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Conference Paper: Corticofugal inhibition on the auditory thalamic neurons: an in-vivo intracellular electrophysiological study
Title | Corticofugal inhibition on the auditory thalamic neurons: an in-vivo intracellular electrophysiological study |
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Authors | |
Keywords | Medial geniculate body Tectothalamic projection Corticofugal modulation Electrical stimulation |
Issue Date | 2002 |
Publisher | Society for Neuroscience (SfN). |
Citation | The 2002 Annual Meeting of the Society for Neuroscience (SfN) - Neuroscience 2002, Orlando, FL., 3-7 November 2002, no. 354.3 How to Cite? |
Abstract | Our recent studies of extracellular and intracellular recordings have shown that the corticofugal projection has a strong inhibition on the medial geniculate body (MGB), especially on its non-lemniscal nuclei. The inhibition is suggested to be caused potentially by the following inhibitory neurons which can be activated by the corticofugal projection: 1) the thalamic interneurons 2) the thalamic reticular neurons, and 3) the inferior collicular inhibitory neurons which directly project to the MGB. In the present study, we examined the contribution of the corticocolliculothalamic pathway on the strong corticothalamic inhibition by comparing neuronal responses to the cortical electrical stimulation between the experimental condition with the colliculothalamic projection sectioned and the control condition in which the colliculothalamic projection was kept intact. 90 thalamic neurons from 8 anesthetized guinea pigs were recorded intracellularly while the auditory cortex was activated through an electrical stimulation of pulse trains. Strong corticofugal inhibitions were confirmed in the thalamic neurons after the section of the auditory colliculothalamic connections. The inhibitory effects lasted for 247.1-317.7 ms in the same order as before the sectioning. Both the sectioning and the recording sites were anatomically confirmed. We conclude that the strong corticofugal inhibition on the MGB is mainly caused by the thalamic reticular nucleus.
Supported by RGC (PolyU5211/99M) and PolyU (G-T253) |
Persistent Identifier | http://hdl.handle.net/10722/105123 |
DC Field | Value | Language |
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dc.contributor.author | Fujimoto, K | en_HK |
dc.contributor.author | Yu, YQ | en_HK |
dc.contributor.author | Chan, YS | en_HK |
dc.contributor.author | He, JF | en_HK |
dc.date.accessioned | 2010-09-25T22:21:08Z | - |
dc.date.available | 2010-09-25T22:21:08Z | - |
dc.date.issued | 2002 | en_HK |
dc.identifier.citation | The 2002 Annual Meeting of the Society for Neuroscience (SfN) - Neuroscience 2002, Orlando, FL., 3-7 November 2002, no. 354.3 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/105123 | - |
dc.description.abstract | Our recent studies of extracellular and intracellular recordings have shown that the corticofugal projection has a strong inhibition on the medial geniculate body (MGB), especially on its non-lemniscal nuclei. The inhibition is suggested to be caused potentially by the following inhibitory neurons which can be activated by the corticofugal projection: 1) the thalamic interneurons 2) the thalamic reticular neurons, and 3) the inferior collicular inhibitory neurons which directly project to the MGB. In the present study, we examined the contribution of the corticocolliculothalamic pathway on the strong corticothalamic inhibition by comparing neuronal responses to the cortical electrical stimulation between the experimental condition with the colliculothalamic projection sectioned and the control condition in which the colliculothalamic projection was kept intact. 90 thalamic neurons from 8 anesthetized guinea pigs were recorded intracellularly while the auditory cortex was activated through an electrical stimulation of pulse trains. Strong corticofugal inhibitions were confirmed in the thalamic neurons after the section of the auditory colliculothalamic connections. The inhibitory effects lasted for 247.1-317.7 ms in the same order as before the sectioning. Both the sectioning and the recording sites were anatomically confirmed. We conclude that the strong corticofugal inhibition on the MGB is mainly caused by the thalamic reticular nucleus. Supported by RGC (PolyU5211/99M) and PolyU (G-T253) | - |
dc.language | eng | en_HK |
dc.publisher | Society for Neuroscience (SfN). | - |
dc.relation.ispartof | Neuroscience 2002 | en_HK |
dc.subject | Medial geniculate body | - |
dc.subject | Tectothalamic projection | - |
dc.subject | Corticofugal modulation | - |
dc.subject | Electrical stimulation | - |
dc.title | Corticofugal inhibition on the auditory thalamic neurons: an in-vivo intracellular electrophysiological study | en_HK |
dc.type | Conference_Paper | en_HK |
dc.identifier.email | Chan, YS: yschan@hkucc.hku.hk | en_HK |
dc.identifier.authority | Chan, YS=rp00318 | en_HK |
dc.identifier.hkuros | 82104 | en_HK |