Antidromic discharges of dorsal root afferents and inhibition of the lumbar monosynaptic reflex in the neonatal rat.
The in vitro brain stem-spinal cord preparation of neonatal (0- to five-day-old) rats was used to establish whether pathways descending from the brain stem are capable of modulating synaptic transmission from primary afferents to lumbar motoneurons within the first few days after birth. We stimulated the ventral funiculus of the spinal cord at the cervical (C1-C2) level. Single-pulse stimulations evoked both excitatory and inhibitory postsynaptic potentials in ipsilateral lumbar (L2-L5) motoneurons which were recorded intracellularly. Twin-pulse stimulations evoked bursts of action potentials in ventral roots. The amplitude of the monosynaptic dorsal root-evoked excitatory postsynaptic potential decreased when a conditioning stimulation was applied to the ventral funiculus 50-300 ms prior to the stimulation of the ipsilateral dorsal root. A decreased input resistance of the motoneurons during the early part (25-100 ms after the artifact) of the ventral funiculus-evoked postsynaptic potentials could account, at least partly, for the decreased amplitude of the dorsal root-evoked response. However, the duration of the inhibition of the dorsal root-evoked excitatory postsynaptic potential was longer than that of the decrease in input resistance. Ventral funiculus stimulation evoked antidromic discharges in dorsal roots. Recordings of dorsal root potentials showed that these discharges were generated by the underlying afferent terminal depolarizations reaching firing threshold. The dorsal root discharge overlapped with most of the time-course of the ventral funiculus-evoked inhibition of the response to dorsal root stimulation, suggesting that part of this inhibition may be exerted at a presynaptic level. The number of antidromic action potentials evoked in dorsal roots by ventral funiculus stimulation increased significantly in saline solution with chloride concentration reduced to 50% of control. Bursts of action potentials disappeared when chloride was removed completely. Antidromic discharges were therefore due to chloride conductance. The number of action potentials evoked in ventral roots was increased in low-chloride saline solutions. Removing chloride from the bathing solution resulted in an unstable ventral root activity. Bath application of the GABA(A) receptor antagonist, bicuculline (5-10 microM), blocked the ventral funiculus-evoked antidromic discharges in the dorsal roots. The increase in chloride conductance which generated the depolarizations underlying the dorsal root discharges was therefore mediated by an activation of GABA(A) receptors. In contrast, bursts of action potentials in the ventral roots were increased in both amplitude and duration under bicuculline. Our data demonstrate that pathways running in the ventral funiculus of the spinal cord exert a control on interneurons mediating presynaptic inhibition at birth.
Vinay
L
L
CNRS, UPR Neurobiologie et Mouvements (UPR 9011), Marseille, France.
Clarac
F
F
D000200:Action Potentials / Q000187:drug effects; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001640:Bicuculline / Q000494:pharmacology; D001933:Brain Stem / Q000502:physiology; D002712:Chlorides / Q000378:metabolism; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology*; D058787:GABA-A Receptor Antagonists; D005727:Ganglia, Spinal / Q000502:physiology*; D007395:Interneurons / Q000502:physiology; D017136:Ion Transport / Q000187:drug effects; D008124:Locomotion / Q000502:physiology; D008161:Lumbosacral Region; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017661:Receptors, Presynaptic / Q000187:drug effects / Q000502:physiology; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
D002712:Chlorides; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D017661:Receptors, Presynaptic; D001640:Bicuculline