Corticospinal transmission to leg motoneurones in human subjects with deficient glycinergic inhibition
Normal coordinated movement requires that the activity of antagonistic motoneurones may be depressed at appropriate times during the movement. Both glycinergic and GABAergic inhibitory mechanisms participate in this control. Patients with the major form of hyperekplexia (hereditary startle disease)...
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| Veröffentlicht in: | The Journal of physiology 2002-10, Vol.544 (2), p.631-640 |
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| creator | Nielsen, J. B. Tijssen, M. A. J. Hansen, N. L. Crone, C. Petersen, N. T. Brown, P. Dijk, J. G. Van Rothwell, J. C. |
| description | Normal coordinated movement requires that the activity of antagonistic motoneurones may be depressed at appropriate times
during the movement. Both glycinergic and GABAergic inhibitory mechanisms participate in this control. Patients with the major
form of hyperekplexia (hereditary startle disease) have impaired inhibition of spinal motoneurones from local glycinergic
interneurones and represent an ideal opportunity for studying the role of glycinergic inhibition in the control of antagonistic
muscles. In the present study we investigated whether impaired glycinergic inhibition affects the corticospinal control of
antagonistic spinal motoneurones in 10 patients with hyperekplexia and whether there are mechanisms that may compensate for
the lack of glycinergic inhibition. In healthy subjects transcranial magnetic stimulation (TMS) produced a short-latency inhibition
of the soleus H-reflex at rest and during tonic dorsiflexion. This inhibition, which has been shown to be mediated by spinal
(glycinergic) inhibitory interneurones, was absent in all four patients in whom this experiment was performed. This confirms
that glycinergic transmission is impaired in the patients. During voluntary dorsiflexion subthreshold TMS produced a depression
of the ongoing EMG activity in the tibialis anterior (TA) muscle in both healthy subjects and all of the six tested patients.
This is consistent with the idea that this EMG depression is caused by activation of cortical (GABAergic) inhibitory interneurones.
Cross-correlation analysis revealed normal short-term synchronization of TA motor units accompanied by coherence in the 8â12
Hz and 18â35 Hz frequency bands in the 10 patients. As in healthy subjects, 8â12 Hz coherence accompanied by decreased tendency
to discharge synchronously (de-synchronization) was found in recordings from the antagonistic TA and soleus muscles in 2 of
the 10 patients. This suggests that glycinergic inhibition is not responsible for de-synchronization of antagonistic motor
units, but that other GABAergic-inhibitory mechanisms must be involved. We propose that such mechanisms may compensate for
the lack of glycinergic reciprocal inhibition in the hyperekplectic patients and explain why voluntary movements are not more
severely affected. |
| doi_str_mv | 10.1113/jphysiol.22.024091 |
| format | Article |
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during the movement. Both glycinergic and GABAergic inhibitory mechanisms participate in this control. Patients with the major
form of hyperekplexia (hereditary startle disease) have impaired inhibition of spinal motoneurones from local glycinergic
interneurones and represent an ideal opportunity for studying the role of glycinergic inhibition in the control of antagonistic
muscles. In the present study we investigated whether impaired glycinergic inhibition affects the corticospinal control of
antagonistic spinal motoneurones in 10 patients with hyperekplexia and whether there are mechanisms that may compensate for
the lack of glycinergic inhibition. In healthy subjects transcranial magnetic stimulation (TMS) produced a short-latency inhibition
of the soleus H-reflex at rest and during tonic dorsiflexion. This inhibition, which has been shown to be mediated by spinal
(glycinergic) inhibitory interneurones, was absent in all four patients in whom this experiment was performed. This confirms
that glycinergic transmission is impaired in the patients. During voluntary dorsiflexion subthreshold TMS produced a depression
of the ongoing EMG activity in the tibialis anterior (TA) muscle in both healthy subjects and all of the six tested patients.
This is consistent with the idea that this EMG depression is caused by activation of cortical (GABAergic) inhibitory interneurones.
Cross-correlation analysis revealed normal short-term synchronization of TA motor units accompanied by coherence in the 8â12
Hz and 18â35 Hz frequency bands in the 10 patients. As in healthy subjects, 8â12 Hz coherence accompanied by decreased tendency
to discharge synchronously (de-synchronization) was found in recordings from the antagonistic TA and soleus muscles in 2 of
the 10 patients. This suggests that glycinergic inhibition is not responsible for de-synchronization of antagonistic motor
units, but that other GABAergic-inhibitory mechanisms must be involved. We propose that such mechanisms may compensate for
the lack of glycinergic reciprocal inhibition in the hyperekplectic patients and explain why voluntary movements are not more
severely affected.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.22.024091</identifier><identifier>PMID: 12381832</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Adult ; Electric Stimulation ; Electromyography ; Glycine - metabolism ; H-Reflex ; Humans ; Leg - innervation ; Magnetics ; Middle Aged ; Motor Neurons - physiology ; Muscle, Skeletal - physiopathology ; Nervous System Diseases - physiopathology ; Neural Inhibition ; Original ; Pyramidal Tracts - physiopathology ; Receptors, Glycine - genetics ; Synaptic Transmission</subject><ispartof>The Journal of physiology, 2002-10, Vol.544 (2), p.631-640</ispartof><rights>2002 The Journal of Physiology © 2002 The Physiological Society</rights><rights>The Physiological Society 2002 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4771-ae43dae4b59900d194e92849192f6da593d84aa97a1e4e45897fbb5a6e75fa423</citedby><cites>FETCH-LOGICAL-c4771-ae43dae4b59900d194e92849192f6da593d84aa97a1e4e45897fbb5a6e75fa423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290587/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290587/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12381832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nielsen, J. B.</creatorcontrib><creatorcontrib>Tijssen, M. A. J.</creatorcontrib><creatorcontrib>Hansen, N. L.</creatorcontrib><creatorcontrib>Crone, C.</creatorcontrib><creatorcontrib>Petersen, N. T.</creatorcontrib><creatorcontrib>Brown, P.</creatorcontrib><creatorcontrib>Dijk, J. G. Van</creatorcontrib><creatorcontrib>Rothwell, J. C.</creatorcontrib><title>Corticospinal transmission to leg motoneurones in human subjects with deficient glycinergic inhibition</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Normal coordinated movement requires that the activity of antagonistic motoneurones may be depressed at appropriate times
during the movement. Both glycinergic and GABAergic inhibitory mechanisms participate in this control. Patients with the major
form of hyperekplexia (hereditary startle disease) have impaired inhibition of spinal motoneurones from local glycinergic
interneurones and represent an ideal opportunity for studying the role of glycinergic inhibition in the control of antagonistic
muscles. In the present study we investigated whether impaired glycinergic inhibition affects the corticospinal control of
antagonistic spinal motoneurones in 10 patients with hyperekplexia and whether there are mechanisms that may compensate for
the lack of glycinergic inhibition. In healthy subjects transcranial magnetic stimulation (TMS) produced a short-latency inhibition
of the soleus H-reflex at rest and during tonic dorsiflexion. This inhibition, which has been shown to be mediated by spinal
(glycinergic) inhibitory interneurones, was absent in all four patients in whom this experiment was performed. This confirms
that glycinergic transmission is impaired in the patients. During voluntary dorsiflexion subthreshold TMS produced a depression
of the ongoing EMG activity in the tibialis anterior (TA) muscle in both healthy subjects and all of the six tested patients.
This is consistent with the idea that this EMG depression is caused by activation of cortical (GABAergic) inhibitory interneurones.
Cross-correlation analysis revealed normal short-term synchronization of TA motor units accompanied by coherence in the 8â12
Hz and 18â35 Hz frequency bands in the 10 patients. As in healthy subjects, 8â12 Hz coherence accompanied by decreased tendency
to discharge synchronously (de-synchronization) was found in recordings from the antagonistic TA and soleus muscles in 2 of
the 10 patients. This suggests that glycinergic inhibition is not responsible for de-synchronization of antagonistic motor
units, but that other GABAergic-inhibitory mechanisms must be involved. We propose that such mechanisms may compensate for
the lack of glycinergic reciprocal inhibition in the hyperekplectic patients and explain why voluntary movements are not more
severely affected.</description><subject>Adult</subject><subject>Electric Stimulation</subject><subject>Electromyography</subject><subject>Glycine - metabolism</subject><subject>H-Reflex</subject><subject>Humans</subject><subject>Leg - innervation</subject><subject>Magnetics</subject><subject>Middle Aged</subject><subject>Motor Neurons - physiology</subject><subject>Muscle, Skeletal - physiopathology</subject><subject>Nervous System Diseases - physiopathology</subject><subject>Neural Inhibition</subject><subject>Original</subject><subject>Pyramidal Tracts - physiopathology</subject><subject>Receptors, Glycine - genetics</subject><subject>Synaptic Transmission</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkbuu1DAURS0E4g4XfoACuYIqg1-J4wYJjXjqSlBcastJThKPEnuwHUb5ezzK8OpojguvvXzkjdBzSvaUUv76eBrXaP20Z2xPmCCKPkA7KipVSKn4Q7QjhLGCy5LeoCcxHgmhnCj1GN1Qxmtac7ZD_cGHZFsfT9aZCadgXJxtzFqHk8cTDHj2yTtYQh4RW4fHZTYOx6U5QpsiPts04g5621pwCQ_T2loHYbBthkfb2JRdT9Gj3kwRnl3PW_Tt_bv7w8fi7suHT4e3d0UrpKSFAcG7PJpSKUI6qgQoVgtFFeurzpSKd7UwRklDQYAoayX7pilNBbLsjWD8Fr3ZvKelmaFr80bBTPoU7GzCqr2x-t8bZ0c9-B-aMUXKWmbBy6sg-O8LxKTzb7QwTcaBX6KWjNakJiKDbAPb4GMM0P9-hBJ9qUf_qie79VZPDr34e70_kWsfGag24GwnWP9Dqe8_f634xfxqC452GM82gN7Q6HMtadWlEJrpC_kTJtKxaw</recordid><startdate>20021015</startdate><enddate>20021015</enddate><creator>Nielsen, J. B.</creator><creator>Tijssen, M. A. J.</creator><creator>Hansen, N. L.</creator><creator>Crone, C.</creator><creator>Petersen, N. T.</creator><creator>Brown, P.</creator><creator>Dijk, J. G. Van</creator><creator>Rothwell, J. C.</creator><general>The Physiological Society</general><general>Blackwell Publishing Ltd</general><general>Blackwell Science Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20021015</creationdate><title>Corticospinal transmission to leg motoneurones in human subjects with deficient glycinergic inhibition</title><author>Nielsen, J. B. ; Tijssen, M. A. J. ; Hansen, N. L. ; Crone, C. ; Petersen, N. T. ; Brown, P. ; Dijk, J. G. Van ; Rothwell, J. C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4771-ae43dae4b59900d194e92849192f6da593d84aa97a1e4e45897fbb5a6e75fa423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Electric Stimulation</topic><topic>Electromyography</topic><topic>Glycine - metabolism</topic><topic>H-Reflex</topic><topic>Humans</topic><topic>Leg - innervation</topic><topic>Magnetics</topic><topic>Middle Aged</topic><topic>Motor Neurons - physiology</topic><topic>Muscle, Skeletal - physiopathology</topic><topic>Nervous System Diseases - physiopathology</topic><topic>Neural Inhibition</topic><topic>Original</topic><topic>Pyramidal Tracts - physiopathology</topic><topic>Receptors, Glycine - genetics</topic><topic>Synaptic Transmission</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nielsen, J. B.</creatorcontrib><creatorcontrib>Tijssen, M. A. J.</creatorcontrib><creatorcontrib>Hansen, N. L.</creatorcontrib><creatorcontrib>Crone, C.</creatorcontrib><creatorcontrib>Petersen, N. T.</creatorcontrib><creatorcontrib>Brown, P.</creatorcontrib><creatorcontrib>Dijk, J. G. Van</creatorcontrib><creatorcontrib>Rothwell, J. C.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nielsen, J. B.</au><au>Tijssen, M. A. J.</au><au>Hansen, N. L.</au><au>Crone, C.</au><au>Petersen, N. T.</au><au>Brown, P.</au><au>Dijk, J. G. Van</au><au>Rothwell, J. C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Corticospinal transmission to leg motoneurones in human subjects with deficient glycinergic inhibition</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2002-10-15</date><risdate>2002</risdate><volume>544</volume><issue>2</issue><spage>631</spage><epage>640</epage><pages>631-640</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Normal coordinated movement requires that the activity of antagonistic motoneurones may be depressed at appropriate times
during the movement. Both glycinergic and GABAergic inhibitory mechanisms participate in this control. Patients with the major
form of hyperekplexia (hereditary startle disease) have impaired inhibition of spinal motoneurones from local glycinergic
interneurones and represent an ideal opportunity for studying the role of glycinergic inhibition in the control of antagonistic
muscles. In the present study we investigated whether impaired glycinergic inhibition affects the corticospinal control of
antagonistic spinal motoneurones in 10 patients with hyperekplexia and whether there are mechanisms that may compensate for
the lack of glycinergic inhibition. In healthy subjects transcranial magnetic stimulation (TMS) produced a short-latency inhibition
of the soleus H-reflex at rest and during tonic dorsiflexion. This inhibition, which has been shown to be mediated by spinal
(glycinergic) inhibitory interneurones, was absent in all four patients in whom this experiment was performed. This confirms
that glycinergic transmission is impaired in the patients. During voluntary dorsiflexion subthreshold TMS produced a depression
of the ongoing EMG activity in the tibialis anterior (TA) muscle in both healthy subjects and all of the six tested patients.
This is consistent with the idea that this EMG depression is caused by activation of cortical (GABAergic) inhibitory interneurones.
Cross-correlation analysis revealed normal short-term synchronization of TA motor units accompanied by coherence in the 8â12
Hz and 18â35 Hz frequency bands in the 10 patients. As in healthy subjects, 8â12 Hz coherence accompanied by decreased tendency
to discharge synchronously (de-synchronization) was found in recordings from the antagonistic TA and soleus muscles in 2 of
the 10 patients. This suggests that glycinergic inhibition is not responsible for de-synchronization of antagonistic motor
units, but that other GABAergic-inhibitory mechanisms must be involved. We propose that such mechanisms may compensate for
the lack of glycinergic reciprocal inhibition in the hyperekplectic patients and explain why voluntary movements are not more
severely affected.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>12381832</pmid><doi>10.1113/jphysiol.22.024091</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Free Content; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals; PubMed Central |
| subjects | Adult Electric Stimulation Electromyography Glycine - metabolism H-Reflex Humans Leg - innervation Magnetics Middle Aged Motor Neurons - physiology Muscle, Skeletal - physiopathology Nervous System Diseases - physiopathology Neural Inhibition Original Pyramidal Tracts - physiopathology Receptors, Glycine - genetics Synaptic Transmission |
| title | Corticospinal transmission to leg motoneurones in human subjects with deficient glycinergic inhibition |
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