Dopaminergic influence on the excitability of antidromically activated Renshaw cells in the lumbar spinal cord of the rat

Maitra, K.K.; Seth, Pallab; Thewissen, Michael; Ross, H.-G.; Ganguly, Dilip

doi:10.1111/j.1748-1716.1993.tb09538.x

Cited by 14 publications

(15 citation statements)

References 26 publications

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“…An important caveat is that DA may not have similar actions in different cells in the ventral horn. Heterogeneity of actions is a hallmark of monoaminergic modulatory actions in the spinal cord (Kemnitz, 1997;Beato and Nistri, 1998;Rekling et al, 2000;Schmidt and Jordan, 2000;Gordon and Whelan, 2006), and there is reason to suspect that DA may also have different effects on different classes of ventral horn neurons depending on DA receptor distribution (Dubois et al, 1986;Maitra et al, 1993;Seth et al, 1993;Levant and McCarson, 2001). In other regions of the brain, DA increases EPSCs in layer II-III pyramidal neurons (GonzalezIslas and Hablitz, 2003) in rat prefrontal cortex but decreases EPSCs in the nucleus of the solitary tract (Kline et al, 2002).…”

Section: Synaptic Transmissionmentioning

confidence: 99%

Dopaminergic Modulation of Spinal Neuronal Excitability

Han¹,

Nakanishi²,

Tran³

et al. 2007

J. Neurosci.

105

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It is well recognized that dopamine (DA) can modulate spinal networks and reflexes. DA fibers and receptors are present in the spinal cord, and evidence for DA release within the spinal cord has been published. A critical gap is the lack of data regarding dopaminergic modulation of intrinsic and synaptic properties of motoneurons and ventral interneurons in the mammalian spinal cord. In this paper, we address this issue by examining the cellular mechanisms underlying the excitatory effect of DA on motor systems. We examine the effects of DA on two classes of cells important for motor control, motoneurons and Hb9 interneurons, located in lamina VIII. We show that DA can boost excitability in spinal motoneurons by decreasing the first spike latency and the afterhyperpolarization. Collectively, this leads to an increase in the frequency-current slope likely attributable to modulation of I A and SK Ca (small-conductance calciumactivated K ϩ channel) currents. We also demonstrate that DA increases glutamatergic transmission onto motoneurons. Our data also suggest that DA stabilizes the rhythmic output of conditionally bursting interneurons. Collectively, these data indicate that DA has widespread actions on intrinsic and synaptic properties of ventral spinal neurons.

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Section: Synaptic Transmissionmentioning

confidence: 99%

Dopaminergic Modulation of Spinal Neuronal Excitability

Han¹,

Nakanishi²,

Tran³

et al. 2007

J. Neurosci.

105

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“…Dopamine enhances ventral horn field potentials during antidromic activation of motoneurons in rat lumbar spinal cord (53) but decreases the synaptic response to dorsal root stimulation in rat and cat motoneurons (189,777). In addition, dopamine modulates Renshaw cell-mediated feedback inhibition of rat motoneurons via effects of both D 1 -and D 2 -type dopamine receptors (778,1129). Intracellular studies on mammalian motoneurons are required to determine if mechanisms identified in lower vertebrates and invertebrates are retained in mammals.…”

Section: G Dopaminementioning

confidence: 99%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

532

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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“…Even more surprising are the volunteers' responses to the treatment L-dopa+benzerazide. One hypothesis to account for this imbalance may involve the maintenance of a monosynaptic pathway, 17 capable of regulating the transmission of dopaminergic stimuli. Dopamine, by stimulating dopaminergic D 2 receptors, might inhibit central cholinergic transmission yielding a neurochemical balance (excitatory/inhibitory) which would prevent the occurrence of such abnormal movements.…”

Section: Discussionmentioning

confidence: 99%

“…Dopaminergic agonists have since been used in the treatment of movement disorders. Maitra 17 observed the involvement of the spinal cord in the pathophysiology of extrapyramidal motor disorders. There are motor nerve terminals containing muscarinic as well as inhibitory dopaminergic receptors that in¯uence acetylcholine release at the spinal cord level.…”

Section: Introductionmentioning

confidence: 99%

“…There are motor nerve terminals containing muscarinic as well as inhibitory dopaminergic receptors that in¯uence acetylcholine release at the spinal cord level. 18 In order to study the inhibitory in¯uence of the dopaminergic system on spinal cholinergic transmission, Maitra 17 used a monosynaptic excitatory pathway from the collateral a motor axon of the Renshaw cells using apomorphine (a dopaminergic agonist) and sulpiride (a D 2 dopaminergic antagonist). Based on their ®ndings, the authors concluded that dopamine inhibited motor activity and in¯uenced central acetylcholine transmission.…”

Section: Introductionmentioning

confidence: 99%

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Treatment of periodic leg movements with a dopaminergic agonist in subjects with total spinal cord lesions

1999

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Objective: To investigate the eect of L-dopa on the PLM/h index of spinal cord injured subjects. Setting: SaÄ o Paulo, Brazil. Methods: Thirteen male volunteers with spinal cord section between T7 ± T12, and mean age of 31.6+8.3 years participated in the study. L-dopa or placebo were administered for 30 days, 1 h before the volunteers went to sleep, in a double blind, crossover design. Polysomnographic recordings were performed on ten occasions: Phase 1: Basal night, following an adaptation night at the sleep laboratory; phase 2: after 1, 7, 21 and 30 days of L-dopa administration; phase 3: ®rst night of L-dopa or placebo withdrawal; phase IV: 1, 7, 21 and 30 days after placebo ingestion. Results: The index of PLM/h on the ®rst night of L-dopa or placebo withdrawal (phase III) was lower than on both the basal night and the ®rst night of L-dopa treatment. At the time of polysomnographic analysis, volunteers were divided into two groups: index of PLM/h below ®ve and those whose index was above ®ve. Comparison between L-dopa and placebo treatments revealed that only those volunteers with an index above ®ve revealed a reduction in PLM in L-dopa. Conclusion: These results indicate that despite the spinal cord lesions, L-dopa treatment is capable of minimizing PLM during sleep.Keywords: sleep; spinal cord lesion(s); L-dopa; periodic leg movements (PLM); paraplegic; restless legs syndrome (RLS) IntroductionThe restless legs syndrome (RLS) was originally described in the general population by Ekbom. There is, however, a lack of consensus regarding dosage and length of administration of these drugs with therapeutic doses ranging between 100 and 250 mg of L-dopa.Recently, a high incidence of PLM and RLS in subjects with spinal cord lesions have been reported, 8 ± 12 allowing the possibility of identifying the origin of these abnormal movements. These subjects spontaneously report sleep problems, and also even mention the need to be tied to the bed so as to avoid falling on the¯oor due to the frequency of lower limb movements during sleep.9 Moreover, reduction of the incidence of PLM and RLS following acute physical activity in these patients may be helpful for the identi®cation of the mechanisms underlying PLM and RLS.10,13 Thus, it is possible that the reduction of limb movements may stem from endorphin secretion induced by physical activity, 14 since treatment with opiates often results in a reduction of PLM and RLS.3 In addition, there is an important positive correlation between PLM and K complexes in spinal cord injured 10,11 and non-paraplegic subjects. 3 To our knowledge, there is no study of PLM in spinal cord lesioned subjects treated with dopaminergic agonists.It is known that dopamine plays an important role in motor activity in general. Demonstrably, dopaminergic agonists induce a decrease in motor activity. Spinal Cord (1999) 37, 634 ± 637 ã 1999 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/99 $15.00http://www.stockton-press.co.uk/sc abnormal movements in Parkinsonian patients....

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Dopaminergic influence on the excitability of antidromically activated Renshaw cells in the lumbar spinal cord of the rat

Cited by 14 publications

References 26 publications

Dopaminergic Modulation of Spinal Neuronal Excitability

Dopaminergic Modulation of Spinal Neuronal Excitability

Synaptic Control of Motoneuronal Excitability

Treatment of periodic leg movements with a dopaminergic agonist in subjects with total spinal cord lesions

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