Trial reportThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Reflex excitability regulates prepulse inhibition.
Trial report in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Target Site of Prepulse Inhibition of the Trigeminal Blink Reflex in Humans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Striatal D1 and D2 receptor availability are selectively associated with eye-blink rates after methylphenidate treatment.Communications biology · 2022Article
- Macaque monkey trigeminal blink reflex circuits targeting orbicularis oculi motoneurons.The Journal of comparative neurology · 2021Article
- Cellular Mechanisms of Cortisol-Induced Changes in Mauthner-Cell Excitability in the Startle Circuit of Goldfish.Frontiers in neural circuits · 2017Article
- Frequency matters: beta-band subthalamic nucleus deep-brain stimulation induces Parkinsonian-like blink abnormalities in normal rats.The European journal of neuroscience · 2014Article
- MitoPark mice, an animal model of Parkinson's disease, show enhanced prepulse inhibition of acoustic startle and no loss of gating in response to the adenosine A(2A) antagonist SCH 412348.Psychopharmacology · 2014Article
- The 5-HT5A receptor regulates excitability in the auditory startle circuit: functional implications for sensorimotor gating.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Animal models for investigating benign essential blepharospasm.Current neuropharmacology · 2013Article
- Characterizing the spontaneous blink generator: an animal model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Comparison of salicylate- and quinine-induced tinnitus in rats: development, time course, and evaluation of audiologic correlates.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2010Article
- Impaired prepulse inhibition and prepulse-elicited reactivity but intact reflex circuit excitability in unmedicated schizophrenia patients: a comparison with healthy subjects and medicated schizophrenia patients.Schizophrenia bulletin · 2009Article
- Suppression of cutaneous reflexes by a conditioning pulse during human walking.Experimental brain research · 2006Article
- Animal models of focal dystonia.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2005Review
- Sensorimotor integration in patients with parkinsonian type multisystem atrophy.Journal of neurology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Presentation of a weak stimulus, a prepulse, before a reflex-evoking stimulus decreases the amplitude of the reflex response relative to reflex amplitude evoked without a preceding prepulse. For example, presenting a brief tone before a trigeminal blink-eliciting stimulus significantly reduces reflex blink amplitude. A common explanation of such data are that sensory processing of the prepulse modifies reflex circuit behavior. The current study investigates the converse hypothesis that the intrinsic characteristics of the reflex circuit rather than prepulse processing determine prepulse modification of trigeminal and acoustic reflex blinks. Unilateral lesions of substantia nigra pars compacta neurons created rats with hyperexcitable trigeminal reflex blinks but normally excitable acoustic reflex blinks. In control rats, presentation of a prepulse reduced the amplitude of both trigeminal and acoustic reflex blinks. In 6-OHDA-lesioned rats, however, the same acoustic prepulse facilitated trigeminal reflex blinks but inhibited acoustic reflex blinks. The magnitude of prepulse modification correlated with reflex excitability. Humans exhibited the same pattern of prepulse modification. An acoustic prepulse facilitated the trigeminal reflex blinks of subjects with hyperexcitable trigeminal reflex blinks caused by Parkinson's disease. The same prepulse inhibited trigeminal reflex blinks of age-matched control subjects. Prepulse modification also correlated with trigeminal reflex blink excitability. These data show that reflex modification by a prepulse reflects the intrinsic characteristics of the reflex circuit rather than an external adjustment of the reflex circuit by the prepulse.
Indexed as
Identifiers
10818160PMC6772660What OpenQuestion holds
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.