The neonate-6-hydroxydopamine-lesioned rat: a model for clinical neuroscience and neurobiological principles
In 1973, a technique of administering 6-hydroxydopamine (2,4,5-trihydroxyphenylethylamine) intracisternally to neonate rats was introduced to selectively reduce brain dopamine (neonate-lesioned rat). This neonate treatment proved unique when compared to rats lesioned as adults with 6-hydroxydopamine...
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| Veröffentlicht in: | Brain Research Reviews 2005-02, Vol.48 (1), p.57-73 |
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| creator | Breese, George R. Knapp, Darin J. Criswell, Hugh E. Moy, Sheryl S. Papadeas, Sophia T. Blake, Bonita L. |
| description | In 1973, a technique of administering 6-hydroxydopamine (2,4,5-trihydroxyphenylethylamine) intracisternally to neonate rats was introduced to selectively reduce brain dopamine (neonate-lesioned rat). This neonate treatment proved unique when compared to rats lesioned as adults with 6-hydroxydopamine—prompting the discovery of differing functional characteristics resulting from the age at which brain dopamine is reduced. A realization was that neonate-lesioned rats modeled the loss of central dopamine and the increased susceptibility for self-injury in Lesch–Nyhan disease, which allowed identification of drugs useful in treating self-injury in mentally retarded patients. The neonate-lesioned rat has also been proposed to model the hyperactivity observed in attention-deficit hyperactivity disorder. Because the neonate-lesioned rat exhibits enhanced sensitization to repeated NMDA receptor antagonist administration and has functional changes characteristic of schizophrenia, the neonate lesioning is believed to emulate the hypothesized NMDA hypofunction in this psychiatric disorder. Besides modeling features of neurological and psychiatric disorders, important neurobiological concepts emerged from pharmacological studies in the neonate-lesioned rats. One was the discovery of coupling of D
1/D
2-dopamine receptor function. Another was the progressive increase in responsiveness to repeated D
1-dopamine agonist administration referred to as “priming” of D
1-dopamine receptor function. Additionally, a unique profile of signaling protein expression related to neonate reduction of dopamine has been identified. Thus, from modeling characteristics of disease to defining adaptive mechanisms related to neonatal loss of dopamine, the neonate-lesioned rat has had a persisting influence on neuroscience. Despite an extraordinary legacy from studies of the neurobiology of this treatment, a host of unknowns remain that will inspire future investigations. |
| doi_str_mv | 10.1016/j.brainresrev.2004.08.004 |
| format | Article |
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1/D
2-dopamine receptor function. Another was the progressive increase in responsiveness to repeated D
1-dopamine agonist administration referred to as “priming” of D
1-dopamine receptor function. Additionally, a unique profile of signaling protein expression related to neonate reduction of dopamine has been identified. Thus, from modeling characteristics of disease to defining adaptive mechanisms related to neonatal loss of dopamine, the neonate-lesioned rat has had a persisting influence on neuroscience. Despite an extraordinary legacy from studies of the neurobiology of this treatment, a host of unknowns remain that will inspire future investigations.</description><identifier>ISSN: 0165-0173</identifier><identifier>EISSN: 1872-6321</identifier><identifier>DOI: 10.1016/j.brainresrev.2004.08.004</identifier><identifier>PMID: 15708628</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>6-Hydroxydopamine ; Age Factors ; Animals ; Animals, Newborn ; Behavioral sensitization ; Biological and medical sciences ; Brain - metabolism ; Brain - physiopathology ; Brain Chemistry - drug effects ; Brain Chemistry - physiology ; D 1-dopamine receptors ; Disease Models, Animal ; Dopamine - metabolism ; Excitatory Amino Acid Agonists - pharmacology ; Excitatory Amino Acid Antagonists - pharmacology ; Medical sciences ; Mental Disorders - metabolism ; Mental Disorders - physiopathology ; Neonate dopamine lesion ; Nervous system involvement in other diseases. Miscellaneous ; Neurology ; Neurology - methods ; Neurology - trends ; NMDA hypofunction ; NMDA receptor antagonists ; Oxidopamine - pharmacology ; Rats ; Receptors, Dopamine - drug effects ; Receptors, Dopamine - metabolism ; Self-injurious behavior ; Serotonin hyperinnervation ; Sympatholytics - pharmacology</subject><ispartof>Brain Research Reviews, 2005-02, Vol.48 (1), p.57-73</ispartof><rights>2004 Elsevier B.V.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-28278c803dc2ef1bdfb7e8ff0c4bed7aff2400517b45fce530c64a2ab125e7793</citedby><cites>FETCH-LOGICAL-c405t-28278c803dc2ef1bdfb7e8ff0c4bed7aff2400517b45fce530c64a2ab125e7793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16540940$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15708628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Breese, George R.</creatorcontrib><creatorcontrib>Knapp, Darin J.</creatorcontrib><creatorcontrib>Criswell, Hugh E.</creatorcontrib><creatorcontrib>Moy, Sheryl S.</creatorcontrib><creatorcontrib>Papadeas, Sophia T.</creatorcontrib><creatorcontrib>Blake, Bonita L.</creatorcontrib><title>The neonate-6-hydroxydopamine-lesioned rat: a model for clinical neuroscience and neurobiological principles</title><title>Brain Research Reviews</title><addtitle>Brain Res Brain Res Rev</addtitle><description>In 1973, a technique of administering 6-hydroxydopamine (2,4,5-trihydroxyphenylethylamine) intracisternally to neonate rats was introduced to selectively reduce brain dopamine (neonate-lesioned rat). This neonate treatment proved unique when compared to rats lesioned as adults with 6-hydroxydopamine—prompting the discovery of differing functional characteristics resulting from the age at which brain dopamine is reduced. A realization was that neonate-lesioned rats modeled the loss of central dopamine and the increased susceptibility for self-injury in Lesch–Nyhan disease, which allowed identification of drugs useful in treating self-injury in mentally retarded patients. The neonate-lesioned rat has also been proposed to model the hyperactivity observed in attention-deficit hyperactivity disorder. Because the neonate-lesioned rat exhibits enhanced sensitization to repeated NMDA receptor antagonist administration and has functional changes characteristic of schizophrenia, the neonate lesioning is believed to emulate the hypothesized NMDA hypofunction in this psychiatric disorder. Besides modeling features of neurological and psychiatric disorders, important neurobiological concepts emerged from pharmacological studies in the neonate-lesioned rats. One was the discovery of coupling of D
1/D
2-dopamine receptor function. Another was the progressive increase in responsiveness to repeated D
1-dopamine agonist administration referred to as “priming” of D
1-dopamine receptor function. Additionally, a unique profile of signaling protein expression related to neonate reduction of dopamine has been identified. Thus, from modeling characteristics of disease to defining adaptive mechanisms related to neonatal loss of dopamine, the neonate-lesioned rat has had a persisting influence on neuroscience. Despite an extraordinary legacy from studies of the neurobiology of this treatment, a host of unknowns remain that will inspire future investigations.</description><subject>6-Hydroxydopamine</subject><subject>Age Factors</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Behavioral sensitization</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>Brain Chemistry - drug effects</subject><subject>Brain Chemistry - physiology</subject><subject>D 1-dopamine receptors</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Excitatory Amino Acid Agonists - pharmacology</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Medical sciences</subject><subject>Mental Disorders - metabolism</subject><subject>Mental Disorders - physiopathology</subject><subject>Neonate dopamine lesion</subject><subject>Nervous system involvement in other diseases. Miscellaneous</subject><subject>Neurology</subject><subject>Neurology - methods</subject><subject>Neurology - trends</subject><subject>NMDA hypofunction</subject><subject>NMDA receptor antagonists</subject><subject>Oxidopamine - pharmacology</subject><subject>Rats</subject><subject>Receptors, Dopamine - drug effects</subject><subject>Receptors, Dopamine - metabolism</subject><subject>Self-injurious behavior</subject><subject>Serotonin hyperinnervation</subject><subject>Sympatholytics - pharmacology</subject><issn>0165-0173</issn><issn>1872-6321</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkM1u3CAURlHUqpn8vELlLpqdHcBgmO6qUZNUitRNukYYLgkjDFPwRJ23D-lYSpdZXQmd73K_g9AXgjuCyXC97casfcxQMjx3FGPWYdnVcYJWRAraDj0lH9CqsrzFRPSn6KyULcZ8zeTwCZ0SLrAcqFyh8PAETYQU9Qzt0D4dbE5_Dzbt9OQjtAGKTxFsk_X8rdHNlCyExqXcmOCjNzrU8D6nYjxEA42O9vgw-hTS4z9gl300fldXXaCPTocCl8s8R79vfjxs7tr7X7c_N9_vW8Mwn1sqqZBG4t4aCo6M1o0CpHPYsBGs0M5RVrsQMTLuDPAem4FpqkdCOQix7s_R1XHvLqc_eyizmnwxEIKuTfdFESEJlwOv4PoImlqhynSqHjvpfFAEq1fVaqv-U61eVSssVR01-3n5ZD9OYN-Si9sKfF0AXaoHl3XVUN64gTO8ZrhymyMHVcmzh6wWm9ZnMLOyyb_jnBd9sKW-</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Breese, George R.</creator><creator>Knapp, Darin J.</creator><creator>Criswell, Hugh E.</creator><creator>Moy, Sheryl S.</creator><creator>Papadeas, Sophia T.</creator><creator>Blake, Bonita L.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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></search><sort><creationdate>20050201</creationdate><title>The neonate-6-hydroxydopamine-lesioned rat: a model for clinical neuroscience and neurobiological principles</title><author>Breese, George R. ; Knapp, Darin J. ; Criswell, Hugh E. ; Moy, Sheryl S. ; Papadeas, Sophia T. ; Blake, Bonita L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-28278c803dc2ef1bdfb7e8ff0c4bed7aff2400517b45fce530c64a2ab125e7793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>6-Hydroxydopamine</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Behavioral sensitization</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain - physiopathology</topic><topic>Brain Chemistry - drug effects</topic><topic>Brain Chemistry - physiology</topic><topic>D 1-dopamine receptors</topic><topic>Disease Models, Animal</topic><topic>Dopamine - metabolism</topic><topic>Excitatory Amino Acid Agonists - pharmacology</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Medical sciences</topic><topic>Mental Disorders - metabolism</topic><topic>Mental Disorders - physiopathology</topic><topic>Neonate dopamine lesion</topic><topic>Nervous system involvement in other diseases. Miscellaneous</topic><topic>Neurology</topic><topic>Neurology - methods</topic><topic>Neurology - trends</topic><topic>NMDA hypofunction</topic><topic>NMDA receptor antagonists</topic><topic>Oxidopamine - pharmacology</topic><topic>Rats</topic><topic>Receptors, Dopamine - drug effects</topic><topic>Receptors, Dopamine - metabolism</topic><topic>Self-injurious behavior</topic><topic>Serotonin hyperinnervation</topic><topic>Sympatholytics - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Breese, George R.</creatorcontrib><creatorcontrib>Knapp, Darin J.</creatorcontrib><creatorcontrib>Criswell, Hugh E.</creatorcontrib><creatorcontrib>Moy, Sheryl S.</creatorcontrib><creatorcontrib>Papadeas, Sophia T.</creatorcontrib><creatorcontrib>Blake, Bonita L.</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Brain Research Reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Breese, George R.</au><au>Knapp, Darin J.</au><au>Criswell, Hugh E.</au><au>Moy, Sheryl S.</au><au>Papadeas, Sophia T.</au><au>Blake, Bonita L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The neonate-6-hydroxydopamine-lesioned rat: a model for clinical neuroscience and neurobiological principles</atitle><jtitle>Brain Research Reviews</jtitle><addtitle>Brain Res Brain Res Rev</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>48</volume><issue>1</issue><spage>57</spage><epage>73</epage><pages>57-73</pages><issn>0165-0173</issn><eissn>1872-6321</eissn><abstract>In 1973, a technique of administering 6-hydroxydopamine (2,4,5-trihydroxyphenylethylamine) intracisternally to neonate rats was introduced to selectively reduce brain dopamine (neonate-lesioned rat). This neonate treatment proved unique when compared to rats lesioned as adults with 6-hydroxydopamine—prompting the discovery of differing functional characteristics resulting from the age at which brain dopamine is reduced. A realization was that neonate-lesioned rats modeled the loss of central dopamine and the increased susceptibility for self-injury in Lesch–Nyhan disease, which allowed identification of drugs useful in treating self-injury in mentally retarded patients. The neonate-lesioned rat has also been proposed to model the hyperactivity observed in attention-deficit hyperactivity disorder. Because the neonate-lesioned rat exhibits enhanced sensitization to repeated NMDA receptor antagonist administration and has functional changes characteristic of schizophrenia, the neonate lesioning is believed to emulate the hypothesized NMDA hypofunction in this psychiatric disorder. Besides modeling features of neurological and psychiatric disorders, important neurobiological concepts emerged from pharmacological studies in the neonate-lesioned rats. One was the discovery of coupling of D
1/D
2-dopamine receptor function. Another was the progressive increase in responsiveness to repeated D
1-dopamine agonist administration referred to as “priming” of D
1-dopamine receptor function. Additionally, a unique profile of signaling protein expression related to neonate reduction of dopamine has been identified. Thus, from modeling characteristics of disease to defining adaptive mechanisms related to neonatal loss of dopamine, the neonate-lesioned rat has had a persisting influence on neuroscience. Despite an extraordinary legacy from studies of the neurobiology of this treatment, a host of unknowns remain that will inspire future investigations.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>15708628</pmid><doi>10.1016/j.brainresrev.2004.08.004</doi><tpages>17</tpages></addata></record> |
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| subjects | 6-Hydroxydopamine Age Factors Animals Animals, Newborn Behavioral sensitization Biological and medical sciences Brain - metabolism Brain - physiopathology Brain Chemistry - drug effects Brain Chemistry - physiology D 1-dopamine receptors Disease Models, Animal Dopamine - metabolism Excitatory Amino Acid Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology Medical sciences Mental Disorders - metabolism Mental Disorders - physiopathology Neonate dopamine lesion Nervous system involvement in other diseases. Miscellaneous Neurology Neurology - methods Neurology - trends NMDA hypofunction NMDA receptor antagonists Oxidopamine - pharmacology Rats Receptors, Dopamine - drug effects Receptors, Dopamine - metabolism Self-injurious behavior Serotonin hyperinnervation Sympatholytics - pharmacology |
| title | The neonate-6-hydroxydopamine-lesioned rat: a model for clinical neuroscience and neurobiological principles |
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