Evidence map›Paper›PMID 19783207›Full record

ReviewClinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology2009

Motoneuron excitability: the importance of neuromodulatory inputs.

C J Heckman, Carol Mottram, Kathy Quinlan, Renee Theiss, Jenna Schuster

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07226284 (The Effects of Vagus Nerve Stimulation on Intrinsic Lower Leg Spinal Motoneuron Excitability in Parkinson's Disease.), which is not on this map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07226284 narecruitingnot on this mapstarted 2026, after this paper: background citation

The Effects of Vagus Nerve Stimulation on Intrinsic Lower Leg Spinal Motoneuron Excitability in Parkinson's Disease.

TypeinterventionalSponsorUniversity of MinnesotaRan2026 to 2029Enrolled75ConditionsPARKINSON DISEASE (Disorder), Parkinson's Disease (PD)ArmsVagal nerve stimulation, No intervention
3 · Its place in the literature

Who cites it

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.

  1. Dopamine agonists for restless legs syndrome.The Cochrane database of systematic reviews · 2011
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  20. A novel protocol to investigate the monoaminergic relationship between descending nociceptive and motor unit neuromodulation.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2025
    Article

61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

C J HeckmanPhysiology, Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL 60126, USA. Electronic address: c-heckman@northwestern.edu.
Carol MottramPhysiology, Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL 60126, USA.
Kathy QuinlanPhysiology, Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL 60126, USA.
Renee TheissPhysiology, Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL 60126, USA.
Jenna SchusterPhysiology, Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL 60126, USA.
Northwestern University · US

Funding

MONOAMINES EFFECTS ON MOTONEURON DISCHARGE PATTERNSR01NS034382 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HECKMAN, CHARLES · 1996 to 2013
$3.9M
Increased persistent sodium current in SOD1 motoneuronsR01NS051462 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HECKMAN, CHARLES · 2005 to 2009
$1.6M
NINDS NIH HHS NS034382NINDS NIH HHS NS51462NINDS NIH HHS R01 NS034382NINDS NIH HHS R01 NS051462
6 · The paper itself

Abstract

The excitability of spinal motoneurons is both fundamental for motor behavior and essential in diagnosis of neural disorders. There are two mechanisms for altering this excitability. The classic mechanism is mediated by synaptic inputs that depolarize or hyperpolarize motoneurons by generating postsynaptic potentials. This "ionotropic" mechanism works via neurotransmitters that open ion channels in the cell membrane. In the second mechanism, neurotransmitters bind to receptors that activate intracellular signaling pathways. These pathways modulate the properties of the voltage-sensitive channels that determine the intrinsic input-output properties of motoneurons. This "neuromodulatory" mechanism usually does not directly activate motoneurons but instead dramatically alters the neuron's response to ionotropic inputs. We present extensive evidence that neuromodulatory inputs exert a much more powerful effect on motoneuron excitability than ionotropic inputs. The most potent neuromodulators are probably serotonin and norepinephrine, which are released by axons originating in the brainstem and can increase motoneuron excitability fivefold or more. Thus, the standard tests of motoneuron excitability (H-reflexes, tendon taps, tendon vibration and stretch reflexes) are strongly influenced by the level of neuromodulatory input to motoneurons. This insight is likely to be profoundly important for clinical diagnosis and treatment.

Indexed as

Action PotentialsAnimalsExcitatory Postsynaptic PotentialsHumansMotor NeuronsNervous System DiseasesNeurotransmitter AgentsNeurotransmitter Agents

Identifiers

PMID19783207
PMCPMC7312725
OpenAlexW1999967173

What OpenQuestion holds

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Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.