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Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat
The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation induced by complete Freund's adju...
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| Published in: | The Journal of physiology 2005-12, Vol.569 (2), p.685-695 |
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| container_title | The Journal of physiology |
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| creator | Matayoshi, Satoru Jiang, Nan Katafuchi, Toshihiko Koga, Kohei Furue, Hidemasa Yasaka, Toshiharu Nakatsuka, Terumasa Zhou, Xin‐Fu Kawasaki, Yasuhiko Tanaka, Nobuyuki Yoshimura, Megumu |
| description | The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop
the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation
induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically
to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not
untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na + channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2â4 days after the CFA injection.
On the other hand, the number of monosynaptic Aβ afferent inputs to the SG significantly increased 1 week after the onset
of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day
before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the
CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released
from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals.
BDNF may thereafter induce monosynaptic Aβ afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation. |
| doi_str_mv | 10.1113/jphysiol.2005.095331 |
| format | article |
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the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation
induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically
to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not
untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na + channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2â4 days after the CFA injection.
On the other hand, the number of monosynaptic Aβ afferent inputs to the SG significantly increased 1 week after the onset
of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day
before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the
CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released
from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals.
BDNF may thereafter induce monosynaptic Aβ afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2005.095331</identifier><identifier>PMID: 16210356</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Animals ; Brain-Derived Neurotrophic Factor - immunology ; Brain-Derived Neurotrophic Factor - physiology ; Excitatory Postsynaptic Potentials - physiology ; Freund's Adjuvant ; Ganglia, Spinal - physiology ; Hyperalgesia - drug therapy ; Hyperalgesia - physiopathology ; Immunization, Passive ; In Vitro Techniques ; Integrative Physiology ; Male ; Myelitis - chemically induced ; Myelitis - drug therapy ; Myelitis - physiopathology ; Nerve Growth Factors - physiology ; Neurons, Afferent - physiology ; Neurotrophin 3 - physiology ; Pain - drug therapy ; Pain - physiopathology ; Rats ; Rats, Sprague-Dawley ; Receptor, trkB - physiology ; Sodium Channels - physiology ; Spinal Cord - physiopathology ; Substantia Gelatinosa - physiopathology ; Synaptic Transmission - physiology ; Time Factors</subject><ispartof>The Journal of physiology, 2005-12, Vol.569 (2), p.685-695</ispartof><rights>2005 The Journal of Physiology © 2005 The Physiological Society</rights><rights>The Physiological society 2005 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5852-9d94e366ef29a905ddc6eff362f32621423f98f0dd3f34277aeeacadd6ebe8763</citedby><cites>FETCH-LOGICAL-c5852-9d94e366ef29a905ddc6eff362f32621423f98f0dd3f34277aeeacadd6ebe8763</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/PMC1464224/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464224/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16210356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matayoshi, Satoru</creatorcontrib><creatorcontrib>Jiang, Nan</creatorcontrib><creatorcontrib>Katafuchi, Toshihiko</creatorcontrib><creatorcontrib>Koga, Kohei</creatorcontrib><creatorcontrib>Furue, Hidemasa</creatorcontrib><creatorcontrib>Yasaka, Toshiharu</creatorcontrib><creatorcontrib>Nakatsuka, Terumasa</creatorcontrib><creatorcontrib>Zhou, Xin‐Fu</creatorcontrib><creatorcontrib>Kawasaki, Yasuhiko</creatorcontrib><creatorcontrib>Tanaka, Nobuyuki</creatorcontrib><creatorcontrib>Yoshimura, Megumu</creatorcontrib><title>Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop
the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation
induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically
to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not
untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na + channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2â4 days after the CFA injection.
On the other hand, the number of monosynaptic Aβ afferent inputs to the SG significantly increased 1 week after the onset
of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day
before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the
CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released
from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals.
BDNF may thereafter induce monosynaptic Aβ afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.</description><subject>Animals</subject><subject>Brain-Derived Neurotrophic Factor - immunology</subject><subject>Brain-Derived Neurotrophic Factor - physiology</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Freund's Adjuvant</subject><subject>Ganglia, Spinal - physiology</subject><subject>Hyperalgesia - drug therapy</subject><subject>Hyperalgesia - physiopathology</subject><subject>Immunization, Passive</subject><subject>In Vitro Techniques</subject><subject>Integrative Physiology</subject><subject>Male</subject><subject>Myelitis - chemically induced</subject><subject>Myelitis - drug therapy</subject><subject>Myelitis - physiopathology</subject><subject>Nerve Growth Factors - physiology</subject><subject>Neurons, Afferent - physiology</subject><subject>Neurotrophin 3 - physiology</subject><subject>Pain - drug therapy</subject><subject>Pain - physiopathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, trkB - physiology</subject><subject>Sodium Channels - physiology</subject><subject>Spinal Cord - physiopathology</subject><subject>Substantia Gelatinosa - physiopathology</subject><subject>Synaptic Transmission - physiology</subject><subject>Time Factors</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqNkUuPFCEUhYnROD2t_8AYVrqqlldRzcZkMlFHM4kuxjWh4dLFpBpKqJpJ_3vpVPvauQLCdw6HexB6RcmGUsrf3Y_9sYQ0bBgh7YaolnP6BK2okKrpOsWfohUhjDW8a-kFuizlnhDKiVLP0QWVjBLeyhWKV3YKKRacPN5lE2LjIIcHcDjCnNOU09gHi72xU8o4RVzGEM2AY7LBwjhVFE_ZxHIIpaaJ2M05xD0O0Q_mcDAn83rAUw84m-kFeubNUODleV2j7x8_3F3fNLdfP32-vrptbLttWaOcEsClBM-UUaR1zta955J5zmp2wbhXW0-c454L1nUGwFjjnIQdbDvJ1-j94jvOuwM4C7GGHPSYw8Hko04m6H9vYuj1Pj3oOj7BmKgGb84GOf2YoUy6ftDCMJgIaS6adoIJIUgFxQLanErJ4H8_Qok-FaV_FaVPRemlqCp7_XfAP6JzMxVQC_AYBjj-l6m--_KNsjqbNXq7aPuw7x9DBr3QpZYG01G3Ummm5bblPwG3wbYK</recordid><startdate>200512</startdate><enddate>200512</enddate><creator>Matayoshi, Satoru</creator><creator>Jiang, Nan</creator><creator>Katafuchi, Toshihiko</creator><creator>Koga, Kohei</creator><creator>Furue, Hidemasa</creator><creator>Yasaka, Toshiharu</creator><creator>Nakatsuka, Terumasa</creator><creator>Zhou, Xin‐Fu</creator><creator>Kawasaki, Yasuhiko</creator><creator>Tanaka, Nobuyuki</creator><creator>Yoshimura, Megumu</creator><general>The Physiological Society</general><general>Blackwell Science 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>7TK</scope><scope>5PM</scope></search><sort><creationdate>200512</creationdate><title>Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat</title><author>Matayoshi, Satoru ; Jiang, Nan ; Katafuchi, Toshihiko ; Koga, Kohei ; Furue, Hidemasa ; Yasaka, Toshiharu ; Nakatsuka, Terumasa ; Zhou, Xin‐Fu ; Kawasaki, Yasuhiko ; Tanaka, Nobuyuki ; Yoshimura, Megumu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5852-9d94e366ef29a905ddc6eff362f32621423f98f0dd3f34277aeeacadd6ebe8763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Brain-Derived Neurotrophic Factor - immunology</topic><topic>Brain-Derived Neurotrophic Factor - physiology</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Freund's Adjuvant</topic><topic>Ganglia, Spinal - physiology</topic><topic>Hyperalgesia - drug therapy</topic><topic>Hyperalgesia - physiopathology</topic><topic>Immunization, Passive</topic><topic>In Vitro Techniques</topic><topic>Integrative Physiology</topic><topic>Male</topic><topic>Myelitis - chemically induced</topic><topic>Myelitis - drug therapy</topic><topic>Myelitis - physiopathology</topic><topic>Nerve Growth Factors - physiology</topic><topic>Neurons, Afferent - physiology</topic><topic>Neurotrophin 3 - physiology</topic><topic>Pain - drug therapy</topic><topic>Pain - physiopathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, trkB - physiology</topic><topic>Sodium Channels - physiology</topic><topic>Spinal Cord - physiopathology</topic><topic>Substantia Gelatinosa - physiopathology</topic><topic>Synaptic Transmission - physiology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matayoshi, Satoru</creatorcontrib><creatorcontrib>Jiang, Nan</creatorcontrib><creatorcontrib>Katafuchi, Toshihiko</creatorcontrib><creatorcontrib>Koga, Kohei</creatorcontrib><creatorcontrib>Furue, Hidemasa</creatorcontrib><creatorcontrib>Yasaka, Toshiharu</creatorcontrib><creatorcontrib>Nakatsuka, Terumasa</creatorcontrib><creatorcontrib>Zhou, Xin‐Fu</creatorcontrib><creatorcontrib>Kawasaki, Yasuhiko</creatorcontrib><creatorcontrib>Tanaka, Nobuyuki</creatorcontrib><creatorcontrib>Yoshimura, Megumu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</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>Matayoshi, Satoru</au><au>Jiang, Nan</au><au>Katafuchi, Toshihiko</au><au>Koga, Kohei</au><au>Furue, Hidemasa</au><au>Yasaka, Toshiharu</au><au>Nakatsuka, Terumasa</au><au>Zhou, Xin‐Fu</au><au>Kawasaki, Yasuhiko</au><au>Tanaka, Nobuyuki</au><au>Yoshimura, Megumu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2005-12</date><risdate>2005</risdate><volume>569</volume><issue>2</issue><spage>685</spage><epage>695</epage><pages>685-695</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop
the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation
induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically
to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not
untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na + channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2â4 days after the CFA injection.
On the other hand, the number of monosynaptic Aβ afferent inputs to the SG significantly increased 1 week after the onset
of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day
before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the
CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released
from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals.
BDNF may thereafter induce monosynaptic Aβ afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>16210356</pmid><doi>10.1113/jphysiol.2005.095331</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 2005-12, Vol.569 (2), p.685-695 |
| issn | 0022-3751 1469-7793 |
| language | eng |
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| source | PubMed (Medline); Wiley |
| subjects | Animals Brain-Derived Neurotrophic Factor - immunology Brain-Derived Neurotrophic Factor - physiology Excitatory Postsynaptic Potentials - physiology Freund's Adjuvant Ganglia, Spinal - physiology Hyperalgesia - drug therapy Hyperalgesia - physiopathology Immunization, Passive In Vitro Techniques Integrative Physiology Male Myelitis - chemically induced Myelitis - drug therapy Myelitis - physiopathology Nerve Growth Factors - physiology Neurons, Afferent - physiology Neurotrophin 3 - physiology Pain - drug therapy Pain - physiopathology Rats Rats, Sprague-Dawley Receptor, trkB - physiology Sodium Channels - physiology Spinal Cord - physiopathology Substantia Gelatinosa - physiopathology Synaptic Transmission - physiology Time Factors |
| title | Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat |
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