Reticulospinal actions on primary afferent depolarization of cutaneous and muscle afferents in the isolated frog neuraxis

1993 ◽  
Vol 95 (2) ◽  
Author(s):  
H. Gonz�lez ◽  
I. Jim�nez ◽  
P. Rudomin
Keyword(s):  
Muscle Afferents ◽  
Primary Afferent Depolarization ◽  
Primary Afferent

Sensory Integration in Presynaptic Inhibitory Pathways During Fictive Locomotion in the Cat

2002 ◽  
Vol 88 (1) ◽  
pp. 163-171 ◽  
Author(s):  
Ariane Ménard ◽  
Hugues Leblond ◽  
Jean-Pierre Gossard
Keyword(s):  
Presynaptic Inhibition ◽  
Muscle Afferents ◽  
Primary Afferent Depolarization ◽  
Skin Area ◽  
Fictive Locomotion ◽  
Step Cycle ◽  
Primary Afferent ◽  
Decerebrate Cat ◽  
Group I ◽  
Group I Afferents

The aim of this study is to understand how sensory inputs of different modalities are integrated into spinal cord pathways controlling presynaptic inhibition during locomotion. Primary afferent depolarization (PAD), an estimate of presynaptic inhibition, was recorded intra-axonally in group I afferents ( n = 31) from seven hindlimb muscles in L6–S1 segments during fictive locomotion in the decerebrate cat. PADs were evoked by stimulating alternatively low-threshold afferents from a flexor nerve, a cutaneous nerve and a combination of both. The fictive step cycle was divided in five bins and PADs were averaged in each bin and their amplitude compared. PADs evoked by muscle stimuli alone showed a significant phase-dependent modulation in 20/31 group I afferents. In 12/20 afferents, the cutaneous stimuli alone evoked a phase-dependent modulation of primary afferent hyperpolarization (PAH, n = 9) or of PADs ( n = 3). Combining the two sensory modalities showed that cutaneous volleys could significantly modify the amplitude of PADs evoked by muscle stimuli in at least one part (bin) of the step cycle in 17/31 (55%) of group I afferents. The most common effect (13/17) was a decrease in the PAD amplitude by 35% on average, whereas it was increased by 17% on average in the others (4/17). Moreover, in 8/13 afferents, the PAD reduction was obtained in 4/5 bins i.e., for most of the duration of the step cycle. These effects were seen in group I afferents from all seven muscles. On the other hand, we found that different cutaneous nerves had quite different efficacy; the superficial peroneal (SP) being the most efficient (85% of trials) followed by Saphenous (60%) and caudal sural (44%) nerves. The results indicate that cutaneous interneurons may act, in part, by modulating the transmission in PAD pathways activated by group I muscle afferents. We conclude that cutaneous input, especially from the skin area on the dorsum of the paw (SP), could subtract presynaptic inhibition in some group I afferents during perturbations of stepping (e.g., hitting an obstacle) and could thus adjust the influence of proprioceptive feedback onto motoneuronal excitability.

Convergence onto interneurons subserving primary afferent depolarization of group I afferents

1984 ◽  
Vol 51 (3) ◽  
pp. 432-449 ◽  
Author(s):  
E. Brink ◽  
E. Jankowska ◽  
B. Skoog
Keyword(s):  
Muscle Afferents ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Neuronal Populations ◽  
Ia Afferents ◽  
Group I ◽  
Spatial Facilitation ◽  
Low Threshold ◽  
Group I Afferents ◽  
Dorsal Root Potentials

The aim of the study was to investigate whether common or independent neuronal pathways are used to evoke primary afferent depolarization (PAD) from selectively activated group Ia and Ib afferents of different muscles. To this end, the spatial facilitation of effects of various afferents, indicating convergence on the same interneurons, was used as a test. Its occurrence was assessed on dorsal root potentials (DRPs) evoked in unspecified fibers or using intra-axonal recording from identified group Ia muscle spindle afferents or group Ib tendon organ afferents. Spatial facilitation has been found in PAD pathways a) from various Ia-afferents, whether of flexors or extensors; b) from various Ib-afferents, whether of flexors or extensors; and c) from flexor Ib-afferents and flexor or extensor Ia-afferents. In contrast, no indications have been found for common pathways from extensor Ib- and any Ia-afferents under conditions that proved effective in other combinations. Latencies of those components of PAD that appeared as a result of the spatial facilitation ranged from 2 to more than 7 ms, indicating that the convergence occurred in the shortest (trisynaptic) as well as longer pathways. The same patterns of convergence have been found in PAD pathways to extensor and flexor Ia-afferents (in experiments with intraaxonal recording from these afferents). The possibility might thus be considered that some neuronal pathways are used to modulate transmission via Ia-afferents independently of their muscle origin. The same might hold true for extensor and flexor Ib-afferents. Generally, it is concluded that the minimal number of distinct neuronal populations subserving PAD of group I afferents may be two to six. Additionally, actions of cutaneous, joint, and interosseous afferents on DRPs from Ia-afferents were reexamined to further the comparison between neurons mediating PAD and those mediating postsynaptic excitation or inhibition of motoneurons. Only depression of Ia DRPs followed stimulation of these afferents at intensities of 1.5-2.0 times threshold and higher; lower threshold afferents were apparently ineffective. On the basis of lack of convergence of extensor Ib and Ia muscle afferents and of low-threshold cutaneous afferents, interneurons mediating PAD may thus be distinguished from the interneurons subserving Ib and Ia-like-Ib postsynaptic actions in motoneurons. The latter are coexcited by these three groups of afferents.

scholarly journals Muscle afferent excitability testing in spinal root-intact rats: dissociating peripheral afferent and efferent volleys generated by intraspinal microstimulation

2017 ◽  
Vol 117 (2) ◽  
pp. 796-807 ◽  
Author(s):  
Saeka Tomatsu ◽  
Geehee Kim ◽  
Joachim Confais ◽  
Kazuhiko Seki
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
Muscle Afferents ◽  
Primary Afferents ◽  
Medial Gastrocnemius ◽  
Primary Afferent Depolarization ◽  
Spinal Root ◽  
Primary Afferent ◽  
Intraspinal Microstimulation ◽  
Spinal Roots

Presynaptic inhibition of the sensory input from the periphery to the spinal cord can be evaluated directly by intra-axonal recording of primary afferent depolarization (PAD) or indirectly by intraspinal microstimulation (excitability testing). Excitability testing is superior for use in normal behaving animals, because this methodology bypasses the technically challenging intra-axonal recording. However, use of excitability testing on the muscle or joint afferent in intact animals presents its own technical challenges. Because these afferents, in many cases, are mixed with motor axons in the peripheral nervous system, it is crucial to dissociate antidromic volleys in the primary afferents from orthodromic volleys in the motor axon, both of which are evoked by intraspinal microstimulation. We have demonstrated in rats that application of a paired stimulation protocol with a short interstimulus interval (ISI) successfully dissociated the antidromic volley in the nerve innervating the medial gastrocnemius muscle. By using a 2-ms ISI, the amplitude of the volleys evoked by the second stimulation was decreased in dorsal root-sectioned rats, but the amplitude did not change or was slightly increased in ventral root-sectioned rats. Excitability testing in rats with intact spinal roots indicated that the putative antidromic volleys exhibited dominant primary afferent depolarization, which was reasonably induced from the more dorsal side of the spinal cord. We concluded that excitability testing with a paired-pulse protocol can be used for studying presynaptic inhibition of somatosensory afferents in animals with intact spinal roots. NEW & NOTEWORTHY Excitability testing of primary afferents has been used to evaluate presynaptic modulation of synaptic transmission in experiments conducted in vivo. However, to apply this method to muscle afferents of animals with intact spinal roots, it is crucial to dissociate antidromic and orthodromic volleys induced by spinal microstimulation. We propose a new method to make this dissociation possible without cutting spinal roots and demonstrate that it facilitates excitability testing of muscle afferents.

γ-Aminobutyric acid and primary afferent depolarization in feline spinal cord

1979 ◽  
Vol 57 (10) ◽  
pp. 1157-1167 ◽  
Author(s):  
B. R. Sastry
Keyword(s):  
Spinal Cord ◽  
Nerve Stimulation ◽  
Muscle Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Antidromic Activation ◽  
Primary Afferent ◽  
Afferent Terminal ◽  
Group I ◽  
Terminal Excitability

The effects of iontophoretically applied γ-aminobutyric acid (GABA), (−)-nipecotic acid (NCA), 2,4-diaminobutyric acid (DABA), and pentobarbital were examined on the thresholds for antidromic activation of single group I muscle afferents, in decerebrated spinal cats. GABA decreased the threshold for antidromic activation of the majority of the afferents. During this decrease in the threshold, the preterminal axons were depolarized. This depolarization was decreased by a prior depolarization, but increased by a hyperpolarization, of the afferent. During the depolarization of the afferent produced by GABA, the size of the orthodromic action potential was decreased. Iontophoretically applied bicuculline antagonized the effect of GABA on the threshold for antidromic activation of the afferents. NCA, DABA, and pentobarbital potentiated the action of GABA on the afferent terminal excitability. Pre-treatment of the animals with semicarbazide, which reportedly depletes spinal GABA, resulted in a reduction in the threshold produced by a conditioning stimulation of other group I afferents. GABA decreased the threshold for antidromic activation of the nonterminal regions of the afferents when applied near the stimulation sites. The amounts of GABA required to produce a decrease in the threshold of the nonterminal afferents were greater than those required to produce a comparable effect on the terminal regions of the fibres. Iontophoretically applied NCA and bicuculline, in amounts that were adequate to alter the effects of applied GABA, failed to affect the nerve stimulation-induced decrease in the threshold for antidromic activation of the fibres. Intravenously injected bicuculline, however, antagonized the actions of GABA as well as of the reduction in the threshold produced by nerve stimulation.These results indicate that (1) GABA-induced increase in the excitability of group I afferent terminals is associated with a depolarization of the afferent, (2) the uptake of iontophoretically applied amino acid into the spinal cord tissue appears to limit its action on the afferent terminal excitability, (3) GABA has a preterminal depolarizing action on group I muscle afferents, and (4) primary afferent depolarization produced by nerve stimulation may be of diffuse origin and, hence, cannot be significantly affected by iontophoretically applied NCA and bicuculline.

Excitability of primary afferents in feline spinal cord: taurine, homotaurine, and γ-aminobutyric acid compared

1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin
Keyword(s):  
Primary Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Conditioning Stimulation ◽  
Primary Afferent ◽  
Antagonistic Muscle ◽  
Consistent Change ◽  
Muscle Nerve ◽  
Gaba Synthesis ◽  
Stimulation Of

Effects of taurine and homotaurine (3-aminopropancsuIfonic acid), on excitability of primary afferents were compared with effects of γ-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazidc, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.

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