JPET Introducing ALZET?ew Model 2006 Pump

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Freeman, J. J.
Right arrow Articles by Jenden, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Freeman, J. J.
Right arrow Articles by Jenden, D. J.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CHOLINE BITARTRATE
*CHOLINE CHLORIDE

Studies on the behavioral and biochemical effects of hemicholinium in vivo

JJ Freeman, JR Macri, RL Choi and DJ Jenden

Hemicholinium (HC-3) causes a behavioral reactivity in rats which is correlated with the depletion of brain acetylcholine (ACh). The decrease in ACh levels and behavioral effects caused by HC-3 are correlated in a dose-dependent manner, maximal effects being achieved at an intraventricular (i.vt.) dose of 1 microgram. The HC-3 concentration in the brain 2 hr after i.vt. injection does not increase further with doses greater than 10 microgram. HC-3 (i.vt.) does not affect the uptake of choline (Ch) into subcellular fractions prepared from treated animals. ACh depletion in the brain areas studied closely parallels the HC-3 distribution. HC-3 pretreatment results in greater effects on newly synthesized than on stored ACh. Utilizing a concentration equal to that found in brain after an in vivo dose, HC-3 does not inhibit the uptake of Ch in synaptosomal preparations in which the neuronal membrane was disrupted with ether. The commonly accepted mechanism of action of HC-3, i.e., an inhibition of high affinity Ch uptake at the cholinergic nerve terminal, appears to provide a satisfactory explanation of its effects in vivo.

Volume 210, Issue 1, pp. 91-97, 07/01/1979
Copyright © 1979 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
S. M. Ferguson, M. Bazalakova, V. Savchenko, J. C. Tapia, J. Wright, and R. D. Blakely
Lethal impairment of cholinergic neurotransmission in hemicholinium-3-sensitive choline transporter knockout mice
PNAS, June 8, 2004; 101(23): 8762 - 8767.
[Abstract] [Full Text] [PDF]


Home page
Mol. Interv.Home page
S. M. Ferguson and R. D. Blakely
The Choline Transporter Resurfaces: New Roles for Synaptic Vesicles?
Mol. Interv., February 1, 2004; 4(1): 22 - 37.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1979 by the American Society for Pharmacology and Experimental Therapeutics.