Charles & others, There are various references on the medical web sites to Cholecystokinin in Parkinsons. They take some finding, but here are two quotes to show we are not barking up the wrong tree: ------------------------------------------------------------------- Details of a grant for research, listed on the Harvard site, <http://neuro-chief-e.mgh.harvard.edu/parkinsonsweb/Main/Support/usgrants.html> details as below: 11.Transmitter and Tropic Regulation of Nigrostrial opamine Neurons at the Pre and Postsynaptic Level by Neruotensin and Cholecystokinin Peptides. Possible Opening for New Treatments of Parkinson's Disease Sergio Tanganelli, Ph.D., Principle Investigator Ist. Pharmacolgy Ferrara, Italy ------------------------------------------------------------------ <Web page http://www.biogenes.ipw-berlin.de/igy.htm> part quote: R. Schade, P. Henklein, A. Hlinak , Humboldt-University Berlin Cholecystokinin octapeptide (CCK-8) is a neuropeptide which is colocalised with dopamine (DA) in mesencephalic brain regions [substantia nigra (SN), ventral tegmental area (VTA)] . Since dopamine is particular involved in degenerative diseases of the CNS as e.g. Parkinson's disease the coexistence of DA with CCK-8 is very interesting. Many investigations were started to study the biological significance of interactions between these both neuronal substances. One animal used for such studies is the unilateral disturbance of the dopaminergic nigrostriatal system by injection of the neurotoxin 6-hydroxydopamine (6-OHDA) into the median forebrain bundle which results in a complete lost of catecholaminergic neurons located in VTA and SN. This lost is also seen in dopaminergic fields of termination as e.g. striatum (STR) and nucleus accumbens (NACC). However, with respect to CCK-8 there are confusing results obtained by radioimmunological, immunocytochemical and in situ hybridisation studies, respectively. These differences certainly are due to the methods used and, in particular, due to the specificity of the utilized antibodies (Ab). The main inconsistency between these methods concerns the following results: CCK and DA are colocalised in a major population of nigral neurons (approximately 70%). There is a dramatical fall in DA in both SN and STR. Despite of the high portion of cells with DA and CCK-8 in colocalisation, the nigral CCK content is substantially reduced in contrast to a nearly unaffected striatal CCK-8. At present this contradiction is not convincingly explained. ------------------------------------------------------------------------------- Ernie. Ernie Peters <[log in to unmask]>