Adjacent Dorsal Root Research Articles

The effects of 4-aminopyridine on the cat spinal cord: rhythmic antidromic discharges recorded from the dorsal roots

In a previous paper, we have reported that 4-aminopyridine (4-AP, i.v., 10 mg/kg) induces in decerebrate spinal and paralyzed cats, a sustained rhythmic activity (2.5–8.5 Hz) in various muscle nerves. We describe here that similar discharges are recorded from the proximal stump of cut cutaneous nerves. The latter rhythmic activity arises from intense antidromic discharges in the dorsal roots. The rhythmic discharges are recorded from dorsal roots of both spinal cord enlargements as well as from thoracic roots. The rhythmic activity is highly synchronous among adjacent dorsal roots. Bilateral activity is also highly cross-correlated, but may be dissociated by unilateral stimulation of one dorsal root. It is not yet possible to determine the precise site where the antidromic discharges recorded from the dorsal roots are generated. 4-AP could act directly at the terminal level of the primary afferents or could activate interneurons impinging upon the terminals.

Effects of depressant amino acids and antagonists on an in vitro spinal cord preparation from the adult rat

A mature sacrococcygeal in vitro spinal preparation from the rat has been used to demonstrate effects of neutral amino acids and their antagonists. γ-Aminobutanoate (GABA), glycine and taurine (0.5–5 mM) produced dose-dependent depression of spontaneous paroxysmal activity generated in Mg 2+-free medium. The depressant effect of GABA was antagonised selectively by picrotoxin (25–50 μM) and the depressant effects of glycine and taurine were antagonised selectively by strychnine (0.2 μM). Glycine (0.5–5 mM) had a dose-dependent depolarizing action which was present at the central ends of isolated ventral roots. γ-Aminobutanoate and taurine, had only weak depolarizing actions on ventral root fibres. Depolarizing responses to glycine showed a marked fading. Reduction in the fading appeared to be responsible for a paradoxical potentiation of glycine-induced depolarizations, which occurred in the presence of strychnine (0.2–2 μM). Strychnine (2–10 μM), picrotoxin (10–50 μM) or bicuculline (10 μM) had little or no effect on the amplitude, duration or latency of the monosynaptic component of ventral root reflexes evoked by supramaximal stimulation of dorsal roots (DR-VRP). However all three antagonists introduced slow, NMDA receptor mediated, components to these ventral root potentials. Picrotoxin and bicuculline, but not strychnine, reversibly depressed the dorsal root potential evoked from an adjacent dorsal root (DR-DRP). The depressant actions of 2-amino-5-phosphonopentanoate (AP5), kynurenate and 3-((±)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) revealed both NMDA and non-NMDA receptor mediated components in the dorsal root potential.

Temperature-dependence of reflex transmission in the neonatal rat spinal cord, in vitro: Influence on strychnineand bicuculline-sensitive inhibition

The amplitude, latency and rise time of the monosynaptic reflex, recorded from the spinal cord of the neonatal rat in vitro, was temperature-dependent with optimal conditions occurring at 25°C. The reflex was inhibited when conditioning stimuli were applied to an adjacent dorsal root at 1–150 msec before the monosynaptic reflex was evoked; the inhibition had both an early and a late phase. The early phase of inhibition occurred at conditioning-test intervals of 1–20 msec with peak inhibition occurring at 7 msec. Raising the temperature of the bath to 31°C or exposing the cord to strychnine blocked the early phase of inhibition. The late phase of inhibition occurred at conditioning-test intervals greater than 20 msec, was unaffected by temperature and was blocked by bicuculline. The early phase of inhibition therefore appears to be postsynaptic in origin and mediated by glycine while the late component of inhibition may be presynaptic in origin and mediated by γ-aminobutyric acid (GABA).

The responses recorded in vitro of deep dorsal horn neurons to direct and orthodromic stimulation in the young rat spinal cord

The electrophysiological properties of 87 neurons in the deep dorsal horn (laminae III VI) of the rat spinal cord have been investigated in vitro. Two preparations have been used; the transverse spinal cord slice preparation from the third or fourth lumbar segments of 14–16 -day-old rats (71 cells) and a hemisected lumbar spinal cord preparation from 10–12-day-old rats (16 cells). The input impedances (range 11–128 MΩ), membrane potentials ( -67 ± 8mVS.D.), action potential amplitude (77 ± 11.8mV) duration (1.4 ± 0.5ms) and afterpotentials, were effectively identical in the neurons recorded from the two preparations. Neurons in both preparations when activated with long-duration (1–2s) outward current pulses showed a single steady-state firing range with little Actaptation of firing frequency or action potential amplitude. This pattern of responses was unaffected by changing the membrane potential. Orthodromic synaptic activity could be elicited in the neurons by stimulating either the small dorsal root remnants in the slice or the dorsal roots in the hemisected spinal cord. The responses evoked by single stimuli of increasing intensity varied in different neurons in both preparations. The commonest response (32/62) consisted of a short-latency, short-duration composite excitatory postsynaptic potential which generated one or two spikes with no further spiking activity at longer latency when the stimulus intensity was increased beyond threshold. In 20 neurons, graded stimulation produced a graded response with recruitment, at high intensities, of a discharge of action potentials lasting several hundred milliseconds. A small number of cells (4) responded to the single stimulus with a train of action potentials lasting several seconds. Stimulating adjacent dorsal roots in the hemisected cord preparation could evoke quite different responses from the neurons. The heterogeneity of the types of orthodromic responses obtained in both preparations, in spite of the almost uniform intrinsic membrane properties, is likely to rcflect differences in the strength, location and type of afferent and interneuronal input to different dorsal horn cells.

Sympathetic and afferent somata projecting in hindlimb nerves and the anatomical organization of the lumbar sympathetic nervous system of the rat.

The anatomy of the sympathetic pathways from the spinal cord to the lumbar sympathetic trunk and the inferior mesenteric ganglion was studied systematically in the rat. Details of the arrangements of white and gray rami communicantes, sympathetic trunk ganglia, the intermesenteric nerve, and the lumbar splanchnic nerves are summarized. A modified nomenclature for the segmental ganglia of the paravertebral sympathetic chain is proposed. Cell bodies of sensory and sympathetic axons projecting to the skin and skeletal muscle of the rat hindlimb were labeled retrogradely with horseradish peroxidase (HRP) in order to study numbers, segmental distribution, and location of the somata of these neurons quantitatively. HRP was applied to the nerves supplying skeletal muscle (gastrocnemius-soleus, GS), hairy skin (sural, SU; saphenous, SA) and to a mixed nerve (tibial, TI). All sensory somata and 96.4% of the sympathetic cell bodies were located ipsilaterally. Sensory somata were commonly restricted to two adjacent dorsal root ganglia (usually L3-4 for SA; L4-5 for GS, TI; L5-6 for SU). Although the sympathetic somata were more widely distributed rostrocaudally (four to six segments), their maximum was always located one or two segments more cranially than the sensory outflow, i.e., corresponding to the rami communicantes grisei. From the data, it is estimated that 420 sympathetic and 530 afferent neurons project into GS, 590 and 3,610 into SU, 920 and 3,750 into SA, and 1,070 and 5,760 into TI. These absolute neuron numbers are compared with electron microscopic fiber counts from the literature.

Regeneration of adult dorsal root axons into transplants of embryonic spinal cord.

Transplants of the embryonic rat spinal cord survive and differentiate in the spinal cords of adult and newborn host rats. Very little is known about the extent to which these homotopic transplants can provide an environment for regeneration of adult host axons that normally terminate in the spinal cord. We have used horseradish peroxidase injury filling and transganglionic transport methods to determine whether transected dorsal roots regenerate into fetal spinal cord tissue grafted into the spinal cords of adult rats. Additional transplants were examined for the presence of calcitonin gene-related peptide-like immunoreactivity, which in the normal dorsal horn is derived exclusively from primary afferent axons. Host animals had one side of the L4-5 spinal cord resected and replaced by a transplant of E14 or E15 spinal cord. Adjacent dorsal roots were sectioned and juxtaposed to the graft. The dorsal roots and their projections into the transplants were then labeled 2-9 months later. The tracing methods that used transport or diffusion of horseradish peroxidase demonstrated that severed host dorsal root axons had regenerated and grown into the transplants. In addition, some donor and host neurons had extended their axons into the periphery to at least the midthigh level as indicated by retrograde labeling following application of tracer to the sciatic nerve. Primary afferent axons immunoreactive for calcitonin gene-related peptide were among those that regenerated into transplants, and the projections shown by this immunocytochemical method exceeded those demonstrated by the horseradish peroxidase tracing techniques. Growth of the host dorsal roots into transplants indicates that fetal spinal cord tissue permits regeneration of adult axotomized neurons that would otherwise be aborted at the dorsal root/spinal cord junction. This transplantation model should therefore prove useful in studying the enhancement and specificity of the regrowth of axons that normally terminate in the spinal cord.

Enhancement of recurrent inhibition of the spinal monosynaptic reflex by preceding stimulation of the medullary raphe´in rats

Recurrent inhibition of the spinal monosynaptic reflex (MSR) elicited by conditioning stimulation of the ventral root in anesthetized rats was weaker than both the recurrent inhibition of the disynaptic reflex and the inhibition of the MSR elicited by conditioning stimulation of the adjacent dorsal root. Among these 3 inhibitions, the recurrent inhibition of the MSR was enhanced to a markedly greater extent by a preceding stimulation of the medullary raphe´nucleus than were the other inhibitions. The magnitude of the enhancement of the recurrent inhibition of MSR also was much greater when the medullary stimulation was delivered 20 ms prior to the ventral root activation, as compared with a 30-ms interval. Recurrent inhibition of the MSR was enhanced by intravenous injection of lysergic acid diethylamide (LSD); however, the enhanced effect on recurrent inhibition elicited by stimulation of the raphe´nucleus was not attenuated by the drug. These results suggest that there is a non-serotonergic, descending pathway which is capable of modulating motor output solely by means of recurrent inhibition of the MSR.

Demonstration of the synaptic origin of primary afferent depolarization (PAD) in the isolated spinal cord of the hamster

Intracellular recordings have been made from 31 primary afferent fibres within the dorsal horn of an isolated mammalian spinal cord. In 17 fibres stimulation of an adjacent dorsal root evoked primary afferent depolarization (PAD); these fibres also showed spontaneous depolarizations. Replacement of the calcium in the perfusing medium by manganese blocked both evoked and spontaneous activity showing them to be of synaptic origin. Observations on the effects of current injection and of bicuculline support an involvement of GABA in the generation of PAD.

Concussive head injury producing suppression of sensory transmission within the lumbar spinal cord in cats.

This study examines the effects of concussive levels of a fluid-percussion head injury on sensory transmission within the lumbar spinal cord of the cat. Primary afferent depolarization (PAD) was suppressed for 2 to 5 minutes following injury, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. Polysynaptic reflex discharges in ventral root potentials evoked by dorsal root stimulation were also profoundly suppressed during this same period, even when spontaneous and monosynaptic reflex discharges were facilitated. Changes in PAD produced by injury were abolished by spinal cord transection, but were not affected by midpontine transection. These findings suggest that concussive head injury can produce suppression of segmental sensory transmission by neurally mediated processes involving the bulbar brain stem. Recordings of dorsal root resting potentials, antidromic dorsal root potentials, and reductions of antidromic dorsal root potentials induced by tetanic root stimulation indicated that depressed segmental sensory function produced by injury was due to suppression of postsynaptic interneuronal transmission rather than to excitability changes in primary afferent fibers. Somatosensory cortical potentials evoked by dorsal root stimulation were profoundly depressed at the same time as segmental sensory transmission was suppressed, suggesting that suppressed segmental sensory transmission may also contribute to suppression of ascending sensory transmission. It is hypothesized that transmission failure of interneuronal systems in the initial period following insult may be a general response occurring in wide areas of the central nervous system, and not restricted to areas to which mechanical stress is directly applied. This response pattern may result from indiscriminate activation of interconnected excitatory and inhibitory elements of interneuronal systems.

Depression of afferent-induced primary afferent depolarization at the lumbar spinal cord following concussive head injury

Afferent-induced primary afferent depolarization (PAD) was depressed for 2–5 min following concussive head injury in the cat, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. These changes in PAD were abolished by spinal cord transection but not affected by midpontine transection. Spontaneous dorsal root potentials, resting amplitudes of antidromic dorsal root potentials and reductions of antidromic dorsal root potentials following tetanic root stimulation were not substantially altered by injury. These findings suggest that concussive head injury depresses spinal interneuronal transmission by neurally mediated processes involving the bulbar brainstem.

An investigation of the dorsal root reflex using an in vitro preparation of the hamster spinal cord

A detailed description is given of an hemisected spinal cord preparation from adult golden hamsters and this preparation has been used to investigate the physiology of the dorsal root reflex. In addition to antidromic reflex discharges which could be recorded from lumbar dorsal roots following stimulation of adjacent dorsal roots or the dorsal columns, spontaneous firing was also recorded from the dorsal roots. This activity reached a peak at 27 °C and was abolished at temperatures above 35 °C. Both the evoked and the spontaneous dorsal root activity were demonstrated to be travelling antidromically along the dorsal roots out of the cord, and replacement of the calcium in the bathing medium by manganese showed them to be of synaptic origin. Stimulation of a lumbar dorsal root was found to evoke a reflex in up to 4 adjacent spinal segments in both rostral and caudal directions, and a period of depressed activity was demonstrated following both evoked and spontaneous discharges. A time-locked relationship was found between the dorsal root reflex and the slow dorsal horn potential recorded from within the spinal cord.

Effects of caroverine and diltiazem on synaptic responses, L-glutamate-induced depolarization and potassium efflux in the frog spinal cord.

The frog spinal cord was used to determine the characteristics of the actions of caroverine and diltiazem, two organic Ca2+-antagonists, on synaptic responses and L-glutamate-induced depolarization. Caroverine and diltiazem (10(-4)M) depressed the dorsal root potential (DR-DRP) induced by electrical stimulation of an adjacent dorsal root. Diltiazem also depressed the ventral root potential (DR-VRP), whereas caroverine augmented both the polysynaptic component in the ventral root reflex and the size of the DR-VRP. The root potentials induced by high frequency stimulation (20 Hz, for 1 s) were markedly depressed by these Ca2+-antagonists at a concentration of 10(-4)M. When the preparation was perfused with normal medium, the compounds depressed L-glutamate-induced depolarizations in ventral and dorsal roots. In preparations treated with tetrodotoxin (TTX) (2 X 10(-7)M), the antagonizing actions of the drugs against L-glutamate-induced depolarizations in the ventral root were markedly reduced or abolished, while significant antagonizing actions on the depolarization in the dorsal root were still observed. The increase in extracellular K+ activity induced by L-glutamate in the TTX-treated preparation was significantly reduced by the compounds. Caroverine and diltiazem had no effect on the presynaptic nerve spike and on the focal synaptic potential induced by a single stimulation of a dorsal root; however, the focal synaptic potential induced by high frequency stimulation (20 Hz, 1 s) was attenuated. Motoneuronal action potentials were abolished by the drugs, while the excitatory postsynaptic potential remained unaffected. 9 The present results suggest that caroverine and diltiazem are not specific L-glutamate antagonists in the frog spinal cord, but that they block the initiation of an action potential without affecting presynaptic nerve conduction, transmitter release or transmitter-receptor interactions. The inhibitory effects of these compounds on L-glutamate-induced K+-efflux are discussed with reference to their Ca2+-antagonizing actions.

Spontaneous dorsal root potentials arise from interneuronal activity in the isolated frog spinal cord

Spontaneous dorsal root potentials (sDRPs) were recorded from the dorsal roots of the isolated frog spinal cord using sucrose gap techniques. sDRPs were always negative (depolarizing) in sign and ranged in size from about 100 μV to 6.0 mV. The largest sDRPs were 25–40% of the amplitude of DRPs evoked by stimulation of adjacent dorsal roots. Hypoxia or accumulation of extracellular K + ions did not appear responsible for the generation of this spontaneous activity since exposing the cord to unoxygenated Ringer's solution decreased sDRPs and K +-sensitive microelectrodes indicated that only small changes in extracellular K + (approximately 0.15 mM) were produced coincidently with the largest sDRPs. Chemically-mediated synaptic transmission was found to be necessary for the production of sDRPs because the addition of Mn 2+ or Mg 2+ ions or tetrodotoxin to the Ringer's solution or reduction of its Na + concentration blocked sDRPs, whereas application of 4-aminopyridine enhanced them. It did not seem that a direct action of GABA on afferent fiber terminals was responsible for the generation of spontaneous potentials since an increase in sDRPs was seen after: application of the GABA antagonists, bicuculline and picrotoxin; exposure to the glutamic acid decarboxylase inhibitor, semicarbazide (which significantly reduced the concentration of GABA in the cord); and lowering of the external Cl − concentration. Similarly taurine is probably not significant since the taurine antagonist, TAG, increased the amount of spontaneous activity. On the other hand, (−)-baclofen, which is thought to reduce excitatory amino acid release, d,l-α-aminoadipic acid, α,ɛ-diaminopimelic acid, and 2-amino-4-phosphonobutyric acid, which are believed to be selective postsynaptic excitatory amino acid antagonists, and [ d-Pro 2- d-Phe 7- d-Trp 9]-substance P, a postsynaptic blocker of the action of substance P, markedly and reversibly reduced sDRPs. Experiments were performed on isolated cords without supraspinal or afferent input; therefore sDRPs must be generated by intraspinal structures. It would seem that interneurons are responsible because addition of mephenesin or pentobarbital — compounds which inhibit polysynaptic reflex transmission involving interneurons — reduced the production of sDRPs. sDRPs may result from the action of excitatory transmitters such as l-glutamate, l-aspartate, or substance P released by interneuronal firing in the spinal cord. Moreover, because sDRPs were increased by application of yohimbine, corynanthine and propanolol and reduced by haloperidol, such interneurons may be under descending control of adrenergic and dopaminergic fibers.

Dendrobine, an antagonist of beta-alanine, taurine and of presynaptic inhibition in the frog spinal cord.

1 The effects of dendrobine and nobiline, alkaloids isolated from Dendrobium nobile, on the electrical activity and on amino acid-induced depolarizations of primary afferent terminals were tested on the frog isolated spinal cord and were compared with those of picrotoxinin and strychnine. 2 Dendrobine (3 X 10(-5) M) caused a slight hyperpolarization in both dorsal and ventral roots and this hyperpolarization was accompanied by the augmentation of the dorsal root potential (DR-DRP) and the ventral root potential and reflex (DR-VRP and DR-VRR). The amplitude of the dorsal root reflex (DR-DRR) however, was reduced significantly. Nobiline (3 X 10(-5) M) had no significant effect on either the root potentials or the reflexes. 3 Dendrobine (3 X 10(-5) M) reduced the dorsal root potential induced by repetitive antidromic stimulation of ventral root (VR-DRP) as well as diminishing the maximum rate of rise of the dorsal root potential induced by the stimulation of adjacent dorsal roots (DR-DRP), during which time the amplitude of the DR-DRP was seen to be augmented. 4 Dendrobine (3 X 10(-5) M) reduced the beta-alanine- and taurine-induced depolarizations of primary afferent terminals, while having little effect upon GABA- and glycine-induced depolarizations. 5 Dendrobine (10(-5) M) reversibly blocked the presynaptic inhibition caused by antidromic conditioning stimulation of the ventral root. 6 These effects of dendrobine were qualitatively similar to those of strychnine but were somewhat different from those of picrotoxinin, a molecule having the same picrotoxane skeleton. 7 The present results are discussed with reference to the likely neurotransmitters involved in presynaptic inhibition in the frog spinal cord, and with respect to the structure-activity relationship of picrotoxane compounds as amino acid antagonists.

The cell bodies of origin of sympathetic and sensory axons in some skin and muscle nerves of the cat hindlimb.

Cell bodies of sensory and sympathetic axons projecting to skin and skeletal muscle of the cat hindlimb have been labeled retrogradely with horseradish peroxidase (HRP) in order to study location, size, and numbers of the somata of these neurons. HRP was applied to the freshly transected axons of nerves supplying hairy skin (superficial peroneal, SP; sural, Su), hairy and hairless skin of the paw (medial plantar, MP), or skeletal muscle (gastrocnemius-soleus, GS). Serial sections of lumbosacral dorsal root and sympathetic ganglia were studied after standard histochemical processing. Additionally, the numbers of myelinated fibers in the same nerves were determined. All sensory somata and 99.4% of sympathetic cell bodies were located ipsilaterally. Sensory somata were commonly restricted to two adjacent dorsal root ganglia (usually L6-7 for SP, MP; L7-S1 for Su, GS). Although sympathetic somata were more widely distributed rostrocaudally, their maximum frequency always occurred in the segmental ganglia immediately rostral to the sensory outflows, i.e., corresponding to rami communicantes grisei. Dimensions of sympathetic somata varied little between populations projecting to different tissues and were unimodally distributed. The size distributions of sensory somata were characterized by a peak between 10 and 20 microns radius, similar to sympathetic somata, and a varying smaller number of cells ranging up to 60 microns radius. Each nerve had a characteristic distribution profile of afferent somata. A population of very small cells was only present in GS, while the largest sensory somata in GS and MP were bigger than those in SP and Su. Numerical analysis of the data disclosed the characteristic composition of both myelinated and unmyelinated fibers in each nerve studied.

GABA-mediated responses are not selectively depressed by 3-mercaptopropionic acid in the spinal cord.

The competitive inhibitor of glutamic acid decarboxylase (GAD), 3-mercaptopropionic acid (MPA), causes depletion of gamma-aminobutyric acid and convulsions. We expected it to be a superior GABA depleting agent for in vivo experiments to the frequently used semicarbazide. The dorsal root potentials (DRP) and monosynaptic reflex responses (MSR) evoked by adjacent dorsal root and peripheral nerve stimulation, respectively, were recorded in spinal unanaesthetized cats. MPA (100-200 mg/kg) caused a gradual decrease in DRP, reaching a peak in about 40 min after drug administration. This was usually associated with convulsive activity. Postsynaptic direct inhibition was not substantially affected. However, the MSR was consistently decreased, within 10 min after injection of MPA. It is concluded that MPA is not a suitable tool, at least in the spinal cord, for the selective reduction of GABAergic transmission.

Selective action of piretanide on primary afferent GABA responses in the frog spinal cord

The effects of piretanide, a drug which blocks active chloride transport in other systems, was examined on amino acid responses and synaptic potentials in the frog spinal cord. It was found that piretanide had no effect on GABA ventral root hyperpolarizing responses, but abolished dorsal root depolarizing responses. Dorsal root glutamate responses were little affected by piretanide. The depression of GABA responses on dorsal root ganglion cells was accompanied by a large decrease in the conductance change elicited by GABA. In addition, there was a small shift of the GABA equilibrium potential toward the resting membrane potential, which is consistent with a reduced inward pumping of chloride ions. Piretanide abolished the dorsal root potential elicited by ventral root stimulation. In addition it reduced the early part of the dorsal root potential evoked by stimulating an adjacent dorsal root but had remarkably little effect on the late phase.

Anisatin, a potent GABA antagonist, isolated from Illicium anisatum

The neuropharmacological properties of anisatin were tested on the frog spinal cord and the crude synaptic membrane from rat brain. Anisatin (10 −5 M) reduced the amplitude of dorsal root potentials induced by stimulation of the adjacent dorsal root and presynaptic inhibition of the ventral root reflex. Anisatin shifted the dose-response curve for GABA-induced depolarization in the primary afferent terminal to the right and also reduced the maximum response to GABA. [ 3H]Muscimol binding to the crude synaptic membrane was not inhibited by anisatin. These results indicate that anisatin is a picrotoxin-like, non-competititve GABA-antagonist.

The immaturity of interactions between GABA-and benzodiazepine binding sites in the frog spinal cord

1. 1. In the isolated frog spinal cord, diazepam had little effect on dorsal root responses to both adjacent dorsal root stimulation and exogenous GABA. 2. 2. [ 3H]diazepam and [ 3H]muscimol bound specifically to the crude synaptic membrane of the spinal cord and both binding sites revealed interactions different from those reported in the case of the rat. 3. 3. [ 3H]muscimol binding to the freshly prepared membrane of the spinal cord showed two different K D values, and here, Triton X-100 treatment was without effect. 4. 4. The lack of the potentiation by diazepam of GABA-mediated synaptic effects in the frog spinal cord is probably due to an immaturity of the functional unit.

Characteristics of dorsal root potentials recorded from the isolated spinal cord of the neonate rat.

Dorsal root potentials (DRP) and dorsal root reflexes (DRR) have been recorded from the isolated cord of the neonate rat. A single stimulus to the adjacent rostral or adjacent caudal dorsal root or dorsal columns evoked a DRP, the peak amplitude of which was reached in 110--115 msec and which decayed exponentially over most of its time course (time constant 800--850 msec). The same stimuli evoked field potentials in the dorsal horn comprising fast negative, slow negative and slow positive potentials. DRP had a lower threshold than DRR and reached a maximal amplitude at stimulus voltages sub-maximal for DRR. Increasing the intensity of stimulation shortened the latency of DRP and prolonged its time course. DRR and DRP were depressed by a prior conditioning stimulus (CS) and by the addition of Mg++ ions to the bathing solution. A CS was more effective in producing depression of responses evoked more rostrally than more caudally.