title: Decrease of GABAergic markers and arc protein expression in the frontal cortex by intraventricular 192 IgG-saporin.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Spatial memory impairment was associated with cholinergic basal forebrain injury as well as frontocortical GABAergic hypofunction and synaptic plasticity deceleration.
authors.affiliation: Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Da Un
authors.initials: DU
authors.lastname: Jeong
authors.forename: Won Seok
authors.initials: WS
authors.lastname: Chang
authors.forename: Yong Sup
authors.initials: YS
authors.lastname: Hwang
authors.forename: Dongkyu
authors.initials: D
authors.lastname: Lee
authors.forename: Jin Woo
authors.initials: JW
authors.lastname: Chang
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology*; D015153:Blotting, Western; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D018678:Cholinergic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D003598:Cytoskeletal Proteins / Q000096:biosynthesis*; D003704:Dementia / Q000139:chemically induced / Q000523:psychology; D004195:Disease Models, Animal; D005625:Frontal Lobe / Q000187:drug effects / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D009473:Neuronal Plasticity / Q000187:drug effects; D010320:Parvalbumins / Q000378:metabolism; D016548:Prosencephalon / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D054789:Ribosome Inactivating Proteins, Type 1 / Q000008:administration & dosage / Q000494:pharmacology*; D000076985:Saporins; D013569:Synapses / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
chemical_list: C085696:192 IgG-saporin; D000911:Antibodies, Monoclonal; D018678:Cholinergic Agents; D003598:Cytoskeletal Proteins; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D054789:Ribosome Inactivating Proteins, Type 1; C092069:activity regulated cytoskeletal-associated protein; D005680:gamma-Aminobutyric Acid; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase; D000076985:Saporins; D005968:Glutamate Decarboxylase