Noradrenaline suppression of the spinal efferent component of the pressor reflexes

Noradrenaline applied to the dorsal surface of spinal cord segments C6-T1 suppressed the pressor components of the blood pressure reflexes evoked by stimulation of radial nerve afferents in anesthetized cats. Noradrenaline applied to spinal cord segments L4-S1 suppressed pressor reflexes elicited by stimulation of tibial nerve afferents. The increase in noradrenaline concentration from 0.05 to 0.2% enhanced the duration and intensity of this effect.     

The effect of morphine on the input neuronal system of the spinal cord, participating in the formation of nociceptive pressor reflexes]

Effect of morphine applied to the spinal cord segments L4-S2 or C6-tI on pressor reflexes evoked by supramaximal stimulation of radial and tibial nerve with low frequency (I-2 Hz) was studied in anesthetized cats. Only pressor reflexes elicited by excitation of the tibial nerve afferents were suppressed by morphine applied to the L4-S2 segments. This effect was characterized by diminution of amplitude and steepness of the reflexes and by augmentation of their latency. Both the degree and the rate of the reflex suppression were found to enhance with increasing of morphine concentration from 0.02 to 0.5%. When applied to C6-tI segments, morphine did not suppress the pressor reflexes to the tibial nerve stimulation while reflexes to the radial nerve signals were decreased considerably. In addition to this local action of morphine, the effects resulting from it's distant action, namely, some reduction in systemic arterial pressure and an increase of pressor reflexes evoked by afferent signals entering into the spinal cord segments remote from the application region, were found to occur. All these effects were reversed by naloxone (0.2 mg/kg i. v.). It is concluded that along with attenuation of different withdrawal components of the defence reaction, action of morphine on the opiate receptors of some neurons situated near the entrance of afferent signals into the spinal cord results in suppression of the circulatory components of this reaction.     

Estrogen attenuates the exercise pressor reflex in female cats.

In humans, the pressor and muscle sympathetic nerve responses to static exercise are less in women than in men. The difference has been attributed to the effect of estrogen on the exercise pressor reflex. Estrogen receptors are abundant in areas of the dorsal horn receiving input from group III and IV muscle afferents, which comprise the sensory limb of the exercise pressor reflex arc. These findings prompted us to investigate the effect of estrogen on the spinal pathway of the exercise pressor reflex arc. Previously, we found that the threshold concentration of 17beta-estradiol needed to attenuate the exercise pressor reflex in male decerebrate cats was 10 microg/ml (Schmitt PM and Kaufman MP. J Appl Physiol 94: 1431-1436, 2003). The threshold concentration for female cats, however, is not known. Consequently, we applied 17beta-estradiol to a well covering the L6-S1 spinal cord in decerebrate female cats. The exercise pressor reflex was evoked by electrical stimulation of the L7 or S1 ventral root, a maneuver that caused the hindlimb muscles to contract statically. We found that the pressor response to contraction averaged 38 +/- 7 mmHg before the application of 17beta-estradiol (0.01 microg/ml) to the spinal cord, whereas it averaged only 23 +/- 4 mmHg 30 min after application (P < 0.05). Recovery of the pressor response to contraction was not obtained for 2 h after application of 17beta-estradiol. Application of 17beta-estradiol in a dose of 0.001 microg/ml had no effect on the exercise pressor reflex (n = 5). We conclude that the concentration of 17beta-estradiol required to attenuate the exercise pressor reflex is 1,000 times more dilute in female cats than that needed to attenuate this reflex in male cats.     

Estrogen's attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats.

Using gonadally intact female cats, we showed previously that estrogen, applied topically to the spinal cord, attenuated the exercise pressor reflex. Although the mechanism by which estrogen exerted its attenuating effect is unknown, this steroid hormone has been shown to influence spinal opioid pathways, which in turn have been implicated in the regulation of the exercise pressor reflex. These findings prompted us to test the hypothesis that opioids mediate the attenuating effect of estrogen on the exercise pressor reflex in both gonadally intact female and ovariectomized cats. We therefore applied 200 microl of 17beta-estradiol (0.01 microg/ml) with and without the addition of 1,000 microg naloxone, a mu- and delta-opioid antagonist, to a spinal well covering the L6-S1 spinal cord in decerebrated female cats that were either gonadally intact or ovariectomized. The exercise pressor reflex was evoked by electrical stimulation of the L7 or S1 ventral root, a maneuver that caused the hindlimb muscles to contract statically. We found that, in gonadally intact cats, the attenuating effect of estrogen was more pronounced than that in ovariectomized cats. We also found that, in gonadally intact female cats, naloxone partly reversed the attenuation of the pressor response to static contraction caused by spinal estrogen application. For example, in intact cats, the pressor response to contraction before estrogen application averaged 39 +/- 4 mmHg (n = 10), whereas the pressor response 60 min afterward averaged only 18 +/- 4 mmHg (P < 0.05). In contrast, the pressor response to contraction before estrogen and naloxone application averaged 33 +/- 5 mmHg (n = 11), whereas afterward it averaged 27 +/- 6 mmHg (P < 0.05). In ovariectomized cats, naloxone was less effective in reversing the attenuating effect of estrogen on the exercise pressor reflex.     

Permanent alterations of spinal cord reflexes following nerve lesion in newborn rats

Sciatic nerve lesion in newborn rats is known to cause degeneration of a large number of axotomized motoneurones and spinal ganglion cells. Some of the surviving motoneurones exhibit abnormal firing properties and the projection pattern of central terminals of sensory neurones is altered. We report here on long-term changes in spinal cord reflexes in adult rats following neonatal nerve crush. In acutely spinalized and anaesthetized adult rats 4-6 months old in which the sciatic nerve had been crushed on one side at birth, the tibial nerve, common peroneal nerve or sural nerve were stimulated on the reinnervated and control side and reflex responses were recorded from the L5 ventral spinal roots. Ventral root responses (VRRs) to tibial and peroneal nerve stimulation on the side of the nerve lesion were significantly smaller in amplitude representing only about 15% of the mean amplitude of VRRs on the control side. The calculated central delay of the first, presumably monosynaptic component of the VRR potential was 1.6 ms on the control side while the earliest VRR wave on the side of the nerve lesion appeared after a mean central latency of 4.0 ms that seems too long to be of monosynaptic origin. These results suggest that neonatal sciatic nerve injury markedly alters the physiological properties and synaptic connectivity in spinal cord neurones and causes a marked depression of spinal cord responses to peripheral nerve stimulation.     

Dorsal root tetrodotoxin-resistant sodium channels do not contribute to the augmented exercise pressor reflex in rats with chronic femoral artery occlusion

We investigated the contribution of tetrodotoxin (TTX)-resistant sodium channels to the augmented exercise pressor reflex observed in decerebrated rats with femoral artery ligation. The pressor responses to static contraction, to tendon stretch, and to electrical stimulation of the tibial nerve were compared before and after blocking TTX-sensitive sodium channels on the L3-L6 dorsal roots of rats whose hindlimbs were freely perfused and rats whose femoral arteries were ligated 72 h before the start of the experiment. In the freely perfused group (n=9), pressor (Δ22±4 mmHg) and cardioaccelerator (Δ32±6 beats/min) responses to contraction were attenuated by 1 μM TTX (Δ4±1 mmHg, P<0.05 and Δ17±4 beats/min, P<0.05, respectively). In the 72 h ligated group (n=9), the augmented pressor response to contraction (32±4 mmHg) was also attenuated by 1 μM TTX (Δ8±2 mmHg, P<0.05). The cardioaccelerator response to contraction was not significantly attenuated in these rats. In addition, TTX suppressed the pressor response to tendon stretch in both groups of rats. Electrical stimulation of the tibial nerve evoked similar pressor responses between the two groups (freely perfused: Δ74±9 mmHg and 72 h ligated: Δ78±5 mmHg). TTX attenuated the pressor response to the tibial nerve stimulation by about one-half in both groups. Application of the TTX-resistant sodium channel blocker A-803467 (1 μM) with TTX (1 μM) did not block the pressor response to tibial nerve stimulation to any greater extent than did application of TTX (1 μM) alone. Although the contribution of TTX-resistant sodium channels to the augmented exercise pressor reflex may be slightly increased in rats with chronic femoral artery ligation, TTX-resistant sodium channels on dorsal roots do not play a major role in the augmented exercise pressor reflex.     

Remote electrodermic response to an algogenic stimulus. Pathway and spinal integration

The pathway of a non-segmental sudomotor reflex was studied in rabbits (New Zealand white). By means of thermic stimulation (45 degrees during 30") at the lateral border of the foot, a sudoral response was evoked in a circumscribed area of the pinna. By sequential sections of different nerves and the nervous network around the saphenous and femoral vessels, it was possible to establish the following afferent pathways to the spinal cord: lateral plantar nerve, tibial nerve up to the tuber calcanei, saphenous perivascular network, femoral perivascular network and femoral nerve. The fibres responsible for the podo-auricular sudomotor reflex penetrate into the spinal cord above L4, because the spinal transection at this level does not alter the auricular response. Since the hemisection of the spinal cord at T6 suppresses this reflex in the pinna of the same side, it must be concluded that the spinal pathway is ipsilateral. The efferent pathway abandons the spinal cord beneath segment C6: in fact, the spinal transection at C6 does not alter the auricular response to plantar stimulation. Finally, the sudomotor impulses reach the pinna sweat glands with the auricular vessels.     

Role of the various groups of afferent fibers of the mesenteric nerves in vasomotor reflexes

The dependence of the magnitude and character of vasomotor reflexes on the amplitude of tetanic stimulation of the mesenteric nerves was investigated in experiments on anesthetized cats. Comparison of the results of analysis of the stimulus amplitude versus reflex magnitude curves with previous data on excitability of the various groups of mesenteric nerve fibers revealed three groups of "vasomotor" afferents with different conduction velocities: fast-conducting Aδ-fibers (conduction velocity over 8 m/sec) evoking depressor or small pressor reflexes; slow-conducting Aδ-fibers (conduction velocity below 8 m/sec), evoking pressor reflexes or, by interaction with impulses of lower-threshold, fast-conducting Aδ-fibers, either reduce the magnitude of the depressor reflexes evoked by those impulses or increase the corresponding pressor reflexes; C-fibers increasing the magnitude of the pressor reflexes evoked by slow-conducting A-fibers.     

AMINO ACID AND SUBSTANCE P CONTENTS IN SPINAL CORD OF CATS WITH EXPERIMENTAL HIND-LIMB RIGIDITY PRODUCED BY OCCLUSION OF SPINAL CORD BLOOD SUPPLY

Abstract— Experimental hind-limb rigidity of spinal origin was produced in cats by temporary occlusion of thoracic aorta and internal mammary arteries. In the lumbar segments (L6- S1) of these rigid cats, the monosynaptic reflex recorded from ventral roots was enhanced whereas the polysynaptic reflexes as well as the dorsal root reflexes were almost abolished. On morphological examination of the lumbar spinal cord, the number of interneurons was greatly reduced, whereas the small sized cells, presumably glial cells, were increased by about two times. Ventral horn motoneurons were also reduced. The lumbar spinal cords of the rigid cats were analysed for amino acid and substance P contents. Four major amino acids, aspartate, glutamate, glycine and GABA, were definitely reduced in both grey and white matter except that the glutamate level in the dorsal white was within the normal range. Content and distribution pattern of substance P were not altered in the lumbar cord of the rigid cats. These results are consistent with the notions that GABA occurs in the dorsal horn interneurons subserving primary afferent depolarisation, and that substance P is concentrated in primary afferent fibre terminals. The implications of the decrease of aspartate, glutamate and glycine in the spinal cord of rigid cats are discussed.     

Interlimb Reflexes Induced by Electrical Stimulation of Cutaneous Nerves after Spinal Cord Injury

Whether interlimb reflexes emerge only after a severe insult to the human spinal cord is controversial. Here the aim was to examine interlimb reflexes at rest in participants with chronic (>1 year) spinal cord injury (SCI, n = 17) and able-bodied control participants (n = 5). Cutaneous reflexes were evoked by delivering up to 30 trains of stimuli to either the superficial peroneal nerve on the dorsum of the foot or the radial nerve at the wrist (5 pulses, 300 Hz, approximately every 30 s). Participants were instructed to relax the test muscles prior to the delivery of the stimuli. Electromyographic activity was recorded bilaterally in proximal and distal arm and leg muscles. Superficial peroneal nerve stimulation evoked interlimb reflexes in ipsilateral and contralateral arm and contralateral leg muscles of SCI and control participants. Radial nerve stimulation evoked interlimb reflexes in the ipsilateral leg and contralateral arm muscles of control and SCI participants but only contralateral leg muscles of control participants. Interlimb reflexes evoked by superficial peroneal nerve stimulation were longer in latency and duration, and larger in magnitude in SCI participants. Interlimb reflex properties were similar for both SCI and control groups for radial nerve stimulation. Ascending interlimb reflexes tended to occur with a higher incidence in participants with SCI, while descending interlimb reflexes occurred with a higher incidence in able-bodied participants. However, the overall incidence of interlimb reflexes in SCI and neurologically intact participants was similar which suggests that the neural circuitry underlying these reflexes does not necessarily develop after central nervous system injury.     

Prolonged poststimulation inhibition of bladder activity induced by tibial nerve stimulation in cats

Inhibition of bladder activity by tibial nerve stimulation was investigated in α-chloralose-anesthetized cats with an intact spinal cord. Short-duration (3-5 min) tibial nerve stimulation at both low (5 Hz) and high (30 Hz) frequencies applied repeatedly during rhythmic isovolumetric bladder contractions was effective in inhibiting reflex bladder activity. Both frequencies of stimulation were also effective in inducing inhibition that persisted after the termination of the stimulation. The poststimulation inhibitory effect induced by the short-duration stimulation significantly increased bladder capacity to 181.6 ± 24.36% of the control capacity measured before applying the stimulation. Thirty-minute continuous stimulation induced prolonged poststimulation inhibition of bladder activity, which lasted for more than 2 h and significantly increased bladder capacity to 161.1 ± 2.9% of the control capacity. During the poststimulation periods, 5-Hz stimulation applied during the cystometrogram elicited a further increase (~30% on average) in bladder capacity, but 30-Hz stimulation was ineffective. These results in cats support the clinical observation that tibial nerve neuromodulation induces a long-lasting poststimulation inhibitory effect that is useful in treating overactive bladder symptoms.     

The influence of the adrenal glands upon acute spinal cord injury

The contribution of the adrenal glands to the pressor and nerve tissue necrotic responses that follow acute paralyzing spinal cord injury was determined in cats by total adrenal gland removal. The study suggests that either epinephrine or endogenous steroids may exert posttraumatic protective influences on the cord since after adrenalectomy, both the systematic pressor response and local hemorrhagic necrosis are significantly increased.     

Dorsal horn administration of muscimol abolishes the muscle pressor reflex.

The purpose of this study was to determine the effect of blocking synaptic transmission in the dorsal horn on the cardiovascular responses produced by activation of muscle afferent neurons. Synaptic transmission was blocked by applying the GABA(A) agonist muscimol to the dorsal surface of the spinal cord. Cats were anesthetized with alpha-chloralose and urethane, and a laminectomy was performed. With the exception of the L(7) dorsal root, the dorsal and ventral roots from L(5) to S(2) were sectioned on one side, and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L(7) and S(1) ventral roots. The dorsal surface of the L(4)--S(3) segments of the spinal cord were enclosed within a "well" created by applying layers of vinyl polysiloxane. Administration of a 1 mM solution of muscimol (based on dose-response data) into this well abolished the reflex pressor response to contraction (change in mean arterial blood pressure before was 47 +/- 7 mmHg and after muscimol was 3 +/- 2 mmHg). Muscle stretch increased mean arterial blood pressure by 30 +/- 8 mmHg before muscimol, but after drug application stretch increased MAP by only 3 +/- 2 mmHg. Limiting muscimol to the L(7) segment attenuated the pressor responses to contraction (37 +/- 7 to 24 +/- 11 mmHg) and stretch (28 +/- 2 to 16 +/- 8 mmHg). These data suggest that the dorsal horn of the spinal cord contains an obligatory synapse for the pressor reflex. Furthermore, these data support the hypothesis that branches of primary afferent neurons, not intraspinal pathways, are responsible for the multisegmental integration of the pressor reflex.     

Alterations in growth-associated protein (GAP-43) expression in lower urinary tract pathways following chronic spinal cord injury

Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways 6 or 8 weeks following complete spinal cord transection (~ T9). In control animals, expression of GAP-43 was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the corticospinal tract; (3) the dorsal horn; and (4) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (5) in the lateral collateral pathway of Lissauer in L6-S1 spinal segments. Densitometry analysis has demonstrated significant increases (p 0.001; 1.3-6.4-fold increase) in GAP-43-immunoreactivity (IR) in these regions of the rostral lumbar (L1-L2) and caudal lumbosacral (L6-S1) spinal cord 6 weeks following spinal cord injury. Changes in GAP-43-IR were restricted to the L1-L2 and L6-S1 segments that are involved in lower urinary tract reflexes. Changes in GAP-43-IR were not observed at the L5 segmental level except for an increase in GAP-43-IR in the superficial, dorsal horn at 6 weeks post-injury. In all segments examined, GAP-43-IR was decreased (2-5-fold) in the corticospinal tract (dorsal division) 6 and 8 weeks following spinal cord injury. Eight weeks following spinal cord injury, changes in GAP-43-IR had returned to control levels except for the persistence of increased GAP-43-IR in the region of the sacral parasympathetic nucleus and the lateral collateral pathway in the S1 spinal segment. Alterations in GAP-43-IR following chronic spinal cord injury may suggest a reorganization of bladder afferent projections and spinal elements involved in urinary bladder reflexes consistent with alterations in urinary bladder function (hyperreflexia) observed in animals following spinal cord injury above the lumbosacral spinal cord.     

Alterations in growth-associated protein (GAP-43) expression in lower urinary tract pathways following chronic spinal cord injury

Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways 6 or 8 weeks following complete spinal cord transection (approximately T9). In control animals, expression of GAP-43 was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the corticospinal tract; (3) the dorsal horn; and (4) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (5) in the lateral collateral pathway of Lissauer in L6-S1 spinal segments. Densitometry analysis has demonstrated significant increases (p < or =0.001; 1.3-6.4-fold increase) in GAP-43-immunoreactivity (IR) in these regions of the rostral lumbar (L1-L2) and caudal lumbosacral (L6-S1) spinal cord 6 weeks following spinal cord injury. Changes in GAP-43-IR were restricted to the L1-L2 and L6-S1 segments that are involved in lower urinary tract reflexes. Changes in GAP-43-IR were not observed at the L5 segmental level except for an increase in GAP-43-IR in the superficial, dorsal horn at 6 weeks post-injury. In all segments examined, GAP-43-IR was decreased (2-5-fold) in the corticospinal tract (dorsal division) 6 and 8 weeks following spinal cord injury. Eight weeks following spinal cord injury, changes in GAP-43-IR had returned to control levels except for the persistence of increased GAP-43-IR in the region of the sacral parasympathetic nucleus and the lateral collateral pathway in the S1 spinal segment. Alterations in GAP-43-IR following chronic spinal cord injury may suggest a reorganization of bladder afferent projections and spinal elements involved in urinary bladder reflexes consistent with alterations in urinary bladder function (hyperreflexia) observed in animals following spinal cord injury above the lumbosacral spinal cord.     

Electrical activity in sympathetic fibres to hind limb muscles of the cat produced by hypothalamic stimulation

Electrical stimulation of the "Defence Area" of the hypothalamus in anaesthetized cats was accomplished by stereotaxic placement of bipolar stainless steel electrodes; the spinal cord was sectioned at L4. The muscle blood flow in one hind limb was recorded with an electromagnetic flowmeter. Increases of between 100% and 300% were observed during hypothalamic stimulation. Electroneurographic recordings from small nerve filaments supplying tibialis anterior muscle revealed two populations of neurones whose activity was abolished by lumbar sympathectomy. It appears that the increased blood flow in skeletal muscle during stimulation of the hypothalamic "Defence Area" is brought about by a simultaneous inhibition of vasoconstrictor activity and increase in cholinergic vasodilator discharge.     

Effects of peripheral inputs from hindlimb on the monosynaptic reflex of motoneurons innervating tail muscles.

The effects of group II muscle (PBSt, GS) and cutaneous afferent (Sur, SPc, Tib) inputs from the hindlimb on the monosynaptic reflexes of motoneurons innervating tail muscles were studied in lower spinalized cats. Stimulation of the cutaneous nerves at the conditioning-test stimulus interval of about 10-20 ms facilitated and inhibited the monosynaptic reflexes of ipsilateral and contralateral tail muscles, respectively. The effects of the muscle nerve stimulation were not so prominent as those elicited by cutaneous nerve stimulation. The monosynaptic reflex was also inhibited by muscle nerve stimulation at 10-50 ms intervals. The effects of conditioning stimulation of the hindlimb peripheral nerves at short intervals were depressed or blocked by section of the ipsilateral lateral funiculus at S1 spinal segment. These findings show that the neuronal pathway from hindlimb afferents to tail muscle motoneurons passed the lateral funiculus of the spinal cord and modulates the motoneuronal activity of tail muscles.     

Mechanism of hypothalamic control of cardiac component of sinus nerve reflex.

The modulatory influence of hypothalamic structures on sinus nerve induced bradycardia was investigated in anaesthetized cats. Stimulation of the hypothalamic defence area inhibits the bradycardia produced by sinus nerve stimulation both in intact animals and also in animals with the spinal cord sectioned at C1 or C6. This inhibition was accompanied in the normal animal by an increased sympathetic discharge and by a sustained inspiration or tachypnoea. The same respiratory effects were noted in a spontaneously breathing C6 spinal animal, while an artificially ventilated C1 spinal animal still displayed a powerful central inspiratory drive in its recurrent laryngeal electroneurogram. The presence of central inspiratory activity was found to be an absolute impediment to the development of bradycardia. If this activity was eliminated by simultaneous stimulation of the superior laryngeal nerve, it was possible to obtain bradycardia during combined sinus nerve and hypothalamic defence area stimulation, though this bradycardia was modified by the presence of sympathetic discharge. The level of sympathetic neural discharge affects the magnitude of the bradycardia produced by sinus nerve stimulation. The bradycardia was less with normal or augmented level of sympathetic activity and was greater if this activity was reduced or absent. A lesion just caudal to the mammillary bodies disclosed a tonic hypothalamic influence both on respiration and on sympathetic discharge; stimulation of the sinus nerve produced a much more powerful bradycardia after the lesion. The existence of a respiratory "gate" through which afferent stimuli pass on their way to the nucleus ambiguus, and which can be operated by the hypothalamic defence and depressor areas, is postulated and discussed.     

Fictive locomotion and scratching inhibit dorsal horn neurons receiving thin fiber afferent input

In decerebrate paralyzed cats, we examined the effects of two central motor commands (fictive locomotion and scratching) on the discharge of dorsal horn neurons receiving input from group III and IV tibial nerve afferents. We recorded the impulse activity of 74 dorsal horn neurons, each of which received group III input from the tibial nerve. Electrical stimulation of the mesencephalic locomotor region (MLR), which evoked fictive static contraction or fictive locomotion, inhibited the discharge of 44 of the 64 dorsal horn neurons tested. The mean depth from the dorsal surface of the spinal cord of the 44 neurons whose discharge was inhibited by MLR stimulation was 1.77 +/- 0.04 mm. Fictive scratching, evoked by topical application of bicuculline to the cervical spinal cord and irritation of the ear, inhibited the discharge of 22 of the 29 dorsal horn neurons tested. Fourteen of the twenty-two neurons whose discharge was inhibited by fictive scratching were found to be inhibited by MLR stimulation as well. The mean depth from the dorsal surface of the cord of the 22 neurons whose discharge was inhibited by fictive scratching was 1.77 +/- 0.06 mm. Stimulation of the MLR or the elicitation of fictive scratching had no effect on the activity of 22 dorsal horn neurons receiving input from group III and IV tibial nerve afferents. The mean depth from the dorsal surface of the cord was 1.17 +/- 0.07 mm, a value that was significantly (P < 0.05) less than that for the neurons whose discharge was inhibited by either MLR stimulation or fictive scratching. We conclude that centrally evoked motor commands can inhibit the discharge of dorsal horn neurons receiving thin fiber input from the periphery.