A significant increase in both basal and maximal calcineurin activity following fluid percussion injury in the rat
Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. This study examined the effects of moderate, central fluid percussion injury on the...
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| Veröffentlicht in: | Journal of neurotrauma 2005-04, Vol.22 (4), p.476-490 |
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| creator | KURZ, Jonathan E PARSONS, J. Travis RANA, Aniruddha GIBSON, Cynthia J HAMM, Robert J CHURN, Severn B |
| description | Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. This study examined the effects of moderate, central fluid percussion injury on the activity of this important neuronal enzyme. Animals were sacrificed at several time-points postinjury and cortical, hippocampal, and cerebellar homogenates were assayed for calcineurin activity by dephosphorylation of p-nitrophenol phosphate. A significant brain injury-dependent increase was observed in both hippocampal and cortical homogenates under both basal and maximally-stimulated reaction conditions. This increase persisted 2-3 weeks post-injury. Brain injury did not alter substrate affinity, but did induce a significant increase in the apparent maximal dephosphorylation rate. Unlike the other brain regions, no change in calcineurin activity was observed in the cerebellum following brain injury. No brain region tested displayed a significant change in calcineurin enzyme levels as determined by Western blot, demonstrating that increased enzyme synthesis was not responsible for the observed increase in activity. The data support the conclusion that fluid percussion injury results in increased calcineurin activity in the rat forebrain. This increased activity has broad physiological implications, possibly resulting in altered cellular excitability or a greater likelihood of neuronal cell death. |
| doi_str_mv | 10.1089/neu.2005.22.476 |
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Travis ; RANA, Aniruddha ; GIBSON, Cynthia J ; HAMM, Robert J ; CHURN, Severn B</creator><creatorcontrib>KURZ, Jonathan E ; PARSONS, J. Travis ; RANA, Aniruddha ; GIBSON, Cynthia J ; HAMM, Robert J ; CHURN, Severn B</creatorcontrib><description>Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. This study examined the effects of moderate, central fluid percussion injury on the activity of this important neuronal enzyme. Animals were sacrificed at several time-points postinjury and cortical, hippocampal, and cerebellar homogenates were assayed for calcineurin activity by dephosphorylation of p-nitrophenol phosphate. A significant brain injury-dependent increase was observed in both hippocampal and cortical homogenates under both basal and maximally-stimulated reaction conditions. This increase persisted 2-3 weeks post-injury. Brain injury did not alter substrate affinity, but did induce a significant increase in the apparent maximal dephosphorylation rate. Unlike the other brain regions, no change in calcineurin activity was observed in the cerebellum following brain injury. No brain region tested displayed a significant change in calcineurin enzyme levels as determined by Western blot, demonstrating that increased enzyme synthesis was not responsible for the observed increase in activity. The data support the conclusion that fluid percussion injury results in increased calcineurin activity in the rat forebrain. This increased activity has broad physiological implications, possibly resulting in altered cellular excitability or a greater likelihood of neuronal cell death.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.2005.22.476</identifier><identifier>PMID: 15853464</identifier><identifier>CODEN: JNEUE4</identifier><language>eng</language><publisher>Larchmont, NY: Liebert</publisher><subject>Animals ; Biochemistry ; Biological and medical sciences ; Brain - metabolism ; Brain - pathology ; Brain - physiopathology ; Brain damage ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Brain Injuries - physiopathology ; Calcineurin - metabolism ; Cell Death - physiology ; Cellular biology ; Cerebellum - metabolism ; Cerebellum - physiopathology ; Cerebral Cortex - metabolism ; Cerebral Cortex - physiopathology ; Disease Models, Animal ; Enzyme Activation - physiology ; Hippocampus - metabolism ; Hippocampus - physiopathology ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Kinetics ; Male ; Medical sciences ; Nerve Degeneration - metabolism ; Neurons ; Neurosciences ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Rodents ; Time Factors ; Traumas. Diseases due to physical agents ; Up-Regulation - physiology</subject><ispartof>Journal of neurotrauma, 2005-04, Vol.22 (4), p.476-490</ispartof><rights>2005 INIST-CNRS</rights><rights>(©) Copyright 2005, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-fe60609f695a23764975e857cdbc6079e12bc171a348411b4ce66f072efd7d783</citedby><cites>FETCH-LOGICAL-c352t-fe60609f695a23764975e857cdbc6079e12bc171a348411b4ce66f072efd7d783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3029,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16729698$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15853464$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KURZ, Jonathan E</creatorcontrib><creatorcontrib>PARSONS, J. Travis</creatorcontrib><creatorcontrib>RANA, Aniruddha</creatorcontrib><creatorcontrib>GIBSON, Cynthia J</creatorcontrib><creatorcontrib>HAMM, Robert J</creatorcontrib><creatorcontrib>CHURN, Severn B</creatorcontrib><title>A significant increase in both basal and maximal calcineurin activity following fluid percussion injury in the rat</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. This study examined the effects of moderate, central fluid percussion injury on the activity of this important neuronal enzyme. Animals were sacrificed at several time-points postinjury and cortical, hippocampal, and cerebellar homogenates were assayed for calcineurin activity by dephosphorylation of p-nitrophenol phosphate. A significant brain injury-dependent increase was observed in both hippocampal and cortical homogenates under both basal and maximally-stimulated reaction conditions. This increase persisted 2-3 weeks post-injury. Brain injury did not alter substrate affinity, but did induce a significant increase in the apparent maximal dephosphorylation rate. Unlike the other brain regions, no change in calcineurin activity was observed in the cerebellum following brain injury. No brain region tested displayed a significant change in calcineurin enzyme levels as determined by Western blot, demonstrating that increased enzyme synthesis was not responsible for the observed increase in activity. The data support the conclusion that fluid percussion injury results in increased calcineurin activity in the rat forebrain. This increased activity has broad physiological implications, possibly resulting in altered cellular excitability or a greater likelihood of neuronal cell death.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Brain damage</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Brain Injuries - physiopathology</subject><subject>Calcineurin - metabolism</subject><subject>Cell Death - physiology</subject><subject>Cellular biology</subject><subject>Cerebellum - metabolism</subject><subject>Cerebellum - physiopathology</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation - physiology</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - physiopathology</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nerve Degeneration - metabolism</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Time Factors</subject><subject>Traumas. 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Travis</au><au>RANA, Aniruddha</au><au>GIBSON, Cynthia J</au><au>HAMM, Robert J</au><au>CHURN, Severn B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A significant increase in both basal and maximal calcineurin activity following fluid percussion injury in the rat</atitle><jtitle>Journal of neurotrauma</jtitle><addtitle>J Neurotrauma</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>22</volume><issue>4</issue><spage>476</spage><epage>490</epage><pages>476-490</pages><issn>0897-7151</issn><eissn>1557-9042</eissn><coden>JNEUE4</coden><abstract>Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. This study examined the effects of moderate, central fluid percussion injury on the activity of this important neuronal enzyme. Animals were sacrificed at several time-points postinjury and cortical, hippocampal, and cerebellar homogenates were assayed for calcineurin activity by dephosphorylation of p-nitrophenol phosphate. A significant brain injury-dependent increase was observed in both hippocampal and cortical homogenates under both basal and maximally-stimulated reaction conditions. This increase persisted 2-3 weeks post-injury. Brain injury did not alter substrate affinity, but did induce a significant increase in the apparent maximal dephosphorylation rate. Unlike the other brain regions, no change in calcineurin activity was observed in the cerebellum following brain injury. No brain region tested displayed a significant change in calcineurin enzyme levels as determined by Western blot, demonstrating that increased enzyme synthesis was not responsible for the observed increase in activity. The data support the conclusion that fluid percussion injury results in increased calcineurin activity in the rat forebrain. This increased activity has broad physiological implications, possibly resulting in altered cellular excitability or a greater likelihood of neuronal cell death.</abstract><cop>Larchmont, NY</cop><pub>Liebert</pub><pmid>15853464</pmid><doi>10.1089/neu.2005.22.476</doi><tpages>15</tpages></addata></record> |
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| subjects | Animals Biochemistry Biological and medical sciences Brain - metabolism Brain - pathology Brain - physiopathology Brain damage Brain Injuries - metabolism Brain Injuries - pathology Brain Injuries - physiopathology Calcineurin - metabolism Cell Death - physiology Cellular biology Cerebellum - metabolism Cerebellum - physiopathology Cerebral Cortex - metabolism Cerebral Cortex - physiopathology Disease Models, Animal Enzyme Activation - physiology Hippocampus - metabolism Hippocampus - physiopathology Injuries of the nervous system and the skull. Diseases due to physical agents Kinetics Male Medical sciences Nerve Degeneration - metabolism Neurons Neurosciences Phosphorylation Rats Rats, Sprague-Dawley Rodents Time Factors Traumas. Diseases due to physical agents Up-Regulation - physiology |
| title | A significant increase in both basal and maximal calcineurin activity following fluid percussion injury in the rat |
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