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Prepulse inhibition of change-related P50m no correlation with P50m gating
Both prepulse inhibition (PPI) of the startle response and P50 sensory gating are important tools to investigate the inhibitory mechanisms of sensory processing. However, previous studies found no or a weak association between these two measures, which may have been due to the different indexes used...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825222/ https://www.ncbi.nlm.nih.gov/pubmed/24255871 http://dx.doi.org/10.1186/2193-1801-2-588 |
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author | Inui, Koji Tsuruhara, Aki Nakagawa, Kei Nishihara, Makoto Kodaira, Minori Motomura, Eishi Kakigi, Ryusuke |
author_facet | Inui, Koji Tsuruhara, Aki Nakagawa, Kei Nishihara, Makoto Kodaira, Minori Motomura, Eishi Kakigi, Ryusuke |
author_sort | Inui, Koji |
collection | PubMed |
description | Both prepulse inhibition (PPI) of the startle response and P50 sensory gating are important tools to investigate the inhibitory mechanisms of sensory processing. However, previous studies found no or a weak association between these two measures, which may have been due to the different indexes used. We examined the relationship between P50 sensory gating and P50 PPI. P50m sensory gating and PPI of Change-related P50m were assessed in 14 subjects using magnetoencephalography. Concerning P50m sensory gating, the amplitudes of the response to the second click relative to that to the first one were reduced by 43 and 47% for the left and right hemisphere, respectively. Change-related P50m was evoked by an abrupt sound pressure increase by 10 dB in a continuous click train of 70 dB. When this test stimulus was preceded by a click (prepulse) with a weaker sound pressure increase (5 dB) at a prepulse-test interval of 30, 60, or 90 ms, Change-P50m was suppressed by 33 ~ 65% while the prepulse itself elicited no or very weak P50m responses. Although the amplitude of the P50m response to the first click and the amplitude of the Change-P50m test alone response were positively correlated (r = 0.6), the degree of the inhibition of the two measures was not (r = -0.06 ~ 0.14). The neural origin was estimated to be located in the supratemporal plane around the superior temporal gyrus or Heschl’s gyrus and did not differ between P50m and Change-P50m. The present results suggest that P50m and Change-P50m are generated by a similar group of neurons in the auditory cortex, while the mechanisms of P50m sensory gating and Change-P50m PPI are different. |
format | Online Article Text |
id | pubmed-3825222 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-38252222013-11-19 Prepulse inhibition of change-related P50m no correlation with P50m gating Inui, Koji Tsuruhara, Aki Nakagawa, Kei Nishihara, Makoto Kodaira, Minori Motomura, Eishi Kakigi, Ryusuke Springerplus Research Both prepulse inhibition (PPI) of the startle response and P50 sensory gating are important tools to investigate the inhibitory mechanisms of sensory processing. However, previous studies found no or a weak association between these two measures, which may have been due to the different indexes used. We examined the relationship between P50 sensory gating and P50 PPI. P50m sensory gating and PPI of Change-related P50m were assessed in 14 subjects using magnetoencephalography. Concerning P50m sensory gating, the amplitudes of the response to the second click relative to that to the first one were reduced by 43 and 47% for the left and right hemisphere, respectively. Change-related P50m was evoked by an abrupt sound pressure increase by 10 dB in a continuous click train of 70 dB. When this test stimulus was preceded by a click (prepulse) with a weaker sound pressure increase (5 dB) at a prepulse-test interval of 30, 60, or 90 ms, Change-P50m was suppressed by 33 ~ 65% while the prepulse itself elicited no or very weak P50m responses. Although the amplitude of the P50m response to the first click and the amplitude of the Change-P50m test alone response were positively correlated (r = 0.6), the degree of the inhibition of the two measures was not (r = -0.06 ~ 0.14). The neural origin was estimated to be located in the supratemporal plane around the superior temporal gyrus or Heschl’s gyrus and did not differ between P50m and Change-P50m. The present results suggest that P50m and Change-P50m are generated by a similar group of neurons in the auditory cortex, while the mechanisms of P50m sensory gating and Change-P50m PPI are different. Springer International Publishing 2013-11-01 /pmc/articles/PMC3825222/ /pubmed/24255871 http://dx.doi.org/10.1186/2193-1801-2-588 Text en © Inui et al.; licensee Springer. 2013 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Inui, Koji Tsuruhara, Aki Nakagawa, Kei Nishihara, Makoto Kodaira, Minori Motomura, Eishi Kakigi, Ryusuke Prepulse inhibition of change-related P50m no correlation with P50m gating |
title | Prepulse inhibition of change-related P50m no correlation with P50m gating |
title_full | Prepulse inhibition of change-related P50m no correlation with P50m gating |
title_fullStr | Prepulse inhibition of change-related P50m no correlation with P50m gating |
title_full_unstemmed | Prepulse inhibition of change-related P50m no correlation with P50m gating |
title_short | Prepulse inhibition of change-related P50m no correlation with P50m gating |
title_sort | prepulse inhibition of change-related p50m no correlation with p50m gating |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825222/ https://www.ncbi.nlm.nih.gov/pubmed/24255871 http://dx.doi.org/10.1186/2193-1801-2-588 |
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