The conditioning-testing P50 paradigm is used to demonstrate sensory gating of responsiveness to auditory stimuli. Sensory gating is measured in terms of a suppression of the second (test) P50 component in that paradigm. The time course of sensory gating can be determined by examining subjects' gating of responsiveness to stimuli repeated at various interpair intervals. In the present study auditory evoked potentials were recorded using a paired click, conditioning-testing P50 paradigm in 11 normal subjects with no family history of any psychotic disorder. Recordings were made at conditioning-testing intervals of 250 ms, 500 ms, 750 ms and 1000 ms. Whereas the grand averages of the P50 conditioning-testing response for the 250- and 500-ms intervals were 3.07% and 37.2%, respectively, indicating almost complete suppression, the grand averages of the ratios for the 750- and 1000-ms intervals were 114.35% and 92.92%, respectively, indicating little or no suppression. There was significant correlation in the C-T ratios with the increasing intervals. Our results suggest that the mechanism(s) responsible for sensory gating is activated mostly during the 500 ms after stimulus presentation. Other gating mechanism(s) functioning at longer intervals appear to be uncertain.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0167-8760(01)00134-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Layer-specific control of inhibition by NDNF interneurons.
Proc Natl Acad Sci U S A
January 2025
Modelling of Cognitive Processes, Berlin Institute of Technology, Berlin 10587, Germany.
Neuronal processing of external sensory input is shaped by internally generated top-down information. In the neocortex, top-down projections primarily target layer 1, which contains NDNF (neuron-derived neurotrophic factor)-expressing interneurons and the dendrites of pyramidal cells. Here, we investigate the hypothesis that NDNF interneurons shape cortical computations in an unconventional, layer-specific way, by exerting presynaptic inhibition on synapses in layer 1 while leaving synapses in deeper layers unaffected.
View Article and Find Full Text PDFNociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.
J Gen Physiol
March 2025
Institute for Neurophysiology, Uniklinik RWTH Aachen University, Aachen, Germany.
Voltage-gated sodium channels (VGSCs) in the peripheral nervous system shape action potentials (APs) and thereby support the detection of sensory stimuli. Most of the nine mammalian VGSC subtypes are expressed in nociceptors, but predominantly, three are linked to several human pain syndromes: while Nav1.7 is suggested to be a (sub-)threshold channel, Nav1.
View Article and Find Full Text PDFThe phenomenon of sensory processing: historical overview, theoretical models, and neurophysiological underpinnings.
Acta Neurobiol Exp (Wars)
January 2025
Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland.
The article provides a review of the sensory processing (SP) phenomenon, its origins, theoretical models, and neurophysiological foundations. Initiated by A. Jean Ayres' research on sensory integration in the 1960s and 70s, this field has evolved, leading to the development of concepts such as Winnie Dunn's four quadrant model and Miller's ecological model of sensory modulation.
View Article and Find Full Text PDFMolecular basis of neurosteroid and anticonvulsant regulation of TRPM3.
Nat Struct Mol Biol
January 2025
Department of Biochemistry, Duke University School of Medicine, Durham, NC, USA.
Transient receptor potential channel subfamily M member 3 (TRPM3) is a Ca-permeable cation channel activated by the neurosteroid pregnenolone sulfate (PregS) or heat, serving as a nociceptor in the peripheral sensory system. Recent discoveries of autosomal dominant neurodevelopmental disorders caused by gain-of-function mutations in TRPM3 highlight its role in the central nervous system. Notably, the TRPM3 inhibitor primidone, an anticonvulsant, has proven effective in treating patients with TRPM3-linked neurological disorders and in mouse models of thermal nociception.
View Article and Find Full Text PDFA bedside sensory phenomenon that can help explain functional sensory symptoms.
Pract Neurol
December 2024
Neurology, University Hospital Essen, Essen, Germany
Explaining basic illness mechanisms is an important step in communicating functional neurological symptoms. Clinical signs for motor symptoms, such as the Hoover test, have proven an excellent basis for mechanistic explanations. Here, I recommend a simple technique for eliciting tingling sensations through directed bodily attention, as a helpful experiential starting point for explanations of sensory gating and somatosensory amplification in patients with functional hyperaesthesia, paraesthesia and chronic pain.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!