ArticleJournal of neurophysiology2011
Polysynaptic excitatory postsynaptic potentials that trigger spasms after spinal cord injury in rats are inhibited by 5-HT1B and 5-HT1F receptors.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01587170 (Phase 2), which is not on this map. Cited by 35 papers.
What it found
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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.
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.
Phase 2: Effects of Zolmitriptan on Sensory Afferent Transmission After Spinal Cord Injury
Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Human motoneurone excitability is depressed by activation of serotonin 1A receptors with buspirone.The Journal of physiology · 2017Trial
- GABAA receptor mediated facilitation of proprioceptive afferent transmission to motoneurons is facilitated by TRPM8 channels on C-fibres that are gated by serotonin.bioRxiv : the preprint server for biology · 2026Article
- Pathophysiology of voluntary motor commands at the level of the spinal motoneuron in patients with multiple sclerosis.medRxiv : the preprint server for health sciences · 2025Article
- Grid-based transcutaneous spinal cord stimulation: probing neuromodulatory effect in spinal flexion reflex circuits.Journal of neural engineering · 2025Article
- Loss of 5-HTFrontiers in neural circuits · 2025Article
- Muscle Spasms after Spinal Cord Injury Stem from Changes in Motoneuron Excitability and Synaptic Inhibition, Not Synaptic Excitation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Mitophagy regulates mitochondrial number following pharmacological induction of mitochondrial biogenesis in renal proximal tubule cells.Frontiers in pharmacology · 2024Article
- Post-activation depression from primary afferent depolarization (PAD) produces extensor H-reflex suppression following flexor afferent conditioning.The Journal of physiology · 2023Article
- GABA facilitates spike propagation through branch points of sensory axons in the spinal cord.Nature neuroscience · 2022Article
- Impaired Ability to Relax Pelvic Floor Muscles in Men With Chronic Prostatitis/Chronic Pelvic Pain Syndrome.Physical therapy · 2022Article
- 5-HTThe European journal of neuroscience · 2022Article
- Review
- FDA-approved 5-HTExperimental neurology · 2021Article
- Enhancing KCC2 activity decreases hyperreflexia and spasticity after chronic spinal cord injury.Experimental neurology · 2021Article
- The Involvement of CaFrontiers in neural circuits · 2021Article
- Vibration attenuates spasm-like activity in humans with spinal cord injury.The Journal of physiology · 2020Article
- Bursting interneurons in the deep dorsal horn develop increased excitability and sensitivity to serotonin after chronic spinal injury.Journal of neurophysiology · 2020Article
- 5-hydroxytryptamine 1F Receptor Agonist Induces Mitochondrial Biogenesis and Promotes Recovery from Spinal Cord Injury.The Journal of pharmacology and experimental therapeutics · 2020Article
- 5-HTJournal of neurophysiology · 2019Article
- Locomotor-related V3 interneurons initiate and coordinate muscles spasms after spinal cord injury.Journal of neurophysiology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Sensory afferent transmission and associated spinal reflexes are normally inhibited by serotonin (5-HT) derived from the brain stem. Spinal cord injury (SCI) that eliminates this 5-HT innervation leads to a disinhibition of sensory transmission and a consequent emergence of unusually long polysynaptic excitatory postsynaptic potentials (EPSPs) in motoneurons. These EPSPs play a critical role in triggering long polysynaptic reflexes (LPRs) that initiate muscles spasms. In the present study we examined which 5-HT receptors modulate the EPSPs and whether these receptors adapt to a loss of 5-HT after chronic spinal transection in rats. The EPSPs and associated LPRs recorded in vitro in spinal cords from chronic spinal rats were consistently inhibited by 5-HT(1B) or 5-HT(1F) receptor agonists, including zolmitriptan (5-HT(1B/1D/1F)) and LY344864 (5-HT(1F)), with a sigmoidal dose-response relation, from which we computed the 50% inhibition (EC(50)) and potency (-log EC(50)). The potencies of 5-HT receptor agonists were highly correlated with their binding affinity to 5-HT(1B) and 5-HT(1F) receptors, and not to other 5-HT receptors. Zolmitriptan also inhibited the LPRs and general muscle spasms recorded in vivo in the awake chronic spinal rat. The 5-HT(1B) receptor antagonists SB216641 and GR127935 and the inverse agonist SB224289 reduced the inhibition of LPRs by 5-HT(1B) agonists (zolmitriptan). However, when applied alone, SB224289, SB216641, and GR127935 had no effect on the LPRs, indicating that 5-HT(1B) receptors do not adapt to chronic injury, remaining silent, without constitutive activity. The reduction in EPSPs with zolmitriptan unmasked a large glycine-mediated inhibitory postsynaptic current (IPSC) after SCI. This IPSC and associated chloride current reversed at -73 mV, slightly below the resting membrane potential. Zolmitriptan did not change motoneuron properties. Our results demonstrate that 5-HT(1B/1F) agonists, such as zolmitriptan, can restore inhibition of sensory transmission after SCI without affecting general motoneuron function and thus may serve as a novel class of antispastic drugs.
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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.