||(+/-)-TETRAHYDROPAPAVEROLINE HYDROBROMIDE; NORLAUDANOSOLINE HYDROBROMIDE; 1,2,3,4-tetrahydro-1-(3,4-dihydroxybenzyl)-6,7-isoquinolinediolhydrobromide; 7-isoquinolinediol,1-((3,4-dihydroxyphenyl)methyl)-1,2,3,4-tetrahydro-hb; 7-isoquinolinediol,1,2,3,4-tetrah
||Data not available, please inquire.
1.Half-lives of salsolinol and tetrahydropapaveroline hydrobromide following intracerebroventricular injection.
Melchor CL, Mueller A, Deitrich RA. Biochem Pharmacol. 1980 Feb 15;29(4):657-8.
2.Ethanol and some tetrahydroisoquinolines alter the discharge of cortical and hippocampal neurons: relationship to endogenous opioids.
Berger T, French ED, Siggins GR, Shier WT, Bloom FE. Pharmacol Biochem Behav. 1982 Oct;17(4):813-21.
The activity of single neurons in rat cortex or hippocampus (HPC) was recorded to test two hypotheses: (1) neuronal effects of ethanol are mediated by an endogenous opiate-like mechanism (for example, by release of an endogenous opioid peptide), and; (2) ethanol-induced formation of aldehyde-catecholamine condensation products (tetrahydroisoquinolines; TIQs) might contribute to some acute actions of ethanol. Ethanol and all TIQs were applied to single neurons from multibarrel micropipettes by electroosmosis or pressure. Ethanol most often inhibited neurons of the parietal cortex, while activating most HPC pyramidal neurons. Tetrahydropapaveroline (THP) most often inhibited the spontaneous and glutamate- or acetylcholine (ACh)-induced firing of neurons in both these regions, although some excitations were also seen. In contrast, salsolinol and 7-O-methyl-salsolinol predominantly excited HPC pyramidal neurons, but depressed most parietal cortical neurons.
3.A re-evaluation of the role of tetrahydropapaveroline in ethanol consumption in rats.
McCoy JG1, Strawbridge C, McMurtrey KD, Kane VB, Ward CP. Brain Res Bull. 2003 Apr 15;60(1-2):59-65.
The role of tetrahydropapaveroline (THP), a condensation product of a dopaldehyde with dopamine, in the regulation of alcohol consumption was investigated. In the first experiment, rats received intraventricular injections of either racemic THP hydrobromide (0.65 or 1.3 microg/microl), R-(+)-THP (0.66 or 1.4 microg/microl), or an equal volume of vehicle. The lower doses of both (+/-)-THP and (+)-THP significantly increased volitional alcohol intake. For the racemic compound, the increase was significant at 7-13% concentrations. The R-(+)-enantiomer increased consumption at 4-11 and 15-20% concentrations of ethanol. The higher doses of both compounds did not significantly alter alcohol preference. A second experiment evaluated the chronic effect of THP delivered subcutaneously via osmotic minipump. Animals receiving THP (0.1, 0.5, 1.0, 2.0, and 4.0 mg/ml) did not differ in their alcohol intake, compared to vehicle-treated controls. Whether or not endogenously formed THP participates in the etiology of alcohol addiction remains unclear.