Propriospinal Neurons Research Articles

Respiration-related control of abdominal motoneurons

The abdominal muscles form part of the expiratory pump in cooperation with the other expiratory muscles, primarily the internal intercostal and triangularis sterni muscles. The discharge of abdominal muscles is divided into four main patterns: augmenting, plateau, spindle and decrementing. The patterns tend to be species-specific and dependent on the state of the central nervous system. Recent studies suggest that the abdominal muscles are more active than classically thought, even under resting conditions. Expiratory bulbospinal neurons (EBSN) in the caudal ventral respiratory group are the final output pathway to abdominal motoneurons in the spinal cord. Electrophysiological and anatomical studies indicated the excitatory monosynaptic inputs from EBSN to the abdominal motoneurons, although inputs from the propriospinal neurons seemed to be necessary to produce useful motor outputs. Respiration-related sensory modulation of expiratory neurons by vagal afferents that monitor the rate of change of lung volume and the end-expiratory lung volume (EELV) play a crucial role in modulating the drive to the abdominal musculature. Studies using in vitro and in situ preparations of neonatal and juvenile rats show bi-phasic abdominal activity, characterized by bursting at the end of expiration, a silent period during the inspiratory period, and another burst that occurs abruptly after inspiratory termination. Since the abdominal muscles rarely show these post-inspiratory bursts in the adult rat, the organization of the expiratory output pathway must undergo significant development alterations.

Loss of propriospinal neurons after spinal contusion injury as assessed by retrograde labeling

We studied the number, location and size of long descending propriospinal tract neurons (LDPT), located in the cervical enlargement (C3–C6 spinal levels), and short thoracic propriospinal neurons (TPS), located in mid-thoracic spinal cord (T5–T7 spinal levels), 2, 6 and 16 weeks following a moderate low thoracic (T9) spinal cord contusion injury (SCI; 25 mm weight drop) and subsequent injections of fluorogold into the upper lumbosacral enlargement (L2–L4 spinal levels). Retrograde labeling showed that ∼23% of LDPT and 10% of TPS neurons were labeled 2 weeks after SCI, relative to uninjured animals. No additional significant decrease in number of labeled LDPT and TPS cells was found at the later time points examined, indicating that the maximal loss of propriospinal neurons in these two subpopulations occurs within the first 2 weeks post-SCI. The distribution of labeled cells post-moderate SCI was similar to normal in terms of their location within the gray matter. However, there was a significant change in the size (cross sectional area) of labeled neurons following injury, relative to uninjured controls, indicating a loss in the number of the largest class of propriospinal neurons. Interestingly, the number of labeled LDPT and TPS neurons was not significantly different following different injury severities. Although the rostro–caudal extent of the lesion site expanded between 2 and 16 weeks following injury, there was no significant difference in the number of propriospinal neurons that could be retrogradely labeled at these time points. Possible reasons for these findings are discussed.

Intrinsic response of thoracic propriospinal neurons to axotomy

BackgroundCentral nervous system axons lack a robust regenerative response following spinal cord injury (SCI) and regeneration is usually abortive. Supraspinal pathways, which are the most commonly studied for their regenerative potential, demonstrate a limited regenerative ability. On the other hand, propriospinal (PS) neurons, with axons intrinsic to the spinal cord, have shown a greater regenerative response than their supraspinal counterparts, but remain relatively understudied in regards to spinal cord injury.ResultsUtilizing laser microdissection, gene-microarray, qRT-PCR, and immunohistochemistry, we focused on the intrinsic post-axotomy response of specifically labelled thoracic propriospinal neurons at periods from 3-days to 1-month following T9 spinal cord injury. We found a strong and early (3-days post injury, p.i) upregulation in the expression of genes involved in the immune/inflammatory response that returned towards normal by 1-week p.i. In addition, several regeneration associated and cell survival/neuroprotective genes were significantly up-regulated at the earliest p.i. period studied. Significant upregulation of several growth factor receptor genes (GFRa1, Ret, Lifr) also occurred only during the initial period examined. The expression of a number of pro-apoptotic genes up-regulated at 3-days p.i. suggest that changes in gene expression after this period may have resulted from analyzing surviving TPS neurons after the cell death of the remainder of the axotomized TPS neuronal population.ConclusionsTaken collectively these data demonstrate that thoracic propriospinal (TPS) neurons mount a very dynamic response following low thoracic axotomy that includes a strong regenerative response, but also results in the cell death of many axotomized TPS neurons in the first week after spinal cord injury. These data also suggest that the immune/inflammatory response may have an important role in mediating the early strong regenerative response, as well as the apoptotic response, since expression of all of three classes of gene are up-regulated only during the initial period examined, 3-days post-SCI. The up-regulation in the expression of genes for several growth factor receptors during the first week post-SCI also suggest that administration of these factors may protect TPS neurons from cell death and maintain a regenerative response, but only if given during the early period after injury.

Propriospinal transmission of the locomotor command signal in the neonatal rat

Long direct bulbospinal projections are known to convey descending activation of locomotor networks. Less is understood about the role, if any, of propriospinal mechanisms in this function. Here we review our recent studies on propriospinal neurons in the in vitro neonatal rat brainstem-spinal cord preparation. Neurochemical suppression of synaptic activity in the cervicothoracic spinal cord blocked locomotor-like activity, suggesting synaptic relays make a critical contribution to descending transmission of the locomotor signal. Staggered contralateral hemisections in the cervicothoracic region, intended to eliminate all long direct bulbospinal transmission, failed to suppress locomotion, suggesting the propriospinal system alone is sufficient. Midsagittal lesion experiments showed that locomotor-related commissural components are required for rhythm generation in response to electrical stimulation of the brainstem and are redundantly distributed. No single segment was essential, although a bi-directional gradient was noted, centered on the thoracolumbar junction. These results strongly favor a role for propriospinal mechanisms in the activation of locomotion and suggest that propriospinal neurons are a logical target for interventions to restore locomotor function after spinal cord injury.

Local axon collaterals of lamina I projection neurons in the spinal cord of young rats

Large, mediolaterally oriented neurons in lamina I of the spinal cord, frequently referred to as marginal cells of Waldeyer, are known to project to supraspinal targets via the anterolateral tract (ALT). Although dendritic organization of lamina I neurons has been extensively studied, little is known about their local axonal morphology and branching. With the help of oblique illumination, we visually identified large lamina I neurons in the isolated lumbar enlargement (L1-L6) of the spinal cord of P14-P20 rats. By using intracellular and cell-attached biocytin injections, we achieved extensive axonal and dendritic labeling in 77 lamina I cells, 40 of which were identified as ALT projection neurons. In the majority of the cases (n = 28), the main axon of these projection neurons gave rise to one or more thin collaterals on the ipsilateral side. Based on their trajectory and location, these collaterals could be divided into three major categories: dorsal, lateral, and ventral. Lamina I projection neurons had dorsal (n = 5), lateral (n = 8), or ventral (n = 6) collaterals only or a combination of these collateral types (n = 9). Our results suggest that lamina I ALT projection neurons can additionally function as local-circuit and propriospinal neurons participating in intra- and intersegmental spinal cord processing.

Function analysis of propriospinal neurons relating to human arm movements

Function analysis of propriospinal neurons relating to human arm movements

Recovery of airway protective behaviors after spinal cord injury.

Pulmonary morbidity is high following spinal cord injury and is due, in part, to impairment of airway protective behaviors. These airway protective behaviors include augmented breaths, the cough reflex, and expiration reflexes. Functional recovery of these behaviors has been reported after spinal cord injury. In humans, evidence for functional recovery is restricted to alterations in motor strategy and changes in the frequency of occurrence of these behaviors. In animal models, compensatory alterations in motor strategy have been identified. Crossed descending respiratory motor pathways at the thoracic spinal cord levels exist that are composed of crossed premotor axons, local circuit interneurons, and propriospinal neurons. These pathways can collectively form a substrate that supports maintenance and/or recovery of function, especially after asymmetric spinal cord injury. Local sprouting of premotor axons in the thoracic spinal cord also can occur following chronic spinal cord injury. These mechanisms may contribute to functional resiliency of the cough reflex that has been observed following chronic spinal cord injury in the cat.

Human Bipeds Use Quadrupedal Coordination during Locomotion

During evolution, the increased influence of a direct cortical-motoneuronal system in parallel with a more specialized hand function might have replaced phylogenetically older systems that organized locomotor movements. However, recent research indicates that interlimb coordination during human locomotion is organized in a way similar to that in the cat. During locomotion, corticospinal excitation of upper-limb motoneurons is mediated indirectly, via propriospinal neurons in the cervical spinal cord. This allows a task-dependent neuronal linkage of cervical and thoracolumbar propriospinal circuits controlling leg and arm movements during human locomotor activities. During obstacle avoidance steps, an anticipatory quadrupedal limb coordination is up-regulated, with an involvement of proximal arm muscles during the acquisition and performance of this precision locomotor task.

Intraspinal sprouting of unmyelinated pelvic afferents after complete spinal cord injury is correlated with autonomic dysreflexia induced by visceral pain

Autonomic dysreflexia is a potentially life-threatening hypertensive syndrome following high thoracic (T) spinal cord injury (SCI). It is commonly triggered by noxious pelvic stimuli below the injury site that correlates with increased sprouting of primary afferent C-fibers into the lumbosacral (L/S) spinal cord. We have recently demonstrated that injury-induced plasticity of (L/S) propriospinal neurons, which relay pelvic visceral sensations to thoracolumbar sympathetic preganglionic neurons, is also correlated with the development of this syndrome. To determine the phenotype of pelvic afferent fiber sprouts after SCI, cholera toxin subunit beta (CTb) was injected into the distal colon 2 weeks post–T4 transection/sham to label colonic visceral afferents. After 1 week of transport, the (L/S) spinal cords were cryosectioned and immunohistochemically stained for CTb, the nociceptive-specific marker calcitonin gene-related peptide (CGRP), and the myelinated fiber marker RT97. Quantitative analysis showed that the density of CGRP+ afferent fibers was significantly increased in the L/S dorsal horns of T4-transected versus sham rats, whereas RT97+ afferent fiber density showed no change. Importantly, CTb-labeled pelvic afferent fibers were co-localized with CGRP+ fibers, but not with RT97+ fibers. These results suggest that the sprouting of unmyelinated nociceptive pelvic afferents following high thoracic SCI, but not myelinated fibers, contributes to hypertensive autonomic dysreflexia induced by pelvic visceral pain.

C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons

During myocardial ischemia, the cranial cervical spinal cord (C1-C2) modulates the central processing of the cardiac nociceptive signal. This study was done to determine 1) whether C2 SCS-induced release of an analgesic neuropeptide in the dorsal horn of the thoracic (T4) spinal cord; 2) if one of the sources of this analgesic peptide was cervical propriospinal neurons, and 3) if chemical inactivation of C2 neurons altered local T4 substance P (SP) release during concurrent C2 SCS and cardiac ischemia. Ischemia was induced by intermittent occlusion of the left anterior descending coronary artery (CoAO) in urethane-anesthetized Sprague-Dawley rats. Release of dynorphin A (1-13), (DYN) and SP was determined using antibody-coated microprobes inserted into T4. SCS alone induced DYN release from laminae I-V in T4, and this release was maintained during CoAO. C2 injection of the excitotoxin, ibotenic acid, prior to SCS, inhibited T4 DYN release during SCS and ischemia; it also reversed the inhibition of SP release from T4 dorsal laminae during C2 SCS and CoAO. Injection of the kappa-opioid antagonist, nor-binaltorphimine, into T4 also allowed an increased SP release during SCS and CoAO. CoAO increased the number of Fos-positive neurons in T4 dorsal horns but not in the intermediolateral columns (IML), while SCS (either alone or during CoAO) minimized this dorsal horn response to CoAO alone, while inducing T4 IML neuronal recruitment. These results suggest that activation of cervical propriospinal pathways induces DYN release in the thoracic spinal cord, thereby modulating nociceptive signals from the ischemic heart.

Plasticity of lumbosacral propriospinal neurons is associated with the development of autonomic dysreflexia after thoracic spinal cord transection

Complete thoracic (T) spinal cord injury (SCI) above the T6 level typically results in autonomic dysreflexia, an abnormal hypertensive condition commonly triggered by nociceptive stimuli below the level of SCI. Overexpression of nerve growth factor in the lumbosacral spinal cord induces profuse sprouting of nociceptive pelvic visceral afferent fibers that correlates with increased hypertension in response to noxious colorectal distension. After complete T4 SCI, we evaluated the plasticity of propriospinal neurons conveying visceral input rostrally to thoracic sympathetic preganglionic neurons. The anterograde tracer biotinylated dextran amine (BDA) was injected into the lumbosacral dorsal gray commissure (DGC) of injured/nontransected rats immediately after injury (acute) or 2 weeks later (delayed). At 1 or 2 weeks after delayed or acute injections, respectively, a higher density (P < 0.05) of BDA(+) fibers was found in thoracic dorsal gray matter of injured vs. nontransected spinal cords. For corroboration, fast blue (FB) or cholera toxin subunit beta (CTb) was injected into the T9 dorsal horns 2 weeks postinjury/nontransection. After 1 week transport, more retrogradely labeled (P < 0.05) DGC propriospinal neurons (T13-S1) were quantified in injured vs. nontransected cords. We also monitored immediate early gene c-fos expression following colorectal distension and found increased (P < 0.01) c-Fos(+) cell numbers throughout the DGC after injury. Collectively, these results imply that, in conjunction with local primary afferent fiber plasticity, injury-induced sprouting of DGC neurons may be a key constituent in relaying visceral sensory input to sympathetic preganglionic neurons that elicit autonomic dysreflexia after high thoracic SCI.

Propriospinal neurons are sufficient for bulbospinal transmission of the locomotor command signal in the neonatal rat spinal cord

We recently showed that propriospinal neurons contribute to bulbospinal activation of locomotor networks in the in vitro neonatal rat brainstem-spinal cord preparation. In the present study, we examined whether propriospinal neurons alone, in the absence of long direct bulbospinal transmission to the lumbar cord, can successfully mediate brainstem activation of the locomotor network. In the presence of staggered bilateral spinal cord hemisections, the brainstem was stimulated electrically while recording from lumbar ventral roots. The rostral hemisection was located between C1 and T3 and the contralateral caudal hemisection was located between T5 and mid-L1. Locomotor-like activity was evoked in 27% of the preparations, which included experiments with staggered hemisections placed only two segments apart. There was no relation between the likelihood of developing locomotor-like activity and the distance separating the two hemisections or specific level of the hemisections. In some experiments, where brainstem stimulation alone was ineffective, neurochemical excitation of propriospinal neurons (using 5-HT and NMDA) at concentrations subthreshold for producing locomotor-like activity, promoted locomotor-like activity in conjunction with brainstem stimulation. In other experiments, involving neither brainstem stimulation nor cord hemisections, the excitability of propriospinal neurons in the cervical and/or thoracic region was selectively enhanced by bath application of 5-HT and NMDA or elevation of bath K(+) concentration. These manipulations produced locomotor-like activity in the lumbar region. In total, the results suggest that propriospinal neurons are sufficient for transmission of descending locomotor command signals. This observation has implications for regeneration strategies aimed at restoration of locomotor function after spinal cord injury.

Short-circuit recovery from spinal injury

Propriospinal neurons, whose axons never leave the spinal cord, aid in recovery after spinal cord injury—even when all axons from the brain have been damaged (pages 69–74 ).

Aspiration of a cervical spinal contusion injury in preparation for delayed peripheral nerve grafting does not impair forelimb behavior or axon regeneration

A peripheral nerve graft model was used to examine axonal growth after a unilateral cervical (C) contusion injury in adult rats and to determine if manipulation of an injury site prior to transplantation affects spontaneous behavioral recovery. After a short delay (7 d) the epicenter of a C4 contusion was exposed and aspirated without harming the cavity walls followed by apposition with one end of a pre-degenerated tibial nerve to the rostral cavity wall. After a longer delay (28 d) the aspirated cavity was treated with GDNF to promote regeneration by chronically injured neurons. In both groups forelimb and hindlimb locomotor scores decreased significantly 2 d after lesion site manipulation, but by 7 d, the forelimb score was not different from the pre-manipulation score. There was no significant difference in grid walking or grip strength scores for the affected forelimb in either group 7 d after contusion vs. 7 d after manipulation. Over 1500 brain stem and propriospinal neurons grew axons into the graft with either delay. These results demonstrate that a contusion injury site can be manipulated prior to transplantation without causing long-lasting forelimb or hindlimb behavioral deficits and that peripheral nerve grafts support axonal growth after acute or chronic contusion injury.

P.4.b.009 Normalization of immune cell imbalance after pharmacological treatments in patients with obsessive-compulsive disorder

Long C3–C5 propriospinal neurones (PNs) are classified in 3 types depending on their pyramidal and vestibular input. Thefirst type of PNs received pyramidal excitation but lacked vestibular effects. Thesecond type of PNs was excited from the medial vestibular nucleus but not from the pyramid. Thethird type of PNs was excited from the lateral vestibular nucleus either from second order neurones or from non-second order neurones. Monosynaptic excitatory postsynaptic potentials from neck afferents and/or oligosynaptic postsynaptic potentials from forelimb afferents were found in some of the PNs of the second and third type but not in those of the first type. Collision experiments revealed that cortico- and rubrospinal fibres to the long C3–C5 PNs terminate in the rostral spinal cord, presumably in the forelimb segments. Vestibular and reticular effects on the PNss are partly from fibres terminating in the rostral spinal cord and partly from fibres projecting to the lumbar cord. It is postulated that the different types of PNs contribute to the adjustment of hindlimb posture which is required during different movements of the forebody. It is suggested that the basic tonus is maintained mainly by the direct projection to the hindlimb segments from lateral vestibulospinal and reticulospinal neurones which excite antigravity muscles via lumbar interneurones and that long C3-C5 PNs converge onto the same interneurones so that they act by modulation of the bsic tonus.

Task‐related changes in propriospinal excitation from hand muscles to human flexor carpi radialis motoneurones

This study addresses whether there is excitation from human hand muscles to flexor carpi radialis (FCR) motoneurones mediated through propriospinal circuits and, if so, whether it is used in specific motor tasks. Electrical stimuli to the ulnar nerve at wrist level produced an excitation in FCR motoneurones with characteristics typical of a propriospinally mediated effect: low threshold (0.6 x motor threshold (MT)), a group I effect that was not reproduced by purely cutaneous stimuli, long central delay (4.1 +/- 0.4 ms in single units), suppression when the stimulus intensity was increased, and facilitation of the corticospinal excitation at the premotoneuronal level. Ulnar-induced propriospinally mediated excitation was compared during selective voluntary contractions of the FCR and, at equivalent level of FCR EMG, during tasks in which the FCR was activated automatically in postural contractions rather than voluntarily (grip, pinching and pointing). The excitation was significantly greater during grip (and pinching) than during voluntary FCR contractions and pointing, whether measured in single motor units or tonic EMG activity, or whether the response to motor cortex stimulation was assessed as the compound motor-evoked potential or the corticospinal peak in single units. The discrepancy between the tasks appeared with ulnar intensities above 0.8 x MT and was then present across a wide range of stimulus intensities. This suggests a reduction in the corticospinal control of 'feedback inhibitory interneurones' mediating peripheral inhibition to propriospinal neurones during grip and pinching. The resulting more effective background excitation of propriospinal neurones by the peripheral input from hand muscles could contribute to stabilizing the wrist during grip.

Muscle fatigue changes cutaneous suppression of propriospinal drive to human upper limb muscles

Some voluntary drive reaches human upper limb muscles via cervical propriospinal premotoneurones. Stimulation of the superficial radial nerve can inhibit these premotoneurones selectively and the resultant suppression of voluntary drive to motoneurones changes on-going electromyographic (EMG) activity. We investigated whether muscle fatigue changes this cutaneous-induced suppression of propriospinal drive to motoneurones of upper limb muscles. EMG was recorded from the extensors and flexors of the wrist and elbow. In the first study (n = 10 subjects), single stimuli (2 x perception threshold; 2PT) to the superficial radial nerve were delivered during contraction of the wrist extensors, before and after sustained fatiguing contractions of wrist extensors. In the second study (n = 10), similar stimuli were applied during elbow extension, before and during fatigue of elbow extensors. In the final study (n = 10), trains of three stimuli (2PT) were delivered during contractions of wrist extensors, before and while they were fatigued. With fatigue of either the wrist or elbow extensors, EMG suppression to single cutaneous stimuli increased significantly (by approximately 75%) for the fatigued muscle (P < 0.05). Conversely, in the other muscles, which were coactivated but not principally involved in the task, inhibition decreased or facilitation increased. Trains of stimuli produced greater suppression of on-going wrist extensor EMG than single stimuli and this difference persisted with fatigue. A control study of the H reflex in extensor carpi radialis showed that the mechanism responsible for the altered EMG suppression in fatigue was not at a motoneurone level. The findings suggest that the proportion of descending drive mediated via the disynaptic propriospinal pathway or the excitability of inhibitory interneurones projecting to propriospinal neurones increases substantially to fatigued muscles, but decreases to other active muscles. This pattern of changes may maintain coordination during multimuscle movements when one group of muscles is fatigued.

Spinal cord stimulation modulates intraspinal colorectal visceroreceptive transmission in rats

Previous studies have shown that spinal cord stimulation (SCS) of upper lumbar segments decreases visceromotor responses to mechanical stimuli in a sensitized rat colon and reduces symptoms of irritable bowel syndrome in patients. SCS applied to the upper cervical spinal dorsal column reduces pain of chronic refractory angina. Further, chemical stimulation of C1–C2 propriospinal neurons in rats modulates the responses of lumbosacral spinal neurons to colorectal distension. The present study was designed to compare the effects of upper cervical and lumbar SCS on activity of lumbosacral neurons receiving noxious colorectal input. Extracellular potentials of L6–S2 spinal neurons were recorded in pentobarbital anesthetized, paralyzed and ventilated male rats. SCS (50 Hz, 0.2 ms) at low intensity (90% of motor threshold) was applied to the dorsal column of upper cervical (C1–C2) or upper lumbar (L2–L3) ipsilateral spinal segments. Colorectal distension (CRD, 20 mmHg, 40 mmHg, 60 mmHg, 20 s) was produced by air inflation of a latex balloon. Results showed that SCS applied to L2–L3 and C1–C2 segments significantly reduced the excitatory responses to noxious CRD from 417.6 ± 68.0 to 296.3 ± 53.6 imp ( P < 0.05, n = 24) and from 336.2 ± 64.5 to 225.0 ± 73.3 imp ( P < 0.05, n = 18), respectively. Effects of L2–L3 and C1–C2 SCS lasted 10.2 ± 1.9 and 8.0 ± 0.9 min after offset of CRD. Effects of SCS were observed on spinal neurons with either high or low-threshold excitatory responses to CRD. However, L2–L3 or C1–C2 SCS did not significantly affect inhibitory neuronal responses to CRD. C1–C2 SCS-induced effects were abolished by cutting the C7–C8 dorsal column but not by spinal transection at cervicomedullary junction. These data demonstrated that upper cervical or lumbar SCS modulated responses of lumbosacral spinal neurons to noxious mechanical stimulation of the colon, thereby, proved two loci for a potential therapeutic effect of SCS in patients with irritable bowel syndrome and other colonic disorders.

Strategies for axonal repair in central nervous system diseases

Significant functional recovery after spinal cord injury can be observed in rodents, in spite of the presence of extensive irreversible structural damage. One potential mechanism for functional regeneration of the corticospinal tract may involve the formation of new spinal circuits remote from the lesion that allow the lesion site to be by-passed and contact re-established with the original targets of the transected axons. In both traumatic and inflammatory lesions of the spinal cord, transection at the thoracic level is followed by extensive collateral sprouting at higher levels of the spinal cord. These collaterals can make contact with long propriospinal neurones in the cervical cord, which project to the lumbar ventral horn via the ventral funiculus. These new connections can serve as a ‘bridge’ to reconnect the corticospinal neurone to its target anterior horn cell. The integrity of this circuitry has been demonstrated by retrograde tracing with pseudorabies virus. Recuperation of electromyographic activity following stimulation of the motor cortex indicates that these new spinal circuits are functionally active. Such remodelling of spinal circuitry following spinal injury may play an important role in determining the extent of functional recovery.

Skilled digit movements in feline and primate – recovery after selective spinal cord lesions

Recovery of voluntary movements after partial spinal cord injury depends, in part, on a take-over of function via unlesioned pathways. Using precise forelimb movements in the cat as model, spinal pathways contributing to motor restitution have been investigated in more detail. The food-taking movement by which the cat graSPS a morsel of food with the digits and brings it to the mouth is governed by interneurones in the forelimb segments (C6-Th1) and is normally controlled via the cortico- and rubrospinal tracts. Food-taking disappears after transection of these pathways in the dorsal part of the lateral funiculus (DLF) in C5/C6, but then recovers during a period of 2-3 weeks. Experiments with double lesions showed that the recovery depends on a take-over via ipsilateral ventral systems; a ventrally descending pathway, most probably cortico-reticulospinal, and a pathway via propriospinal neurones in the C3-C4 segments. It is postulated that the recovery involves a plastic reorganization of these systems. Dexterous finger movements in the macaque monkey are generally considered to depend on the monosynaptic cortico-motoneuronal (CM) connexion, which is lacking in the cat. Such movements are abolished after pyramidotomy at the level of the trapezoid body. However, experiments with transection of the corticospinal tract in the DLF and partly ventral part of the lateral funiculus in C5, showed a fast (1-28 days) recovery of precision grip and, to some extent, independent finger movements. Deficits in preshaping during the final approach to the morsel as well as lack of force were observed. A C5 DLF lesion spares corticofugal pathways to the brainstem and upper cervical segments. It is suggested that indirect corticomotoneuronal pathways may provide for recovery of dexterous finger movements and that the role of CM pathways for such movements should be broadened to include not only the monosynaptic connexion.