Decrease of GABAergic markers and arc protein expression in the frontal cortex by intraventricular 192 IgG-saporin

Da Un Jeong, Won Seok Chang, Yong Sup Hwang, Dongkyu Lee, Jin Woo Chang

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background/Aims: Previous studies used 192 IgG-saporin to study cholinergic function because of its facility for selective lesioning; however, results varied due to differences in the methods of administration and behavioral tests used. We examined an animal model of dementia using 192 IgG-saporin to confirm its features before applying this model to research of therapeutic drugs or electrical stimulation techniques. Methods: Features were verified by the Morris water maze test, immunochemistry, and Western blotting. Animals were examined after intraventricular injection of 192 IgG-saporin (0.63 μg/μl; 6, 8, and 10 μl) or phosphate-buffered saline. Results: In the acquisition phase of the Morris water maze test, the latencies of the injection groups were significantly delayed, but recovered within 1 week. In the probe test, 2 of 4 indices (time in the platform zone and the number of crossings) were significantly different in the 8-μl injection group. Immunohistochemistry revealed the extent of cholinergic destruction. Activity-regulated cytoskeleton-associated protein and glutamate decarboxylase expression significantly decreased in the frontal cortex (8- and 10-μl groups), but not in the hippocampus. Conclusion: Spatial memory impairment was associated with cholinergic basal forebrain injury as well as frontocortical GABAergic hypofunction and synaptic plasticity deceleration.

Original languageEnglish
Pages (from-to)70-78
Number of pages9
JournalDementia and Geriatric Cognitive Disorders
Volume32
Issue number1
DOIs
Publication statusPublished - 2011 Sep 1

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Frontal Lobe
Cholinergic Agents
Intraventricular Injections
Therapeutic Human Experimentation
Immunochemistry
Injections
Proteins
Neuronal Plasticity
Glutamate Decarboxylase
Deceleration
Water
Cytoskeleton
Electric Stimulation
Dementia
Hippocampus
Animal Models
Western Blotting
Immunohistochemistry
Phosphates
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Geriatrics and Gerontology
  • Cognitive Neuroscience
  • Psychiatry and Mental health

Cite this

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title = "Decrease of GABAergic markers and arc protein expression in the frontal cortex by intraventricular 192 IgG-saporin",
abstract = "Background/Aims: Previous studies used 192 IgG-saporin to study cholinergic function because of its facility for selective lesioning; however, results varied due to differences in the methods of administration and behavioral tests used. We examined an animal model of dementia using 192 IgG-saporin to confirm its features before applying this model to research of therapeutic drugs or electrical stimulation techniques. Methods: Features were verified by the Morris water maze test, immunochemistry, and Western blotting. Animals were examined after intraventricular injection of 192 IgG-saporin (0.63 μg/μl; 6, 8, and 10 μl) or phosphate-buffered saline. Results: In the acquisition phase of the Morris water maze test, the latencies of the injection groups were significantly delayed, but recovered within 1 week. In the probe test, 2 of 4 indices (time in the platform zone and the number of crossings) were significantly different in the 8-μl injection group. Immunohistochemistry revealed the extent of cholinergic destruction. Activity-regulated cytoskeleton-associated protein and glutamate decarboxylase expression significantly decreased in the frontal cortex (8- and 10-μl groups), but not in the hippocampus. Conclusion: Spatial memory impairment was associated with cholinergic basal forebrain injury as well as frontocortical GABAergic hypofunction and synaptic plasticity deceleration.",
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Decrease of GABAergic markers and arc protein expression in the frontal cortex by intraventricular 192 IgG-saporin. / Jeong, Da Un; Chang, Won Seok; Hwang, Yong Sup; Lee, Dongkyu; Chang, Jin Woo.

In: Dementia and Geriatric Cognitive Disorders, Vol. 32, No. 1, 01.09.2011, p. 70-78.

Research output: Contribution to journalArticle

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