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Notes: Summary 1. The functional organization of synaptic connexions to the ventral spinocerebellar tract (VSCT) has been investigated with intracellular recording from 89 spinal border cells (SBCs). 2. EPSPs from primary afferents. Monosynaptic group I EPSPs were evoked in 62 SBCs, in 50 of them from Ia afferents. Ia EPSPs were from knee extensors in 34 cells and knee flexors in 14 cells. No monosynaptic EPSP was evoked by stimulation of peripheral nerves in 27 SBCs. Dorsal column stimulation was tested in 15 of these cells; the absence of monosynaptic EPSPs in 14 of them proves the existence of VSCT cells without monosynaptic connexions from group I afferents. Polysynaptic EPSPs were woked in some cells from Ib afferents, high threshold muscle and cutaneous afferents. 3. IPSPs from primary afferents. Disynaptic IPSPs were evoked from Ia or Ib afferents in many cells. Ib IPSPs were common in SBCs without monosynaptic group I EPSPs. SBCs with Ia EPSPs received Ia or Ib IPSPs mainly from knee muscles. Convergence of Ia EPSPs and IPSPs from the same nerve was observed in 10 cells. Polysynaptic IPSPs were commonly evoked from Ib afferents and invariably evoked from high threshold muscle and skin afferents. 4. Stimulation of the ipsilateral dorsal and/or ventral quadrant of the spinal cord evoked monosynaptic EPSPs and/or IPSPs in many SBCs. 5. The results show that the synaptic input to the VSCT is much more complex than hitherto believed. It is pointed out that all investigated afferent systems, peripheral or descending, which evoke excitation also give inhibition.

Notes: Summary Discharges evoked by mesencephalic stimulation have been recorded from the contralateral dissected dorsal and ventral quadrants in the lower thoracic region of the spinal cord in cats. The effect of this activity on different spinal cord mechanisms was analysed. After interruption of the rubrospinal tract in the lateral part of the medulla, stimulation just dorsal to the red nucleus still evokes a discharge in the contralateral dorsal quadrant. The discharge which requires repetitive stimulation is probably mediated by a two-neurone pathway. Since the stimuli giving this dorsal discharge produces inhibition of interneuronal transmission from the flexor reflex afferents to motoneurones, which is the characteristic effect of activity in the dorsal reticulospinal system (Engberg et al., 1968) it is suggested that the second order neurones belong to this pathway. Stimulation just dorsal to the red nucleus also evokes a synchronized discharge in the contralateral ventral quadrant, mediated by a two-neurone pathway. The first order neurones are at least partly of tectal origin; the second order neurones originate from the brain stem and their axons descend in the medial longitudinal fasciculus. Activity in these fibres has no detectable effect on spinal cord mechanism controlling hindlimb muscles but produces monosynaptic EPSPs in motoneurones of the upper lumbar segments. Some observations are reported regarding long propriospinal excitatory and inhibitory connexions to upper lumbar motoneurones.

Notes: Summary Stimulation of the red nucleus evokes a two-component descending discharge in the contralateral dorsal quadrant of the spinal cord; the first component is caused by direct and the second by synaptic activation of rubrospinal neurones projecting to the lumbosacral cord. Threshold maps for direct and synaptic activation are given. The low threshold focus for direct activation covers not only the hindlimb region of the red nucleus where the antidromic field potential is large but also the medial part of the nucleus where the axons leave. Direct activation can also be evoked from a region extending caudally from the medial part of the red nucleus. Synaptic activation of rubrospinal neurones, evoked at very low threshold from the ventro-medio-caudal border zone of the red nucleus, is due to stimulation of interposito-rubral efferents. The threshold, indicated by unitary EPSPs in rubral cells and antidromic activation of cells in interpositus, is about 1 μA, which is 1/10 of the strength required for direct activation of rubrospinal neurones. There is neither evidence that rubral stimuli activate collaterals of corticospinal axons to the lumbosacral cord, nor that antidromic activation of interposito-rubral fibres evokes descending effect via their collaterals to the reticular formation.

Notes: Summary Interaction between volleys in the vestibulospinal tract and contralateral primary afferents in transmission to motoneurones has been investigated with intracellular recording from motoneurones in cats. Stimulation of Deiters' nucleus facilitates crossed reflex action, excitatory to extensor and inhibitory to flexor motoneurones, evoked from the flexor reflex afferents (FRA; high threshold muscle afferents and cutaneous afferents tested). It is postulated that vestibulospinal fibres and contralateral (co) FRA converge on common interneurones. Reversed conditioning-testing revealed that volleys in the coFRA facilitated disynaptic vestibulospinal PSPs. Control experiments showed that this facilitation was not due to an action by the FRA volleys at the level of Deiters' nucleus or other brain centres. It is postulated that vestibulospinal fibres have monosynaptic connexions with last order interneurones in certain crossed reflex pathways from the FRA, mainly excitatory to extensors and inhibitory to flexors. Some exceptions are described notably that in toe flexor motoneurones the dominating connexion is with last order excitatory interneurones. Mixed excitatory and inhibitory effects are evoked in motor nuclei to some muscles among them hip abductors. In knee flexor motoneurones volleys in the coFRA gave a parallel facilitation of the disynaptic vestibulospinal IPSP and of the Ia IPSP, while in ankle flexor motoneurones there was no concomitant facilitation of the Ia IPSP. From this difference it is postulated that the disynaptic vestibulospinal IPSP in knee flexor motoneurones is evoked largely or entirely via Ia inhibitory interneurones (which are also excited from the coFRA) but in ankle flexors by monosynaptic excitation of last order interneurones in an inhibitory pathway from the coFRA not shared with Ia afferents. The results are discussed in relation to vestibular regulation of extension and sideways limb movements, to interaction between the two limbs in standing and to feed-back control from the FRA of vestibulospinal actions.

Notes: Summary Stimulation of the lateral funicle was performed at different segmenta levels in the cat in order to investigate the connecxions of long propriospinal neurones with ipsilateral lumbosacral motoneurones and interneurones projecting directly to them. In one series of experiments the propriospinal contribution was assessed from the difference between the effect of maximal stimulation in C 1 (activating supraspinal descending fibres) and in more caudal segments (activating supraspinal and propriospinal fibres). In another series on cats with chronic hemisection in C 3 pure propriospinal effects were evoked by stimulation of the thoracic spinal cord. In both series it was shown that volleys in long propriospinal neurones evoke monosynaptic EPSPs and disynaptic EPSP and/or IPSP in many flexor and extensor motoneurones; an extracellular monosynaptic focal synaptic potential was recorded in lamina VII of Rexed. The effects evoked by stimulation of the Th 11 segment after chronic C 3 hemisection were not found after chronic Th 10 hemisection. It is therefore tentatively suggested that they were due to stimulation of long descending propriospinal neurones originating in the lower cervical and upper thoracic segments, their axon trajectory being in the middle of the lateral funiculus and conduct at velocity 100 m/sec. Other effects evoked by stimulation of Th 11 after chronic Th 10 hemisection are ascribed to antidromic activation of axons of ascending neurones.

Notes: Summary The purpose of this study was to elucidate the relative role of the C3-C4 propriospinal neurones (PNs) and of neuronal networks within the forelimb segments for precise forelimb movements. The effects of different spinal cord lesions were investigated on the ability of cats to retrieve food with the forelimb from the bottom of a narrow horizontal or vertical tube. The test movements, which are known to depend on the cortico- and/or rubrospinal tracts (Gorska and Sybirska 1980a, b), are subdivided into the target-reaching movement by which the paw is brought in contact with the food, and the food-taking movement, consisting of toe grasping and paw supination which are components of the movement by which the cat brings the food to the mouth. The following lesions were made ipsilaterally to the tested limb: 1. A dorsal lesion in C5 interrupting the cortico- and rubrospinal input to the forelimb segments (four cats). 2. A dorsal lesion in C2 interrupting the cortico- and rubrospinal input to the C3-C4 PNs and the forelimb segments (four cats). 3. A ventral lesion in C5 interrupting the descending axons of the C3-C4 PNs and bulbospinal fibres to forelimb segments (three cats). 4. A ventral lesion in C2 interrupting bulbospinal fibres and ascending collaterals from the C3-C4 PNs (two cats). 5. A ventral lesion in C2 and a dorsal lesion in C5 sparing the cortico- and rubrospinal input to the C3-C4 PNs and their axons to the forelimb segments (one cat). 6. Hemisection in C2, except the dorsal column (two cats). Severe short-term impairment of the food-taking movement was observed after lesion 1, 2, 5, or 6, but not after lesion 3 or 4. The target-reaching movement was severely impaired after lesion 2, 3, or 6 but not after lesion 1, 4, or 5. The defect after lesion 3 was not in the lifting of the limb but in the appearance of gross ataxia in aiming at the target with the paw. It is postulated that the C3-C4 PNs can transmit to forelimb motoneurones the command for target-reaching but not for food-taking, which depends on direct activation of neuronal networks within the forelimb segments from the cortico- and/or rubrospinal tracts. Long-term recovery of the limb lifting in the target-reaching movement occurred after all lesions. A partial recovery of the food-taking movement occurred after lesions 1 and 2 but not after lesions 5 and 6 which also included the ventral part of the lateral funicle; the recovery is assumed to depend on reticulospinal control of networks within the forelimb segments.

Notes: Summary A further analysis has been made of inhibitory pathways to motoneurones via C3-C4 propriospinal neurones (PNs). Intracellular recording was made from triceps brachi motoneurones and effects from higher centres and forelimb afferents on corticospinal IPSPs were investigated after transection of the corticospinal tract at the C5/C6 border. The shortest latencies of the IPSPs evoked by stimulation of the pyramid were as brief as those of the pyramidal EPSPs (Illert et al. 1977). It is postulated that the minimal linkage of the pyramidal IPSPs is disynaptic via inhibitory C3-C4 PNs projecting directly to motoneurones. It was confirmed that pyramidal IPSPs usually are depressed by volleys in forelimb motor axon collaterals (Illert and Tanaka 1978). A quantitative comparison was made of the recurrent depression of pyramidal IPSPs and of IPSPs caused by activation of the Ia inhibitory interneurones. The result support the hypothesis of two parallel inhibitory cortico-motoneuronal pathways via C3-C4 PNs, one disynaptic via the inhibitory PNs and the other trisynaptic via excitatory PNs and Ia inhibitory interneurones. Pyramidal volleys also evoked late IPSPs which in some cases were not depressed from forelimb motor axon collaterals. It is postulated that the late IPSPs are partly due to activation of inhibitory C3-C4 PNs. Disynaptic pyramidal IPSPs were effectively facilitated by volleys in rubro-, tecto- and reticulospinal fibres — but not from vestibulospinal fibres — showing a convergence from the former descending tracts on common inhibitory C3-C4 PNs. Projection from forelimb afferents and corticospinal fibres on common inhibitory C3-C4 PNs was revealed by strong facilitation of disynaptic pyramidal IPSPs from cutaneous forelimb afferents. No corresponding effect was evoked from C2 neck afferents. Stimulation in the lateral reticular nucleus (LRN) evoked monosynaptic IPSPs in some motoneurones. The results of threshold mapping in and around the LRN suggest that the IPSPs are caused by antidromic stimulation of ascending collaterals of inhibitory neurones also projecting to motoneurones, possibly the inhibitory C3-C4 PNs.

Notes: Summary Intracellular recording was made in the C3-C4 segments from cell bodies of a previously described system of propriospinal neurones (PNs), which receive convergent monosynaptic excitation from different higher motor centres and mediate disynaptic excitation and inhibition from them to forelimb motoneurones. Inhibitory effects in these PNs have now been investigated with electrical stimulation of higher motor centres and forelimb nerves. Short-latency IPSPs were evoked by volleys in the cortico-, rubro- and tectospinal tracts and from the reticular formation. Latency measurements showed that those IPSPs which required temporal summation were disynaptically mediated. After transection of the corticospinal tract in C2, only small and infrequent disynaptic IPSPs were evoked from the pyramid. It is postulated that disynaptic pyramidal IPSPs only to a small extent are evoked by monosynaptic excitation of reticulospinal inhibitory neurones known to project directly to the PNs, and that they are mainly mediated by inhibitory interneurones in the C3-C4 segments. Tests with spatial facilitation revealed monosynaptic excitatory convergence from tecto-, rubro- and probably also from reticulospinal fibres on inhibitory interneurones monosynaptically excited from corticospinal fibres (interneuronal system I). Disynaptic IPSPs were also evoked in the great majority of the PNs by volleys in forelimb muscle and skin nerves. A short train of volleys was usually required to evoke these IPSPs from group I muscle afferents. In the case of cutaneous nerves and mixed nerves single volleys were often effective, and the lack of temporal facilitation of IPSPs produced by a train of volleys showed strong linkage from these nerves. The results obtained after transection of the dorsal column at different levels show that the relay is almost entirely rostral to the forelimb segments. Test with spatial facilitation revealed that interneurones monosynaptically activated from forelimb afferents receive convergent excitation from corticospinal but not or only weakly so from tecto- or rubrospinal fibres. There was also convergence from group I muscle afferents and low threshold cutaneous afferents on common interneurones. It is postulated that the disynaptic IPSPs from forelimb afferents are mediated by inhibitory interneurones (interneuronal system II) other than those receiving convergent descending excitation. Volleys in corticospinal fibres, in addition to the disynaptic IPSPs, evoke late IPSPs in the PNs. Similar late IPSPs were evoked from the ipsilateral forelimb by stimulation of the FRA. Monosynaptic IPSPs were evoked in the majority of the PNs on weak stimulation of the lateral reticular nucleus (LRN) and from regions dorsal to it. Results from threshold mapping suggest that these IPSPs are due to antidromic stimulation of ascending inhibitory neurones which also project to the C3-C4 PNs, and that the ascending collaterals terminate in the LRN or/and the base of the cuneate nuclei. Activity in the ascending collaterals may give higher centres information regarding inhibitory control of the PNs. It is postulated that interneuronal system I subserves descending feed-forward inhibition and interneuronal system II feed-back inhibition from the forelimb of transmission through the C3-C4 PNs to motoneurones.

Notes: Summary The interneuronally mediated reflex actions evoked by electrical stimulation of group II muscle afferents in low spinal cats have been reinvestigated with intracellular recording from motoneurones to knee flexors and ankle extensors. The results of Eccles and Lundberg (1959) have been confirmed and extended. There was wide convergence from flexors and extensors of group II excitation to flexor and group II inhibition to extensor motoneurones. Some quantitative differences in the effect from the different nerves are described. Latency measurements suggest that the minimal linkage is disynaptic in the excitatory interneuronal pathways and trisynaptic in the inhibitory pathways. Disynaptic group II EPSPs were found in 14% of the ankle extensor motoneurones but were much more common in unanaesthetized high spinal cats (Wilson and Kato 1965). From these results and corresponding ones on flexors (Holmqvist and Lundberg 1961) it is postulated that secondary afferents in addition to the weak monosynaptic connexions (Kirkwood and Sears 1975) have disynaptic excitatory pathways and trisynaptic inhibitory pathways to both flexor and extensor motoneurones. It is proposed that the group II actions of the flexor reflex pattern characterizing the anaesthetized low spinal cat are due to suppression of the inhibitory pathway to flexor motoneurones and the excitatory pathway to extensor motoneurones. In some ankle extensor motoneurones the disynaptic group II EPSPs occurred in combination with IPSPs from the FRA (including group II and III muscle afferents). The possibility is considered that these group II EPSPs are mediated by an interneuronal group II pathway with little or no input from group III muscle afferents but probably from extramuscular receptors. In other ankle extensor motoneurones group II EPSPs were combined with EPSPs from group III muscle afferents, cutaneous afferents and joint afferents. It is postulated that these group II EPSPs are mediated by an interneuronal pathway from the FRA which also supply interneuronal pathways giving inhibition to extensor or/and flexor motoneurones and excitation to flexors as postulated by Eccles and Lundberg (1959) and Holmqvist and Lundberg (1961).

Notes: Summary The convergence of group II muscle afferents on interneurones in reflex pathways has been elucidated by investigating interaction in transmission to motoneurones. Recording was also made from interneurones activated from group II afferents. Maximal group II EPSPs evoked in motoneurones from different muscles (extensors or flexors and extensors) did not summate linearly but with a deficit of 35–40%. The corresponding deficit in summation with Ia EPSPs was 7%. It is suggested that the difference in deficit is caused largely by occlusion due to shared interneuronal discharge zones and that it gives an approximate minimal measure of the convergence of group II afferents from different muscles on the interneurones. Tests with weak group II volleys from different muscles gave no or little evidence for spatial facilitation in the disynaptic excitatory pathway to flexor motoneurones, and there was no or little temporal facilitation of transmission in this pathway. It is suggested that group II excitation of the interneurones in this pathway depends on few afferents giving large unitary EPSPs. Convergence of cutaneous afferents and joint afferents on the interneurones was evidenced by spatial facilitation from these afferents of group II transmission to motoneurones. Convergence on interneurones in the trisynaptic inhibitory pathway from group II afferents to extensor motoneurones was also investigated with the spatial facilitation technique. There was convergence on common interneurones of group II afferents from different muscles (extensors or flexors and extensors) and from cutaneous afferents as well as joint afferents. Trisynaptic group II IPSPs, including those depending on spatial facilitation from different muscles were resistant to recurrent depression from motor axon collaterals and are therefore not mediated by the reciprocal Ia inhibitory pathway. Interneurones with monosynaptic group II EPSPs were recorded from in the dorsal horn and intermediate region. Graded stimulation revealed large unitary EPSPs from few group II afferents. The EPSP evoked by a single group II afferent may produce firing (extracellular recording). Convergence of monosynaptic group II EPSPs from different muscles was rather limited but could be from flexors and extensors. Extensive multisensory convergence onto some of these interneurones was indicated by di-or polysynaptic EPSPs from group II and III muscle afferents, from joint afferents and from cutaneous afferents. The discussion of the functional role of the group II reflex pathways is based on previous findings suggesting the existence of alternative pathways to both flexors and extensors and demonstrating that the reciprocity of the spinal state is not obligatorily under control from the brain (Holmqvist and Lundberg 1961). It is postulated that the excitatory group II pathways mediate commands from the brain for movements engaging flexors and/or extensors and that group II inhibition may contribute spatial selectivity by lateral inhibition.