|1.||Wattanathorn, Jintanaporn: 2 articles (07/2011 - 01/2010)|
|2.||Bae, Dae-Kwon: 1 article (04/2012)|
|3.||Matsuo, Akinori: 1 article (04/2012)|
|4.||Kim, Yun-Bae: 1 article (04/2012)|
|5.||Tooyama, Ikuo: 1 article (04/2012)|
|6.||Lee, Hong Jun: 1 article (04/2012)|
|7.||Yang, Goeun: 1 article (04/2012)|
|8.||Lim, Inja: 1 article (04/2012)|
|9.||Kim, Seung U: 1 article (04/2012)|
|10.||Yang, Yun-Hui: 1 article (04/2012)|
05/01/1992 - "Relatively selective lesions produced by bilateral 50 nl microinjections of 75 pmol of the cholinergic neurotoxin ethylcholine mustard aziridinium ion (AF64A) resulted in a significant reduction in the threshold of myoclonic and facial-forelimb clonic seizures but not tonic seizures when PTZ was infused 7 days later. "
05/01/1998 - "While these studies do not allow us to conclude that AF64A is specific for N-myc, the data do, nevertheless, suggest that AF64A affects cell growth and/or replication by down-regulating the expression of N-myc which is involved in differentiation and cell growth in neuroblastomas. "
09/01/1995 - "The LA-N-2 neuroblastoma cell line thus serves well as an in vitro model of the cholinergic neuron and provides a useful system to study the mode of cholinotoxicity induced by AF64A."
04/01/1993 - "As revealed by the measurement of lactate dehydrogenase activity in the culture medium, AF64A produced similar concentration-dependent cellular damage in cultures of bovine cerebral endothelial cells and in the human cholinergic neuroblastoma cell line SK-N-MC, but not in bovine cerebral smooth muscle cells. "
02/01/1985 - "We report that in further studies on its mechanism of action incubation of the cholinergic neuroblastoma X glioma cell line, NG-108-15, with 100 microM AF64A resulted in a rapid decrease in cellular choline acetyltransferase (ChAT) activity which preceded cytotoxicity. "
09/01/1995 - "We have examined the effects of AF64A in the human neuroblastoma cell line, LA-N-2, which has an intact sodium-coupled choline uptake system, and is capable of synthesizing acetylcholine (ACh). "
|4.||Alzheimer Disease (Alzheimer's Disease)
01/01/1992 - "Using the cholinergic neurotoxin AF64A we have developed a rodent model of cholinergic hypofunction that exhibits behavioral, anatomical, and neurochemical deficits very analogous to those observed in Alzheimer's disease. "
03/15/1988 - "Since the primary cholinergic innervation to the FP cortex, originating in the nucleus basalis of Meynert, appears to become dysfunctional (but not totally degenerative) in Alzheimer's disease, cortical AF64A infusions may closely reflect this cholinergic dysfunction by 'functionally' eliminating cortical cholinergic terminals."
04/30/1986 - "These results suggest that AF64A can be used to produce specific lesions of cholinergic neurons, and therefore may be useful in developing animal models of human disorders involving cholinergic hypofunction, such as senile dementia of the Alzheimer type. "
10/29/1984 - "Furthermore, based upon the behavioral and biochemical data presented, it is suggested that AF64A could be a useful pharmacological tool for examining the neurobiological substrates of putative cholinergic disorders such as senile dementia of the Alzheimer's type."
07/02/1984 - "The neurochemical and behavioral consequences of AF64A administration are reminiscent of similar measures in patients with Alzheimer's disease (5, 6). "
|5.||Memory Disorders (Memory Loss)
08/01/1995 - "A memory deficits-induced animal model was used that involved AF64A (3 nmol/2 microliters/side) bilaterally injected ICV. "
01/01/1994 - "Treatment with AF64A (3.5 nmol, i.c.v.) produced memory deficits and decreased hippocampal ACh content. "
12/18/1989 - "These findings indicate that the memory deficits resulting from intraventricular administration of AF64A are a consequence of the compound's cholinotoxic properties and in particular its interaction with the HAChT carrier. "
04/01/1989 - "These data indicate that memory deficits are observed during a period of cortical cholinergic hypofunction induced by cortical AF64A infusions and that a recovery from such hypofunction occurs by 6 months after these infusions."
07/01/2011 - "Young adult male Wistar rats, weighing 180-220 g, were orally given rice berry once daily at doses of 180, 360, and 720 mg/kg of body weight for a period of 2 weeks before and 1 week after the induction of memory deficit and cholinergic lesions with AF64A, a specific cholinotoxin, via bilateral intracerebroventricular administration. "
|2.||Choline O-Acetyltransferase (Choline Acetyltransferase)
|3.||Choline (Choline Chloride)
|5.||Excitatory Amino Acid Antagonists
|6.||Cholinergic Agents (Cholinergics)
|7.||1- Methyl- 4- phenyl- 1,2,3,6- tetrahydropyridine (MPTP)