Mechanisms involved in presynaptic depolarization of group I and rubrospinal fibers in cat spinal cord.

Rudomín, P.; Engberg, I.; Jiménez, Ismael

doi:10.1152/jn.1981.46.3.532

Cited by 81 publications

(41 citation statements)

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“…The majority (80%) of viral-labeled neurons express markers for GAD1, GAD2, or GlyT2, consistent with previous EM studies, indicating that GABA is the main neurotransmitter at the axo-axonic synapses onto sensory afferents ( Figure 7B). GABA induces PAD that suppresses action potentials arriving at the afferent terminals, resulting in presynaptic inhibition of sensory transmission (8)(9)(10).…”

Section: Discussionmentioning

confidence: 99%

“…The main neurotransmitter of these axo-axonic and dendro-axonic inputs was shown to be GABA (5)(6)(7). GABA released at these axo-axonic synapses causes primary afferent depolarization (PAD) that depresses action potentials arriving at the afferent terminal (8)(9)(10). Thus, these inputs onto sensory afferents are thought to control pain and touch sensory transmission through presynaptic inhibition.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identifying local and descending inputs for primary sensory neurons

Zhang¹,

Zhao²,

Rodriguez³

et al. 2015

Journal of Clinical Investigation

103

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identifying local and descending inputs for primary sensory neurons

Zhang¹,

Zhao²,

Rodriguez³

et al. 2015

Journal of Clinical Investigation

103

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“…Antidromic discharges were blocked by picrotoxin and bumetanide, demonstrating that GABA A receptors and NKCC1 cotransporters were involved. It is well established that GABA, through the activation of GABA A receptors, plays a major role in generating PADs (Rudomín et al, 1981). PADs rely on a high [Cl Ϫ ] I , which is maintained by the chloride intruders NKCC1 cotransporters (Alvarez-Leefmans et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Primary Afferent Terminals Acting as Excitatory Interneurons Contribute to Spontaneous Motor Activities in the Immature Spinal Cord

Bos¹,

Brocard²,

Vinay³

2011

Journal of Neuroscience

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Patterned, spontaneous activity plays a critical role in the development of neuronal networks. A robust spontaneous activity is observed in vitro in spinal cord preparations isolated from immature rats. The rhythmic ventral root discharges rely mainly on the depolarizing/ excitatory action of GABA and glycine early during development, whereas at later stages glutamate drive is primarily responsible for the rhythmic activity and GABA/glycine are thought to play an inhibitory role. However, rhythmic discharges mediated by the activation of GABA A receptors are recorded from dorsal roots (DRs). In the present study, we used the in vitro spinal cord preparation of neonatal rats to identify the relationship between discharges that are conducted antidromically along DRs and the spontaneous activity recorded from lumbar motoneurons. We show that discharges in DRs precede those in ventral roots and that primary afferent depolarizations (PADs) start earlier than EPSPs in motoneurons. EPSP-triggered averaging revealed that the action potentials propagate not only antidromically in the DR but also centrally and trigger EPSPs in motoneurons. Potentiating GABAergic antidromic discharges by diazepam increased the EPSPs recorded from motoneurons; conversely, blocking DR bursts markedly reduced these EPSPs. High intracellular concentrations of chloride are maintained in primary afferent terminals by the sodium-potassium-chloride cotransporter NKCC1. Blocking these cotransporters by bumetanide decreased both dorsal and ventral root discharges. We conclude that primary afferent fibers act as excitatory interneurons and that GABA, through PADs reaching firing threshold, is still playing a key role in promoting spontaneous activity in neonates.

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“…Presynaptic inhibition, estimated from indirect measurements in human subjects, is often proposed as a mechanism to explain changes in the gain of reflex pathways during movement (Simonsen and DyhrePoulsen, 1999;Roche et al, 2011;Robertson et al, 2012), motor disorders (Calancie et al, 1993;Morita et al, 2000), and age or fatigue (Butchart et al, 1993). Presynaptic inhibition is produced by spinal interneurons with GABAergic axo-axonic synapses on primary afferent terminals (Eccles et al, 1962;Rudomin and Schmidt, 1999;Hughes et al, 2005). With GABAergic activation, Cl Ϫ anions escape the negative intra-axonal environment, thus producing a primary afferent depolarization (PAD) (Eccles et al, 1963;Nicoll and Alger, 1979;Cattaert and El Manira, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…PAD can thus be evoked by stimulating sensory inputs, supraspinal structures, or central pattern generators (CPGs) (Rudomin and Schmidt, 1999;Rossignol et al, 2006). However, how these systems interact during movement remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Independent Control of Presynaptic Inhibition by Reticulospinal and Sensory Inputs at Rest and during Rhythmic Activities in the Cat

2013

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To be functionally relevant during movement, the transmission from primary afferents must be efficiently controlled by presynaptic inhibition. Sensory feedback, central pattern generators, and supraspinal structures can all evoke presynaptic inhibition, but we do not understand how these inputs interact during movement. Here, we investigated the convergence of inputs from the reticular formation and sensory afferents on presynaptic inhibitory pathways and their modulation at rest and during two fictive motor tasks (locomotion and scratch) in decerebrate cats. The amplitude of primary afferent depolarization (PAD), an estimate of presynaptic inhibition, was recorded in individual afferents with intra-axonal recordings and in a mix of afferents in lumbar dorsal rootlets (dorsal root potential [DRP]) with bipolar electrodes. There was no spatial facilitation between inputs from reticulospinal and sensory afferents with DRPs or PADs, indicating an absence of convergence. However, spatial facilitation could be observed by combining two sensory inputs, indicating that convergence was possible. Task-dependent changes in the amplitude of responses were similar for reticulospinal and sensory inputs, increasing during fictive locomotion and decreasing during fictive scratch. During fictive locomotion, DRP and PAD amplitudes evoked by reticulospinal inputs were increased during the flexion phase, whereas sensory-evoked DRPs and PADs showed maximal amplitude in either flexion or extension phases. During fictive scratch, the amplitudes of DRPs and PADs evoked by both sources were maximal in flexion. The absence of spatial facilitation and different phase-dependent modulation patterns during fictive locomotion are consistent with independent presynaptic inhibitory pathways for reticulospinal and sensory inputs.

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Mechanisms involved in presynaptic depolarization of group I and rubrospinal fibers in cat spinal cord.

Cited by 81 publications

References 0 publications

Identifying local and descending inputs for primary sensory neurons

Identifying local and descending inputs for primary sensory neurons

Primary Afferent Terminals Acting as Excitatory Interneurons Contribute to Spontaneous Motor Activities in the Immature Spinal Cord

Independent Control of Presynaptic Inhibition by Reticulospinal and Sensory Inputs at Rest and during Rhythmic Activities in the Cat

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