented that this inhibition includes a presynaptic component. Similar effects were seen with field potentials evoked by sural nerve stimulation. It is concluded that diffuse DRPs are mediated through propriospinal networks which may contribute to the gating of sensory information flow during natural behaviour as they respond to weak mechanical stimuli and provoke presynaptic inhibition.
(Received 30 March 2006;
accepted after revision 20 July 2006;
first published online 27 July 2006)
Corresponding author M. Lidierth: King's College London, Hodgkin Building, Guy's Hospital Campus, London SE1 1UL, UK. Email: malcolm.lidierth{at}kcl.ac.uk
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