Accelerated cognitive aging in diabetic rats is prevented by lowering corticosterone levels
Diabetes and normal aging are both characterized by increases in levels of glucocorticoids. Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippoc...
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| Veröffentlicht in: | Neurobiology of learning and memory 2008-09, Vol.90 (2), p.479-483 |
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| creator | Stranahan, Alexis M. Lee, Kim Pistell, Paul J. Nelson, Christopher M. Readal, Nathaniel Miller, Marshall G. Spangler, Edward L. Ingram, Donald K. Mattson, Mark P. |
| description | Diabetes and normal aging are both characterized by increases in levels of glucocorticoids. Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippocampal deficits. To assess the contribution of diabetes-induced elevations in corticosterone levels, we examined maze learning in diabetic rats that had levels of corticosterone ‘clamped’ through adrenalectomy and low-dose corticosterone replacement. For comparison, we also tested a separate group of young and aged rats in the maze. Adrenally intact diabetic rats learned poorly in the 14-unit T-maze. Preventing the increases in corticosterone levels that accompanies the onset of experimental diabetes also prevented deficits in complex maze learning. The pattern of errors made by adrenally intact diabetic rats was similar to the pattern of errors made by aged rats, suggesting that the cognitive profiles of diabetic and aged rats share common features. |
| doi_str_mv | 10.1016/j.nlm.2008.05.005 |
| format | Article |
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Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippocampal deficits. To assess the contribution of diabetes-induced elevations in corticosterone levels, we examined maze learning in diabetic rats that had levels of corticosterone ‘clamped’ through adrenalectomy and low-dose corticosterone replacement. For comparison, we also tested a separate group of young and aged rats in the maze. Adrenally intact diabetic rats learned poorly in the 14-unit T-maze. Preventing the increases in corticosterone levels that accompanies the onset of experimental diabetes also prevented deficits in complex maze learning. The pattern of errors made by adrenally intact diabetic rats was similar to the pattern of errors made by aged rats, suggesting that the cognitive profiles of diabetic and aged rats share common features.</description><identifier>ISSN: 1074-7427</identifier><identifier>EISSN: 1095-9564</identifier><identifier>DOI: 10.1016/j.nlm.2008.05.005</identifier><identifier>PMID: 18579418</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Adrenalectomy ; Aging ; Aging - physiology ; Animals ; Arousal - physiology ; Avoidance Learning - physiology ; Behavioral psychophysiology ; Biological and medical sciences ; Cognition & reasoning ; Corticosterone - blood ; Diabetes ; Diabetes Mellitus, Experimental - physiopathology ; Diabetes. Impaired glucose tolerance ; Electroshock ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Escape Reaction - physiology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fear - physiology ; Fundamental and applied biological sciences. Psychology ; Hippocampus ; Hippocampus - physiopathology ; Learning ; Male ; Maze Learning - physiology ; Medical sciences ; Mental Recall - physiology ; Motor Activity - physiology ; Neuronal Plasticity - physiology ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Sensory Thresholds - physiology ; Stone maze ; Streptozocin ; Stress</subject><ispartof>Neurobiology of learning and memory, 2008-09, Vol.90 (2), p.479-483</ispartof><rights>2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright © 2008 Elsevier B.V. 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Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippocampal deficits. To assess the contribution of diabetes-induced elevations in corticosterone levels, we examined maze learning in diabetic rats that had levels of corticosterone ‘clamped’ through adrenalectomy and low-dose corticosterone replacement. For comparison, we also tested a separate group of young and aged rats in the maze. Adrenally intact diabetic rats learned poorly in the 14-unit T-maze. Preventing the increases in corticosterone levels that accompanies the onset of experimental diabetes also prevented deficits in complex maze learning. The pattern of errors made by adrenally intact diabetic rats was similar to the pattern of errors made by aged rats, suggesting that the cognitive profiles of diabetic and aged rats share common features.</description><subject>Adrenalectomy</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Arousal - physiology</subject><subject>Avoidance Learning - physiology</subject><subject>Behavioral psychophysiology</subject><subject>Biological and medical sciences</subject><subject>Cognition & reasoning</subject><subject>Corticosterone - blood</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Electroshock</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Escape Reaction - physiology</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fear - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus</subject><subject>Hippocampus - physiopathology</subject><subject>Learning</subject><subject>Male</subject><subject>Maze Learning - physiology</subject><subject>Medical sciences</subject><subject>Mental Recall - physiology</subject><subject>Motor Activity - physiology</subject><subject>Neuronal Plasticity - physiology</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. 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Impaired glucose tolerance</topic><topic>Electroshock</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Escape Reaction - physiology</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fear - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus</topic><topic>Hippocampus - physiopathology</topic><topic>Learning</topic><topic>Male</topic><topic>Maze Learning - physiology</topic><topic>Medical sciences</topic><topic>Mental Recall - physiology</topic><topic>Motor Activity - physiology</topic><topic>Neuronal Plasticity - physiology</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. 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Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippocampal deficits. To assess the contribution of diabetes-induced elevations in corticosterone levels, we examined maze learning in diabetic rats that had levels of corticosterone ‘clamped’ through adrenalectomy and low-dose corticosterone replacement. For comparison, we also tested a separate group of young and aged rats in the maze. Adrenally intact diabetic rats learned poorly in the 14-unit T-maze. Preventing the increases in corticosterone levels that accompanies the onset of experimental diabetes also prevented deficits in complex maze learning. The pattern of errors made by adrenally intact diabetic rats was similar to the pattern of errors made by aged rats, suggesting that the cognitive profiles of diabetic and aged rats share common features.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>18579418</pmid><doi>10.1016/j.nlm.2008.05.005</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neurobiology of learning and memory, 2008-09, Vol.90 (2), p.479-483 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adrenalectomy Aging Aging - physiology Animals Arousal - physiology Avoidance Learning - physiology Behavioral psychophysiology Biological and medical sciences Cognition & reasoning Corticosterone - blood Diabetes Diabetes Mellitus, Experimental - physiopathology Diabetes. Impaired glucose tolerance Electroshock Endocrine pancreas. Apud cells (diseases) Endocrinopathies Escape Reaction - physiology Etiopathogenesis. Screening. Investigations. Target tissue resistance Fear - physiology Fundamental and applied biological sciences. Psychology Hippocampus Hippocampus - physiopathology Learning Male Maze Learning - physiology Medical sciences Mental Recall - physiology Motor Activity - physiology Neuronal Plasticity - physiology Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Rats Rats, Sprague-Dawley Rodents Sensory Thresholds - physiology Stone maze Streptozocin Stress |
| title | Accelerated cognitive aging in diabetic rats is prevented by lowering corticosterone levels |
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