Depth cues,rather than perceived depth,govern vergence

Transmission of information from the terminals group II muscle afferents is subject to potent presynaptic modulation by both segmental group II and cutaneous afferents and by descending monoaminergic systems. Currently it is unknown whether descending corticospinal fibres affect this transmission. Here we have examined whether corticospinal tract activation modulates the size of monosynaptic focal synaptic potentials (FSPs) evoked by group II muscle afferents, and the excitability of intraspinal terminals of group II afferents, both of which are indices used to show presynaptic control. Conditioning stimulation of corticospinal pathways had no effects on the sizes of group II evoked FSPs in the midlumbar or sacral segments at either dorsal horn or intermediate zone locations. These stimuli also had no effect on the excitability of single group II afferent terminals in the dorsal horn of the midlumbar segments. As positive controls, we verified that the corticospinal conditioning stimuli used did effectively depress FSPs evoked from cutaneous afferents recorded at the same spinal locations as the group II field potentials in all experiments. Corticospinal tract conditioning stimuli did not consistently enhance or reduce the depression of group II FSPs that was evoked by stimulation of ipsilateral segmental group II or cutaneous afferents; in the large majority of cases there was no effect. The results reveal that the control of transmission of information from group II afferents in these regions of the spinal cord is independent of direct corticospinal control. N.C. Aggelopoulos and S. Chakrabarty equally contributed to this work.     

John Eccles' studies of spinal cord presynaptic inhibition

Presynaptic inhibition is one of many areas of neurophysiology in which Sir John Eccles did pioneering work. Frank and Fuortes first described presynaptic inhibition in 1957. Subsequently, Eccles and his colleagues characterized the process more fully and showed its relationship to primary afferent depolarization. Eccles' studies emphasized presynaptic inhibition of the group Ia monosynaptic reflex pathway but also included group Ib, II and cutaneous afferent pathways, and the dorsal column nuclei. Presynaptic inhibition of the group Ia afferent pathway was demonstrated by depression of monosynaptic excitatory postsynaptic potentials and inhibition of monosynaptic reflex discharges. Primary afferent depolarization was investigated by recordings of dorsal root potentials, dorsal root reflexes, cord dorsum and spinal cord field potentials, and tests of the excitability of primary afferent terminals. Primary afferent depolarization was proposed to result in presynaptic inhibition by reducing the amplitude of the action potential as it invades presynaptic terminals. This resulted in less calcium influx and, therefore, less transmitter release. Presynaptic inhibition and primary afferent depolarization could be blocked by antagonists of GABA(A) receptors, implying a role of interneurons that release gamma aminobutyric acid in the inhibitory circuit. The reason why afferent terminals were depolarized was later explained by a high intracellular concentration of Cl(-) ions in primary sensory neurons. Activation of GABA(A) receptors opens Cl(-) channels, and Cl(-) efflux results in depolarization. Another proposed mechanism of depolarization was an increase in extracellular concentration of K(+) following neural activity. Eccles' work on presynaptic inhibition has since been extended in a variety of ways.     

Combined effect of motor imagery and peripheral nerve electrical stimulation on the motor cortex

Although motor imagery enhances the excitability of the corticospinal tract, there are no peripheral afferent inputs during motor imagery. In contrast, peripheral nerve electrical stimulation (ES) can induce peripheral afferent inputs; thus, a combination of motor imagery and ES may enhance the excitability of the corticospinal tract compared with motor imagery alone. Moreover, the level of stimulation intensity may also be related to the modulation of the excitability of the corticospinal tract during motor imagery. Here, we evaluated whether a combination of motor imagery and peripheral nerve ES influences the excitability of the corticospinal tract and measured the effect of ES intensity on the excitability induced during motor imagery. The imagined task was a movement that involved touching the thumb to the little finger, whereas ES involved simultaneous stimulation of the ulnar and median nerves at the wrist. Two different ES intensities were used, one above the motor threshold and another above the sensory threshold. Further, we evaluated whether actual movement with afferent input induced by ES modulates the excitability of the corticospinal tract as well as motor imagery. We found that a combination of motor imagery and ES enhanced the excitability of the motor cortex in the thenar muscle compared with the other condition. Furthermore, we established that the modulation of the corticospinal tract was related to ES intensity. However, we found that the excitability of the corticospinal tract induced by actual movement was enhanced by peripheral nerve ES above the sensory threshold.     

The differential effects of baclofen on segmental and descending excitation of spinal interneurones in the cat

Summary Intravenous baclofen (1–6.25 mg kg^-1) substantially reduced the monosynaptic excitation of neurones in the intermediate nucleus of the cat spinal cord by impulses in group I extensor muscle primary afferent fibres, but had little or no effect on excitation by stimulating fibres of the ipsilateral dorsolateral funiculus or the contralateral red nucleus. Relatively low concentrations of baclofen thus appear not to influence the release of excitatory transmitter from the terminals of rubrospinal, corticospinal and long descending propriospinal fibres, in contrast to the reduction of the release of primary afferent transmitters.     

Amino acids and presynaptic inhibition in the rat cuneate nucleus

1. Presynaptic inhibition was evoked in the rat cuneate nucleus by a peripheral conditioning stimulus. The dicarboxylic amino acid salts glutamate and aspartate and the neutral amino acids glycine and gamma-aminobutyric acid (GABA) were topically applied to a restricted area of the cuneate nucleus and their effects on both resting primary afferent terminal excitability and the increase in excitability of afferent terminals during presynaptic inhibition determined.2. Aspartate had no effect on either resting primary afferent terminal excitability or on the increase in excitability during presynaptic inhibition.3. Glycine reduced both resting primary afferent terminal excitability and presynaptic inhibition.4. Glutamate increased both resting primary afferent terminal excitability and presynaptic inhibition while GABA increased resting primary afferent terminal excitability but reduced the increase in excitability during presynaptic inhibition.5. The convulsant alkaloids picrotoxin (given intravenously) and bicuculline (topically applied) blocked presynaptic inhibition. The blocking action of picrotoxin was overcome by topical application of GABA but not glutamate.6. Simultaneous measurement of pre- and post-synaptic excitability in the cuneate nucleus showed that while glutamate increased excitability at both sites, GABA increased primary afferent terminal excitability but depressed post-synaptic excitability.7. It is concluded that glycine and glutamate exert non-specific actions on primary afferent terminals similar to their effects at post-synaptic sites elsewhere in the C.N.S. while GABA depolarizes primary afferent terminals by a specific action at the same receptor site as the presynaptic inhibitory transmitter. The possibility is discussed that the presynaptic inhibitory transmitter in the cuneate nucleus is GABA or a closely related substance.     

The effect of electrical stimulation of the corticospinal tract on motor units of the human biceps brachii

In healthy human subjects, descending motor pathways including the corticospinal tract were stimulated electrically at the level of the cervicomedullary junction to determine the effects on the discharge of motoneurones innervating the biceps brachii. Post-stimulus time histograms (PSTHs) were constructed for 15 single motor units following electrical stimulation of the corticospinal tract and for 11 units following electrical stimulation of large diameter afferents at the brachial plexus. Responses were assessed during weak voluntary contraction. Both types of stimulation produced a single peak at short latency in the PSTH (mean 8.5 and 8.7 ms, respectively) and of short duration (< 1.4 ms). In separate studies, we compared the latency of the responses to electrical stimulation of the corticospinal tract in the relaxed muscle with that in the contracting muscle. The latency was the same in the two conditions when the intensity of the stimulation was adjusted so that responses of the same size could be compared. Estimates of the descending conduction velocity and measurements of presumed peripheral conduction time suggest that there is less than 0.5 ms for spinal events (including synaptic delays). We propose that in response to electrical stimulation of the descending tract fibres, biceps motoneurones receive a large excitatory input with minimal dispersion and it presumably contains a dominant monosynaptic component.     

Primary afferent depolarization and inhibory interactions in spinal cord of the stingray, Dasyatis sabina

1. Excitability changes in primary afferents and inhibitory interactions in evoked spinal cord activity were investigated in unanesthetized stingrays (Dasyatis subina) with high cervical spinal transections. 2. Primary afferent excitability increases following a conditioning stimulus to an adjacent segmental nerve were demonstrated with the Wall (31) technique. 3. Stimulation of A-alpha,beta and A-delta afferent fibers produced excitability increases in both A-alpha,beta and delta-fibers of the adjacent segment. 4. The excitability increase had a latency of about 10 ms, it peaked around 25 ms, and the change lasted more than 100 ms. 5. The central afferent volley in A-alpha,beta fibers and the N1- and late negative waves due to postsynaptic activity of dorsal horn interneurons were reduced by conditioning volleys in adjacent afferent nerves. The time course of the inhibition paralleled that of the excitability increases in afferent terminal arborizations, suggesting that the depression of postsynaptic activity is, at least in part, due to presynaptic inhibition. 6. Reduction of evoked discharges and excitatory postsynaptic potentials was observed in recordings from interneurons with a time course similar to that of the primary afferent depolarization (PAD). 7. Conditioning volleys in afferents of adjacent peripheral nerves produced facilitation or inhibition of segmental reflexes.     

Ammonium decreases excitatory synaptic transmission in cat spinal cord in vivo

1. Glutamine is thought to be a precursor of the pool of glutamate that is used as synaptic transmitter. NH4+ inhibits glutaminase, the enzyme presumed to cleave glutamine into glutamate in synaptic terminals. Therefore a decrease by NH4+ of excitatory synaptic transmission in hippocampus was suggested to be due to the inability to utilize glutamine as a precursor for glutamate and subsequent transmitter depletion. This study reexamines the effects of NH4+ on excitatory synaptic transmission. 2. The effects of NH4+ on excitatory synaptic transmission from low-threshold afferent fibers, presumably Ia-afferent fibers, to motoneurons was investigated in the spinal cord of anesthetized cats in vivo. 3. Action potentials of low-threshold afferent fibers were recorded at the entry of the dorsal roots into the spinal cord. An extracellular electrode within a motoneuron nucleus recorded the action potential of low-threshold afferent fibers and the extracellular monosynaptic excitatory postsynaptic potential, i.e., the focal synaptic potential (FSP). This extracellular electrode also recorded the antidromic field potential (AFP) in response to ventral root stimulation. Electrodes on the ventral roots recorded the monosynaptic reflex (MSR) and the monosynaptic excitatory postsynaptic potential in motoneurons electrotonically conducted into the ventral roots (VR-EPSP). 4. Intravenous infusion of ammonium acetate (AA) reversibly decreased MSR, VR-EPSP, and FSP, i.e., decreased excitatory synaptic transmission. 5. The decrease of VR-EPSP and FSP was accompanied initially by a decrease of conduction and, eventually, a conduction block in presynaptic terminals of low-threshold afferent fibers. 6. The decreases of VR-EPSP and FSP were also accompanied by the transient appearance of a reflex discharge, triggered by VR-EPSPs of decreased amplitude, and changes of the AFP indicating increased invasion of motoneuron somata by antidromic action potentials. 7. It is suggested that NH4+ depolarizes intraspinal Ia-afferent fibers and motoneurons. This depolarization initially decreases and then blocks conduction of action potentials into the presynaptic terminals of Ia-afferent fibers. The conduction block prevents the release of excitatory transmitter and decreases excitatory synaptic transmission. 8. The suggested depolarizing action of NH4+ may be due to K+-like ionic properties of NH4+ and/or an inhibition of K+-uptake into astrocytes. 9. The conduction block in presynaptic terminals of low-threshold afferent fibers can fully explain the decrease of excitatory synaptic transmission by NH4+. Because of the conduction block in presynaptic terminals, this study does not permit a conclusion as to an inhibition by NH4+ fo the utilization of glutamine as a precursor for glutamate used as synaptic transmitter.     

Presynaptic inhibition in the vertebrate spinal cord revisited

The present review examines the experimental evidence supporting the existence of central mechanisms able to modulate the synaptic effectiveness of sensory fibers ending in the spinal cord of vertebrates. The first section covers work on the mode of operation and the synaptic mechanisms of presynaptic inhibition, in particular of the presynaptic control involving axo-axonic synapses made by GABAergic interneurons with the terminal arborizations of the afferent fibers. This includes reviewing of the ionic mechanisms involved in the generation of primary afferent depolarization (PAD) by GABAergic synapses, the ultrastructural basis underlying the generation of PAD, the relationship between PAD and presynaptic inhibition, the conduction of action potentials in the terminal arborizations of the afferent fibers, and the modeling of the presynaptic inhibitory synapse. The second section of the review deals with the functional organization of presynaptic inhibition. This includes the segmental and descending presynaptic control of the synaptic effectiveness of group-I and group-II muscle afferents, the evidence dealing with the local character of PAD as well as the differential inhibition of PAD in selected collaterals of individual muscle-spindle afferents by cutaneous and descending inputs. This section also examines observations on the presynaptic modulation of large cutaneous afferents, including the modulation of the synaptic effectiveness of thin myelinated and unmyelinated cutaneous fibers and of visceral afferents, as well as the presynaptic control of the synaptic actions of interneurons and descending tract neurons. The third section deals with the changes in PAD occurring during sleep and fictive locomotion in higher vertebrates and with the changes of presynaptic inhibition in humans during the execution of a variety of voluntary movements. In the final section, we examine the non-synaptic presynaptic modulation of transmitter release, including the possibility that the intraspinal endings of primary afferents also release colocalized peptides in a similar way as in the periphery. The outcome of the studies presently reviewed is that intraspinal terminals of sensory fibers are not hard-wired conductors of the information generated in their peripheral sensory receptors, but dynamic systems that convey information that can be selectively addressed by central mechanisms to specific neuronal targets. This central control of information flow in peripheral afferents appears to play an important role in the generation of integrated movements and processing of sensory information, including nociceptive information. Received: 16 December 1998 / Accepted: 1 June 1999     

Effects of γ-aminobutyrate and bicuculline on primary afferent depolarization of cutaneous fibres in the cat spinal cord

The excitability of single cutaneous primary afferent fibres (sural nerve) was tested by focal stimulation in the dorsal horn of the cat spinal cord, and recording the antidromically conducted action potential in the peripheral nerve. To induce primary afferent depolarization, which is an expression of presynaptic inhibition, the superficial peroneal nerve was stimulated. The primary afferent depolarization was measured as the concomitant excitability change in the antidromically excited sural fibre. This primary afferent depolarization was reduced by 32% during microelectrophoretic release of bicuculline methochloride near the microstimulation electrode in the dorsal horn. Microelectrophoresis of γ-aminobutyrate increased excitability in sural nerve fibres which correlated with the primary afferent depolarization induced by stimulation of the superficial peroneal nerve.The results suggest a possible role for γ-aminobutyrate in presynaptic inhibition of cutaneous afferent fibres in the cat.     

Effects of motor cortex stimulation on spinal interneurones in intact man

Summary The effect of a descending corticospinal volley on a spinal inhibitory pathway, has been studied in five intact human subjects. Approximately 63% inhibition of the H-reflex evoked in wrist and finger flexor muscles, was produced by motor threshold stimulation of the radial nerve. When a submotor threshold cortical shock was given 2 to 4 ms before the H-reflex, this inhibition was reduced to approximately 38%. The timing of this effect is compatible with either a monosynaptic or disynaptic corticospinal tract projection onto the spinal inhibitory interneurone.     

Calcium facilitation of group Ia EPSPs evoked in cat spinal motoneurones in vivo

The extracellular environment of motoneurones in the cat spinal cord in vivo was altered by means of local perfusion of the central canal. Intracellular recordings were made to determine the effects of raised extracellular Ca2+ or Mg2+ concentration on the monosynaptic afferent excitatory postsynaptic potential (EPSP). Raised extracellular Mg2+ concentration reversibly reduced the EPSP amplitude, whereas raised extracellular Ca2+ concentration produced extremely large increases in the monosynaptic EPSP amplitude, up to almost an order of magnitude. In some cases, a reduction in amplitude of the EPSP and a delay in its onset were also observed, following raised extracellular Ca2+ concentration. This effect was thought to be due to a divalent cation block of the presynaptic action potential. A major conclusion from this study is that group Ia afferent terminals have a much greater transmitter release capacity than suggested by previous studies at this connection.     

Action of baclofen on mammalian synaptic transmission.

Microiontophoretic and systemic injections were used to investigate the mechanism of baclofen's powerful depressant action on transmission at primary afferent synapses in the cat. Iontophoretic applications depressed the spontaneous and evoked activity of cuneate cells and reduced the excitability and input resistance of spinal motoneurones. These effects, which were quick to reverse, resemble those of γ-aminobutyrate and may be due to activation of γ-aminobutyrate receptors by high concentrations of baclofen. Systemic doses of baclofen (0.1–5 mg/kg i.V.), which are known to give only a very low tissue concentration (<10^?7M), induced a very prolonged depression of synaptic responses in the spinal cord (motoneuronal excitatory postsynaptic potentials) and the cuneate nucleus (medial lemniscal potentials); but there was no increase in motoneuronal conductance, and responses of cuneate neurones to direct stimulation by electrical pulses, glutamate, or substance P were not diminished. On the other hand, there was some reduction in the excitability of primary afferent fibres, and the dorsal column reflex and primary afferent depolarization (as revealed by tests of terminal excitability) were nearly abolished.These observations are most simply explained if systemic baclofen blocks primary afferent synapses by a presynaptic action, which leads to a depression of transmitter release; this would be in keeping with evidence that, in cortical slices, baclofen selectively inhibits the release of excitatory amino acids.     

Evidence for corticospinal excitation of presumed propriospinal neurones in man.

1. The possibility that stimulation of the motor cortex facilitates transmission in the pathway mediating non-monosynaptic ('propriospinal') excitation from low-threshold afferents to upper limb motoneurones was investigated. 2. Convergence between peripheral afferent volleys (from the ulnar or musculo-cutaneous nerve) and corticospinal volleys (evoked by magnetic stimulation of the motor cortex) was investigated using the spatial facilitation technique. Thus the effects of these volleys on the flexor carpi radialis H reflex were compared when applied separately and together. When cortical stimulation was optimal for the muscle from which the conditioning volley originated the facilitation of the reflex on combined stimulation was significantly larger than the algebraic sum of the effects of separate stimuli. 3. The extra facilitation on combined stimulation had all the characteristics of 'propriospinal' excitation (low threshold, long central delay, brief duration and depression when the afferent input was increased), and it is suggested that this reflects corticospinal excitation of 'propriospinal' neurones. 4. When varying the time interval between cortical and test stimulations, it was shown that extra facilitation on combined stimulation began 1 ms later than the onset of the control reflex facilitation. Assuming that the latter onset reflects the arrival of the monosynaptic corticospinal volley at the motoneurone pool, this 1 ms delay suggests a disynaptic pathway for the cortical excitation of motoneurones through 'propriospinal' neurones. 5. As at the onset of voluntary movement, the pattern of the cortical excitation of 'propriospinal' neurones was quite specific: extra facilitation of the reflex on combined stimulation only occurred when the cortical volley was preferentially directed to motoneurones supplying the muscle from which the afferents used for the peripheral volley originated. 6. It is concluded that corticospinal axons activate human 'propriospinal' neurones and thereby produce disynaptic excitation of the motoneurone pool. Given temporal summation with the monosynaptic excitation, this 'propriospinally mediated' disynaptic excitation might make a significant contribution to the evoked EMG potential.     

Somatosensory responses in the cat motor cortex. I. Identification and course of an afferent pathway.

1. The main aim of the present series of experiments was to demonstrate with electrophysiological methods that the spinothalamocortical system may send somesthetic information to the pyramidal and corticospinal tract cells in the motor cortex of the cat. 2. Experiments were carried out on acutely prepared cats anesthetized with alpha-chloralose. Extra- and intracellular recordings were made from the cells located in the pericruciate motor cortex (the lateral portion of area 4 gamma). They were identified by their antidromic responses to pyramidal stimulation and/or stimulation of the dorsolateral funiculus of the spinal cord. The animals were subjected to a set of nervous tissue lesions to prevent any transit of extereoceptive information to the motor cortex via the cerebellum and the somatosensory cortex. A lesion of the dorsal part of the spinal cord was also made, leaving intact only the afferent inflow ascending in the spinal ventral half, i.e., the spinothalamic system. 3. In this cat preparation it was observed that both electrical and natural stimulation of the limbs still efficiently activated the motor cortical efferent cells. 4. The pathway was mapped by applying microstimulation along its whole course in the spinal cord and brain stem. Stimulation of the primary afferent fibers running in the dorsal columns caudally to the spinal cord lesion produced activation and/or inhibition of the cortical cells. The existence of these responses may be attributable to the existence of collaterals from primary afferent fibers located in the dorsal columns, which activate the spinothalamic tract cells either mono- or polysynaptically. In the brain stem the fibers join the medial lemniscus. 5. In view of the short latency of the responses (mean latency 10.5 ms from the spinal cord) it is suggested that this component of the spinothalamic system may play an important role in the sensory regulation of ongoing movements.     

The organization of primary afferent depolarization in the isolated spinal cord of the frog

1. The organization of primary afferent depolarization (PAD) produced by excitation of peripheral sensory and motor nerves was studied in the frog cord isolated with hind limb nerves.2. Dorsal root potentials from sensory fibres (DR-DRPs) were evoked on stimulation of most sensory nerves, but were largest from cutaneous, joint and flexor muscle afferents. With single shock stimulation the largest cutaneous and joint afferent fibres gave DR-DRPs, but potentials from muscle nerves resulted from activation of sensory fibres with thresholds to electrical stimulation higher than 1.2-1.5 times the threshold of the most excitable fibres in the nerve. This suggests that PAD from muscle afferents is probably due to excitation of extrafusal receptors.3. Dorsal root potentials produced by antidromic activation of motor fibres (VR-DRPs) were larger from extensor muscles and smaller or absent from flexor muscles. The VR-DRPs were produced by activation of the lowest threshold motor fibres.4. Three types of interactions were found between test and conditioning DRPs from the same or different nerves. With maximal responses occlusion was usually pronounced. At submaximal levels linear summation occurred. Near threshold the conditioning stimulus frequently resulted in a large facilitation of the test DRP. All three types of interactions were found with two DR-DRPs, two VR-DRPs or one DR-DRP and one VR-DRP.5. The excitability of sensory nerve terminals from most peripheral nerves was increased during the DR-DRP. The magnitude of the excitability increase varied roughly with the magnitude of the DR-DRP evoked by the conditioning stimulus.6. There was a marked excitability increase of cutaneous and extensor muscle afferent terminals during the VR-DRP. Flexor muscle afferent terminals often showed no excitability changes to ventral root stimulation. In those experiments where afferent terminals from flexor muscles did show an excitability increase, the effects were smaller than those of cutaneous and extensor terminals.7. The VR-DRPs appear to reflect activity of a negative feed-back loop from extensor motoneurones on to sensory fibres from cutaneous and extensor muscles. This system may have a role in modulating the ballistic movement of the frog. DR-DRPs, on the contrary, are widespread in origin and distribution. PAD from sensory fibres may function to sharpen contrast between incoming afferent information.     

Effects of red nucleus ablation and exogenous neurotrophin-3 on corticospinal axon terminal distribution in the adult rat

Collateral sprouting of undamaged descending axons is one potential mechanism for recovery of function after incomplete spinal cord injury. In this study, we have investigated whether terminals of the intact corticospinal tract in the rat would sprout following ablation of a parallel descending pathway, the rubrospinal tract. No sprouting was detected after this injury alone. However, the combination of rubrospinal tract ablation with administration of 100ng neurotrophin-3 to neurons of the corticospinal tract resulted in marked increased density of corticospinal innervation in the superficial dorsal horn. There was no effect of administration of neurotrophin-3 alone and increase in axon density was not detected in the deep dorsal horn.These results imply that spontaneous sprouting of undamaged corticospinal axons does not occur following ablation of a parallel tract system, although collateral sprouting can be induced through a combination of the lesion plus exogenous growth factor. Induced change in corticospinal terminal density is detected in the superficial dorsal horn only, supporting the hypothesis that this is an area particularly supportive of circuit reorganisation.     

Sites of action of segmental and descending control of transmission on pathways mediating PAD of Ia- and Ib-afferent fibers in cat spinal cord

The present series of investigations was aimed to disclose the possible sites of action of excitatory and inhibitory inputs on tho-interneuron pathway mediating the primary afferent depolarization (PAD) of group I afferents of extensor muscles in the cat spinal cord. To this end we compared the effects produced by stimulation of segmental and descending pathways on the PAD generated either by stimulation of group I fibers of flexor muscles or by intraspinal microstimulation. It was assumed that under the appropriate conditions the PAD produced by intraspinal microstimulation results from the activation of the last-order interneurons in the PAD pathway and may, therefore, allow detection pathway. The PAD of single group I afferent fibers was determined in barbiturate-anesthetized preparations by measuring the test stimulus current required to maintain a constant probability of antidromic firing. This was achieved by means of a feedback system that continuously adjusted the test stimulus current to the required values. The PAD of individual group Ia gastrocnemius soleus (GS) fibers that is produced by activation of the low-threshold afferents of the posterior biceps and semitendinosus nerve was found to be inhibited by conditioning stimulation of the relatively low-threshold cutaneous fibers and also by stimulation of supraspinal structures such as the ipsilateral brain stem reticular formation, the contralateral red nucleus, and the contralateral pyramidal tract. In contrast, the PAD of group Ia fibers produced by microstimulation applied in the intermediate nucleus could be inhibited only by stimulation of the brain stem reticular formation but not by stimulation of the other descending inputs presently tested or by stimulation of cutaneous nerves. PAD of group Ia fibers was produced also by microstimulation applied within the motor nucleus. However, in most fibers the resulting PAD could not be inhibited either by stimulation of the brain stem reticular formation, the red nucleus, the pyramidal tract, or cutaneous nerves. Stimulation of cutaneous and of flexor muscle nerves of the brain stem reticular formation, the red nucleus, and the pyramidal tract all produced PAD of the group Ib GS fibers.(ABSTRACT TRUNCATED AT 400 WORDS)     

Control by Preynaptic Correlation: a mechanism affecting information transmission from Ia fibers to motoneurons.

1. In the unanesthetized spinal cord of the cat, simultaneous intracellular recordings were made from two motoneurons belonging to the gastronemius motor nucleus. 2. Supramaximal iterative stimulation of small branches of the gastrocnemius nerve produced monosynaptic EPSPs (Ia EPSPs) of varying amplitude superimposed on a fluctuating base line. 3. In most cases the variance of the motoneuron membrane potential was increased above base-line levels with a time course approximately matching the Ia EPSP. This suggests that Ia EPSP fluctuations are greater than can be accounted for by the base-line fluctuations alone. 4. For a given series of Ia EPSPs, the smaller responses in the series had about the same decay phase as the larger EPSPs, suggesting that most of the Ia EPSP fluctuations were not due to systematic changes in postsynaptic conductances produced by ongoing activity, but rather to a presynaptic mechanism. 5. Simultaneous recording from two motoneurons showed that base-line fluctuations were positively correlated. In most cases, however, there was an additional increased correlation above base-line levels resembling the time course of the Ia EPSPs, indicating positive correlation between EPSP fluctuations which is attributed to a presynaptic mechanism. 6. Conditioning volleys to group I muscle afferents or to low-threshold cutaneous afferents reduced the variance of the Ia EPSPs and also their correlation in motoneuron pairs, often without changing the mean Ia EPSPs. 7. It is concluded that, in the unanesthetized spinal cord, in addition to the random process which governs transmitter release intrinsic to a given synaptic terminal, there is another stochastic process affecting, in a correlated manner, transmitter release in large sets of Ia synaptic terminals. Most likely, the correlation in transmitter release is achieved by membrane potential fluctuations imposed on the Ia terminal arborizations by ongoing activity of the segmental mechanism mediating primary afferent depolarization. 8. The effects of such a correlating influence on cell firing behavior have been analyzed. The results suggest that this mechanism, referred to as control by presynaptic correlation, is able to modulate the information transmitted from Ia fibers to motoneurons.     

Sensory input to primate spinal cord is presynaptically inhibited during voluntary movement

During normal voluntary movements, re-afferent sensory input continuously converges on the spinal circuits that are activated by descending motor commands. This time-varying input must either be synergistically combined with the motor commands or be appropriately suppressed to minimize interference. The earliest suppression could be produced by presynaptic inhibition, which effectively reduces synaptic transmission at the initial synapse. Here we report evidence from awake, behaving monkeys that presynaptic inhibition decreases the ability of afferent impulses to affect postsynaptic neurons in a behaviorally dependent manner. Evidence indicates that cutaneous afferent input to spinal cord interneurons is inhibited presynaptically during active wrist movement, and this inhibition is effectively produced by descending commands. Our results further suggest that this presynaptic inhibition has appropriate functional consequences for movement generation and may underlie increases in perceptual thresholds during active movement.