Utilization of sodium-dependent high affinity choline uptake [formula omitted] as a measure of the activity of cholinergic neurons [formula omitted

Abstract

Previous reports indicate that alterations of activity of cholinergic neurons in vivo are followed by parallel changes in sodium-dependent high affinity choline uptake in vitro . These results are consistent with the proposal that this portion of choline uptake is regulatory in the synthesis of ACh. These results also suggest the possibility of utilizing sodium-dependent high affinity choline uptake as a measure of the relative state of cholinergic activity in vivo . In this study, we administer a number of drugs reported to alter turnover and release of ACh (both are measures of cholinergic activity in vivo , and subsequently examine sodium-dependent high affinity choline uptake in vitro . Administration of pentobarbital, chloral hydrate, morphine, physostigmine, Δ 9 THC, hemicholinium-3 and oxotremorine, drugs which decrease ACh turnover and release, caused a reduction in choline uptake. Conversely, administration of pentylenetetrazol, atropine, scopolamine, and haloperidol, drugs which increase ACh turnover and release, caused an increase in choline uptake in vitro . These findings support the proposal that sodium-dependent high affinity choline uptake can be used as a relative measure of the activity of cholinergic neurons in vivo .