Striatal neurones show sustained recovery from severe hypoglycaemic insult
Glucose deprivation provides a reliable model to investigate cellular responses to metabolic dysfunction, and is reportedly associated with permanent cell death in many paradigms. Consistent with previous studies, primary cultures of rat striatal neurones exposed to 24‐h hypoglycaemia showed dramati...
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| Veröffentlicht in: | Journal of neurochemistry 2003-07, Vol.86 (2), p.383-393 |
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| creator | McDermott, C. J. Bradley, K. N. McCarron, J. G. Palmer, A. M. Morris, B. J. |
| description | Glucose deprivation provides a reliable model to investigate cellular responses to metabolic dysfunction, and is reportedly associated with permanent cell death in many paradigms. Consistent with previous studies, primary cultures of rat striatal neurones exposed to 24‐h hypoglycaemia showed dramatically decreased sodium 2,3‐bis(2‐methoxy‐4‐nitro‐5‐sulfophenyl)‐2H‐tetrazolium‐5‐carboxanilide (XTT) metabolism (used as a marker of cell viability) and increased TUNEL staining, suggesting widespread DNA damage typical of apoptotic cell death. Remarkably, restoration of normal glucose levels initiated a sustained recovery in XTT staining, along with a concomitant decrease in TUNEL staining, even after 24 h of hypoglycaemia, suggesting recovery of damaged neurones and repair of nicked DNA. No alterations in the levels of four DNA repair proteins could be detected during hypoglycaemia or recovery. A reduction in intracellular calcium concentration was seen in recovered cells. These data suggest that striatal cells do not die after extended periods of glucose deprivation, but survive in a form of suspended animation, with sufficient energy to maintain membrane potential. |
| doi_str_mv | 10.1046/j.1471-4159.2003.01853.x |
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J. ; Bradley, K. N. ; McCarron, J. G. ; Palmer, A. M. ; Morris, B. J.</creator><creatorcontrib>McDermott, C. J. ; Bradley, K. N. ; McCarron, J. G. ; Palmer, A. M. ; Morris, B. J.</creatorcontrib><description>Glucose deprivation provides a reliable model to investigate cellular responses to metabolic dysfunction, and is reportedly associated with permanent cell death in many paradigms. Consistent with previous studies, primary cultures of rat striatal neurones exposed to 24‐h hypoglycaemia showed dramatically decreased sodium 2,3‐bis(2‐methoxy‐4‐nitro‐5‐sulfophenyl)‐2H‐tetrazolium‐5‐carboxanilide (XTT) metabolism (used as a marker of cell viability) and increased TUNEL staining, suggesting widespread DNA damage typical of apoptotic cell death. Remarkably, restoration of normal glucose levels initiated a sustained recovery in XTT staining, along with a concomitant decrease in TUNEL staining, even after 24 h of hypoglycaemia, suggesting recovery of damaged neurones and repair of nicked DNA. No alterations in the levels of four DNA repair proteins could be detected during hypoglycaemia or recovery. A reduction in intracellular calcium concentration was seen in recovered cells. These data suggest that striatal cells do not die after extended periods of glucose deprivation, but survive in a form of suspended animation, with sufficient energy to maintain membrane potential.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.2003.01853.x</identifier><identifier>PMID: 12871579</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; apoptosis ; bcl-2-Associated X Protein ; Biochemistry and metabolism ; Biological and medical sciences ; Caspases - metabolism ; Cell Survival - drug effects ; Cell Survival - physiology ; Cells, Cultured ; Central nervous system ; Corpus Striatum - cytology ; Corpus Striatum - metabolism ; DNA Damage - physiology ; DNA Repair - physiology ; Fundamental and applied biological sciences. 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J.</creatorcontrib><creatorcontrib>Bradley, K. N.</creatorcontrib><creatorcontrib>McCarron, J. G.</creatorcontrib><creatorcontrib>Palmer, A. M.</creatorcontrib><creatorcontrib>Morris, B. J.</creatorcontrib><title>Striatal neurones show sustained recovery from severe hypoglycaemic insult</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Glucose deprivation provides a reliable model to investigate cellular responses to metabolic dysfunction, and is reportedly associated with permanent cell death in many paradigms. Consistent with previous studies, primary cultures of rat striatal neurones exposed to 24‐h hypoglycaemia showed dramatically decreased sodium 2,3‐bis(2‐methoxy‐4‐nitro‐5‐sulfophenyl)‐2H‐tetrazolium‐5‐carboxanilide (XTT) metabolism (used as a marker of cell viability) and increased TUNEL staining, suggesting widespread DNA damage typical of apoptotic cell death. Remarkably, restoration of normal glucose levels initiated a sustained recovery in XTT staining, along with a concomitant decrease in TUNEL staining, even after 24 h of hypoglycaemia, suggesting recovery of damaged neurones and repair of nicked DNA. No alterations in the levels of four DNA repair proteins could be detected during hypoglycaemia or recovery. A reduction in intracellular calcium concentration was seen in recovered cells. These data suggest that striatal cells do not die after extended periods of glucose deprivation, but survive in a form of suspended animation, with sufficient energy to maintain membrane potential.</description><subject>Animals</subject><subject>apoptosis</subject><subject>bcl-2-Associated X Protein</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Caspases - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Central nervous system</subject><subject>Corpus Striatum - cytology</subject><subject>Corpus Striatum - metabolism</subject><subject>DNA Damage - physiology</subject><subject>DNA Repair - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose - metabolism</subject><subject>Glucose - pharmacology</subject><subject>hypoglycaemia</subject><subject>Hypoglycemia - metabolism</subject><subject>In Situ Nick-End Labeling</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>neurotoxicity</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>recovery</subject><subject>Recovery of Function - drug effects</subject><subject>Recovery of Function - physiology</subject><subject>striatum</subject><subject>Tetrazolium Salts - metabolism</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtP3DAURq2qqAy0f6Hypt0l9bUdO150gUYtDyFYQNeW49yUjPIY7IQh_56kMypLWN1Puuc-dAihwFJgUv3YpCA1JBIyk3LGRMogz0T6_IGs_jc-khVjnCeCSX5MTmLcMAZKKvhEjoHnGjJtVuTqbgi1G1xDOxxD32Gk8aHf0TjGwdUdljSg758wTLQKfUsjzhnpw7Tt_zaTd9jWntZdHJvhMzmqXBPxy6Gekj-_f92vL5Lr2_PL9dl14qVWIikKAU6UmQZTIShuCqGZc4BYIjfclIXGrPQG55bwjIscpDRMcc01E0UpTsn3_d5t6B9HjINt6-ixaVyH_RitFpnMlII3QciN5EIsYL4HfehjDFjZbahbFyYLzC7C7cYuXu3i1S7C7T_h9nke_Xq4MRYtlq-DB8Mz8O0AuOhdUwXX-Tq-ctJIZnI1cz_33K5ucHr3A_bqZr0k8QKK_Jvl</recordid><startdate>200307</startdate><enddate>200307</enddate><creator>McDermott, C. 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Psychology</topic><topic>Glucose - metabolism</topic><topic>Glucose - pharmacology</topic><topic>hypoglycaemia</topic><topic>Hypoglycemia - metabolism</topic><topic>In Situ Nick-End Labeling</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>neurotoxicity</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>recovery</topic><topic>Recovery of Function - drug effects</topic><topic>Recovery of Function - physiology</topic><topic>striatum</topic><topic>Tetrazolium Salts - metabolism</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McDermott, C. J.</creatorcontrib><creatorcontrib>Bradley, K. N.</creatorcontrib><creatorcontrib>McCarron, J. G.</creatorcontrib><creatorcontrib>Palmer, A. M.</creatorcontrib><creatorcontrib>Morris, B. 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Remarkably, restoration of normal glucose levels initiated a sustained recovery in XTT staining, along with a concomitant decrease in TUNEL staining, even after 24 h of hypoglycaemia, suggesting recovery of damaged neurones and repair of nicked DNA. No alterations in the levels of four DNA repair proteins could be detected during hypoglycaemia or recovery. A reduction in intracellular calcium concentration was seen in recovered cells. These data suggest that striatal cells do not die after extended periods of glucose deprivation, but survive in a form of suspended animation, with sufficient energy to maintain membrane potential.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12871579</pmid><doi>10.1046/j.1471-4159.2003.01853.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals apoptosis bcl-2-Associated X Protein Biochemistry and metabolism Biological and medical sciences Caspases - metabolism Cell Survival - drug effects Cell Survival - physiology Cells, Cultured Central nervous system Corpus Striatum - cytology Corpus Striatum - metabolism DNA Damage - physiology DNA Repair - physiology Fundamental and applied biological sciences. Psychology Glucose - metabolism Glucose - pharmacology hypoglycaemia Hypoglycemia - metabolism In Situ Nick-End Labeling Neurons - cytology Neurons - metabolism neurotoxicity Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 Rats Rats, Wistar recovery Recovery of Function - drug effects Recovery of Function - physiology striatum Tetrazolium Salts - metabolism Time Factors Vertebrates: nervous system and sense organs |
| title | Striatal neurones show sustained recovery from severe hypoglycaemic insult |
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