Interneurones mediating presynaptic inhibition of group II muscle afferents in the cat spinal cord (original) (raw)
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Observations on neuronal pathways subserving primary afferent depolarization
Journal of neurophysiology, 1981
AND CONCLUSIONS 1. Latencies of presynaptic depolarization of group I muscle afferents and cutaneous afferents have been reinvestigated in an attempt to define the minimal number of interneurons interposed in the pathways of the presynaptic depolarization. Intra-axonal records from individual afferents, records of dorsal root potentials, and measurements of changes in excitability of individual afferents were used for this purpose. Some of the animals were treated with 4-aminopyridine to facilitate transmission via neuronal pathways.
The Journal of Physiology, 2000
used spike triggered averaging of dorsal root and ventral root potentials to disclose possible connections of intermediate nucleus interneurones with afferent fibres andÏor spinal motoneurones. They found one set of interneurones (class I) whose spontaneous activity was associated with short-latency glycinergic inhibitory potentials in motoneurones as well as in the ventral roots (iVRPs), which were produced without concurrent dorsal root potentials (DRPs). These inhibitory neurones had collaterals to Clarke's column and appeared to be the same as those mediating non-reciprocal postsynaptic inhibition of Ib origin . The activity of the second set of interneurones (class II) was instead associated with the generation of short-latency DRPs and iVRPs. It was suggested that these were GABAergic interneurones directly connected with the intraspinal terminals of group I muscle afferents and spinal motoneurones, where they produced PAD and postsynaptic inhibition, respectively . The spontaneous activity of class I and class II interneurones usually appeared in synchrony with a negative cord dorsum potential lasting 40-60 ms that was initiated 20-30 ms before the interneuronal action potentials. It was assumed that this cord dorsum potential was generated by the spontaneous activity of a population of neurones located in the most superficial regions of the spinal cord. It was not clear, however, if these were 'command' interneurones modulating transmission along the pathways 1. We examined, in the anaesthetised cat, the influence of the neuronal ensembles producing spontaneous negative cord dorsum potentials (nCDPs) on segmental pathways mediating primary afferent depolarisation (PAD) of cutaneous and group I muscle afferents and on Ia monosynaptic activation of spinal motoneurones. 2. The intraspinal distribution of the field potentials associated with the spontaneous nCDPs indicated that the neuronal ensembles involved in the generation of these potentials were located in the dorsal horn of lumbar segments, in the same region of termination of lowthreshold cutaneous afferents. 3. During the occurrence of spontaneous nCDPs, transmission from low-threshold cutaneous afferents to second order neurones in laminae III-VI, as well as transmission along pathways mediating PAD of cutaneous and Ib afferents, was facilitated. PAD of Ia afferents was instead inhibited. 4. Monosynaptic reflexes of flexors and extensors were facilitated during the spontaneous nCDPs. The magnitude of the facilitation was proportional to the amplitude of the 'conditioning' spontaneous nCDPs. This led to a high positive correlation between amplitude fluctuations of spontaneous nCDPs and fluctuations of monosynaptic reflexes. 5. Stimulation of low-threshold cutaneous afferents transiently reduced the probability of occurrence of spontaneous nCDPs as well as the fluctuations of monosynaptic reflexes. 6. It is concluded that the spontaneous nCDPs were produced by the activation of a population of dorsal horn neurones that shared the same functional pathways and involved the same set of neurones as those responding monosynaptically to stimulation of large cutaneous afferents. The spontaneous activity of these neurones was probably the main cause of the fluctuations of the monosynaptic reflexes observed under anaesthesia and could provide a dynamic linkage between segmental sensory and motor pathways. 0925
Brain Research, 1984
Intersegmentally evoked primary afferent depolarization (PAD) was analysed to investigate whether an}' lower lumbar propriospinal neurones are involved in mediating PAD from group I afferents to group I afferents both in the same segments and in Clarke's column. The intersegmental PAD of lower lumbar afferents, as judged by recording dorsal root potentials, was evoked by stimuli applied in the grey matter of L3 and L4 segments. With intraspinal stimuli of I(I,,A or less PAD was evoked from two foci: from within the middle part of the dorsal columns and from the dorsal part of the dorsal horn. Dorsal root potentials evoked from the dorsal horn focus appeared with longer latencies. When the dorsal columns were transected PAD was evoked only from the dorsal horn focus. No PAD appeared upon stimulation of Clarke's column after transection of the dorsal columns even with stronger (2(I/,A) stimuli. Interactions between the actions of the intraspinal stimuli and of different groups of afferents were analysed to define the neuronal pathways via which the intersegmental PAD was evoked. Neurones located within both the lower and the upper lumbar segments were found to be involved. Indications have only been found for a contribution of neurones mediating PAD from afferents other than group I afferents. Lesions of the ipsilateral and contralateral, lateral and ventral funiculi (in addition to the dorsal columns) were made in order to define which of these funiculi are required for the appearance of the intersegmental PAD. The intersegmental PAD coukt be evoked from the dorsal horn when either the contralateral or the ipsilateral funiculi were left intact.
Patterns of connectivity of spinal interneurons with single muscle afferents
Experimental Brain Research, 1997
A technique was developed to measure, in the anesthetized and paralyzed cat under artificial ventilation, changes of excitability to intraspinal stimulation simultaneously in two different afferent fibers or in two collaterals of the same afferent fiber. Intraspinal stimulation reduced the threshold of single muscle afferent fibers ending in the intermediate nucleus. This effect was seen with strengths below those required to activate the afferent fiber tested (1.5-12 µA), occurred at a short latency (1.5-2.0 ms), reached a maximum between 15 and 30 ms, and lasted up to 100 ms. The effects produced by graded stimulation applied at the shortest conditioningtesting stimulus time intervals increased by fixed steps, suggesting recruitment of discrete elements, most likely of last-order interneurons mediating primary afferent depolarization (PAD). The short-latency increases in excitability produced by the weakest effective intraspinal stimuli were usually detected only in the collateral closest to the stimulating micropipette, indicating that the stimulated interneurons mediating PAD have spatially restricted actions. The short-latency PAD produced by intraspinal stimuli, as well as the PAD produced by stimulation of the posterior biceps and semitendinosus (PBSt) nerve or by stimulation of the bulbar reticular formation (RF), was depressed 19-30 min after the i.v. injection of 0.5 mg/kg of picrotoxin, suggesting that all these effects were mediated by GABAergic mechanisms. The PAD elicited by stimulation of muscle and/or cutaneous nerves was depressed following the i.v. injection of (-)baclofen, whereas the PAD elicited in the same collateral by stimulation of the RF was baclofen-resistant. The short-latency PAD produced by intraspinal stimulation was not always depressed by i.v. injections of (-)-baclofen.
The Journal of Neuroscience, 1997
We present evidence that the electrical excitability of the terminals of a group of spinal premotor interneurons can be increased after stimulation of sensory afferents. The interneurons were located in the midlumbar segments of the spinal cord and had projections to the lower lumbar motor nuclei. Thresholds for antidromic activation of a substantial number of interneurons were reduced after electrical stimulation of group II muscle afferents. Several observations suggest that the excitability changes are unlikely to have arisen from electrotonic spread of depolarization from the interneuron soma to its terminals or by environmental changes in the vicinity of the terminals related to neuronal activity. A particularly interesting possibility is that the excitability of the central terminals of the interneurons is increased because they are depolarized by a mechanism similar to that acting at the terminals of primary sensory afferents (primary afferent depolarization, PAD), which accompanies one type of presynaptic inhibition. This type of presynaptic action has been shown in premotor interneurons in the lamprey but not in the mammalian spinal cord. From our observations the organization of the systems generating excitability changes at the interneuron terminals seem in general to parallel the organization of the systems generating PAD at afferent terminals, raising the possibility that common principles might underlie the operation of this form of presynaptic control.
Brain Research, 1984
The origin of presynaptic depolarization of group I afferents in Clarke's column has been re-investigated, using changes in excitability of single fibres as a measure of their depolarization. In contrast to the previously reported lack of effects following conditioning stimulation of group Ia afferents, these afferents have been found to increase the excitability of other group la afferent terminals in Clarke's column. Flexor la and Ib afferents were found to be more effective than extensor afferents. The group I origin of the presynaptic depolarization of group I afferents in Clarke's column thus appears to be as of other terminals of these afferents. In order to define the location of interneurones mediating primary afferent depolarization in Clarke's column, changes in the excitability of afferents in Clarke's column were measured after isolating L4 and more rostral segments from the sacral and caudal lumbar segments, except for the dorsal columns, or after transection of ipsilateral lateral and ventral funiculi. Primary afferent depolarization of group Ia, or unspecified group I origin, was also found after such lesions and its effectiveness appeared to be as in intact preparations. It may thus be evoked primarily by interneurones located in the same segments as Clarke's column.
Areas of operation of interneurons mediating presynaptic inhibition in sacral spinal segments
Experimental Brain Research, 2000
Sources of primary afferent depolarization (PAD) of skin afferents in the sural (Sur) nerve and of group-II muscle afferents in the posterior biceps and semitendinosus (PBST) nerve were compared at several sites, about 2 mm apart, within the L7-S2 segments in order to define areas of projection of sacral interneurons mediating PAD of these afferents. Just rostral to the pudendal nucleus, strong PAD of Sur afferents was evoked by stimulation of skin nerves, while stimulation of muscle nerves had only marginal effects. This indicates that sacral PAD interneurons co-excited by skin and muscle afferents operate primarily within the regions overlying the pudendal nucleus. Furthermore, PAD evoked by muscle afferents was weaker over the rostral part of the pudendal nucleus than over the caudal part of this nucleus, where hamstring afferents became its main source, both in Sur and in PBST group-II afferents. By correlating the relative strength of PAD at the levels of the rostral and caudal parts of the pudendal nucleus with the previously established input from muscle and cutaneous afferents to interneurons at these levels, it is therefore proposed that sacral PAD interneurons operate over shorter distances than indicated by previous experiments: over either rostral or caudal parts of the pudendal nucleus, i.e., about 2 mm, rather than over the whole length of this nucleus, i.e., 4-5 mm. Sacral PAD interneurons may, thus, modulate synaptic transmission to even more spatially restricted neuronal populations than previously proposed.
Convergence of excitatory and inhibitory action on interneurones in the lumbosacral cord
Experimental Brain Research, 1966
Intracellular recording has been made in spinal cats from more than 100 interneurones in the dorsal horn and intermediary region of the lum-bosacrM spinal cord. The majority of interneurones receive not only EPSPs but also IPSPs from primary afferents. The IPSPs are evoked from three different systems, group I muscle afferents (probably Ib), low threshold cutaneous affcrents and the FI{A. The shortest central latency of the IPSPs indicates a disynaptic linkage from primary afferents. Interneurones with monosynaptic EPSPs from group I muscle affercnts may receive IPSPs from all the above mentioned afferent systems. Interneurones with monosynaptic EPSPs from cutaneous afferents receive their inhibition from the two latter afferent systems. Convergence of EPSPs and IPSPs from the FI~A may occur on the same interneurone. The results are discussed mainly with respect to inhibitory interaction between spinal reflex pathways.
Journal of Neurophysiology, 2006
The aim of the study was to analyze interactions between neuronal networks mediating centrally initiated movements and reflex reactions evoked by peripheral afferents; specifically whether interneurons in pathways from group Ib afferents and from group II muscle afferents mediate actions of reticulospinal neurons on spinal motoneurons by contralaterally located commissural interneurons. To this end reticulospinal tract fibers were stimulated in the contralateral medial longitudinal fascicle (MLF) in chloralose-anesthetized cats in which the ipsilateral half of the spinal cord was transected rostral to the lumbosacral enlargement. In the majority of interneurons mediating reflex actions of group Ib and group II afferents, MLF stimuli evoked either excitatory or inhibitory postsynaptic potentials (EPSPs and IPSPs, respectively) or both EPSPs and IPSPs attributable to disynaptic actions by commissural interneurons. In addition, in some interneurons EPSPs were evoked at latencies compat...