Mechanisms Causing Plateau Potentials in Spinal Motoneurones

Alaburda, Aidas; Perrier, Jean‐François; Hounsgaard, Jørn

doi:10.1007/978-1-4615-0713-0_27

Cited by 65 publications

(47 citation statements)

References 41 publications

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“…19,20 5-HT and NE act on spinal motor neurons yielding plateau potentials, which may amplify excitatory inputs including reflex inputs. [21][22][23] Plateau potentials originate on dendrites and amplify excitatory inputs up to six-fold, thus leading to sustained firing with minimal excitatory input. 24 This effect may be due to prolonged activation of Ca 2 þ channels.…”

Section: Historical Perspectivementioning

confidence: 99%

Spinal shock revisited: a four-phase model

et al. 2004

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Spinal shock has been of interest to clinicians for over two centuries. Advances in our understanding of both the neurophysiology of the spinal cord and neuroplasticity following spinal cord injury have provided us with additional insight into the phenomena of spinal shock. In this review, we provide a historical background followed by a description of a novel fourphase model for understanding and describing spinal shock. Clinical implications of the model are discussed as well.

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Section: Historical Perspectivementioning

confidence: 99%

Spinal shock revisited: a four-phase model

et al. 2004

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“…In adult chronic spinal (t13) cats, 5-HT modulates treadmill-induced locomotor patterns (Barbeau and Rossignol 1990;Edgerton et al 1997) and depresses the sAHP in motorneurons (White and Fung 1989). Application of 5-HT also modulates fictive locomotion in turtles, presumably by activation of plateau potentials by 5-HT 2 receptors (Alaburda et al 2002) and inhibition of K ϩ conductance by 5-HT 1A receptors (Perrier et al 2003).…”

Section: Introductionmentioning

confidence: 99%

5-HT Prolongs Ventral Root Bursting Via Presynaptic Inhibition of Synaptic Activity During Fictive Locomotion in Lamprey

Schwartz¹,

Gerachshenko²,

Alford³

2005

Journal of Neurophysiology

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. Locomotor pattern generation is maintained by integration of the intrinsic properties of spinal central pattern generator (CPG) neurons in conjunction with synaptic activity of the neural network. In the lamprey, the spinal locomotor CPG is modulated by 5-HT. On a cellular level, 5-HT presynaptically inhibits synaptic transmission and postsynaptically inhibits a Ca 2ϩ -activated K ϩ current responsible for the slow afterhyperpolarization (sAHP) that follows action potentials in ventral horn neurons. To understand the contribution of these cellular mechanisms to the modulation of the spinal CPG, we have tested the effect of selective 5-HT analogues against fictive locomotion initiated by bath application of N-methyl-D-aspartate (NMDA). We found that the 5-HT 1D agonist, L694-247, dramatically prolongs the frequency of ventral root bursting. Furthermore, we show that L694-247 presynaptically inhibits synaptic transmission without altering postsynaptic Ca 2ϩ -activated K ϩ currents. We also confirm that 5-HT inhibits synaptic transmission at concentrations that modulate locomotion. To examine the mechanism by which selective presynaptic inhibition modulates the frequency of fictive locomotion, we performed voltage-and current-clamp recordings of CPG neurons during locomotion. Our results show that 5-HT decreases glutamatergic synaptic drive within the locomotor CPG during fictive locomotion. Thus we conclude that presynaptic inhibition of neurotransmitter release contributes to 5-HT-mediated modulation of locomotor activity.

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“…Two types of L-type VDCC α-subunits, Ca V 1.2 and Ca V 1.3, are expressed in the spinal cord (21,22). Ca V 1.3-containing channels have a much lower activation threshold than Ca V 1.2 channels and are preferentially involved in genesis of the plateau potential (26,48). Although Ca V 1.3-containing channels are 10 -20 times less sensitive to dihydropyridine than Ca V 1.2 channels (49), nicardipine showed a selective effect on after-discharges (Fig.…”

Section: Figmentioning

confidence: 99%

“…The dose of nicardipine used in this study was thought to be enough for inhibition of after-discharges. Ca V 1.3 are expressed not only in the spinal dorsal horn (21) but also the ventral horn (24,48) and contribute to the generation of plateau potentials in motoneurons (26,50). However during-and after-discharges were not inhibited by injection of nicardipine into the spinal cord ventral horn (Fig.…”

Section: Figmentioning

confidence: 99%

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N- and L-Type Voltage-Dependent Ca<SUP>2+</SUP> Channels Contribute to the Generation of After-Discharges in the Spinal Ventral Root After Cessation of Noxious Mechanical Stimulation

2012

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Abstract. Voltage-dependent Ca2+ channels (VDCCs) play a crucial role in the spinal pain transduction. We previously reported that nociceptive mechanical stimuli to the rat hindpaw evoked two types of ventral root discharges that increased during stimulation (during-discharges) and after cessation of stimulation (after-discharges). To explore the involvement of VDCCs in these ventral root discharges, several VDCC blockers were applied directly to the surface of the spinal cord. Spinalized rats were laminectomized. The fifth lumbar ventral root was sectioned and used for multi-unit efferent discharges recording. An agar pool was constructed on the first lumbar vertebra for drug application. Ethosuximide (a T-type VDCC blocker) had no effect on ventral root discharges. ω-Conotoxin GVIA (an N-type VDCC blocker) preferentially suppressed after-discharges. ω-Agatoxin IVA (a P/Q-type VDCC blocker), diltiazem, and verapamil (L-type VDCC blockers) nonselectively depressed both during-and after-discharges. The more selective L-type VDCC blocker nicardipine depressed only after-discharges and the depression was exhibited when nicardipine was microinjected into the dorsal horn, but not into the ventral horn. These findings suggested that N-and L-type VDCCs in the dorsal horn were involved in the generation of afterdischarges and these blockers might be useful for treatment of persistent pain that involves the spinal pathway.

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Mechanisms Causing Plateau Potentials in Spinal Motoneurones

Cited by 65 publications

References 41 publications

Spinal shock revisited: a four-phase model

Spinal shock revisited: a four-phase model

5-HT Prolongs Ventral Root Bursting Via Presynaptic Inhibition of Synaptic Activity During Fictive Locomotion in Lamprey

N- and L-Type Voltage-Dependent Ca<SUP>2+</SUP> Channels Contribute to the Generation of After-Discharges in the Spinal Ventral Root After Cessation of Noxious Mechanical Stimulation

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