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At least 55 records · Page 3Linked to original sources
PubMed1978

[Examination of psychic effects of a new analgesic agent of the cyclohexanols series. A contribution to a possible psychic dependence potential of tramadol (author's transl)].

A double-blind trial was performed with 30 male students of the University of Düsseldorf. The volunteers were divided at random into two groups containing 15 subjects each. One group received 1-(m-methoxyphenyl)-2-(dimethylaminomethyl)-cyclohexan-1-ol (tramadol; Tramal), and the other placebo. The latter served as the controls. On three occasions at regular intervals in the course of one week the volunteers were questioned on the basis of Janke and Debus's "Eigenschaftswörterliste" (EWL) (attribution word list). The interviews were carried out 1 h after the injection (1 ampoule 100 mg i.m.). The results in the sense of any euphoretic or dysphoretic effects are discussed.

Adult↗
PubMed1986

2-(4-phenylpiperidino) cyclohexanol (AH5183) decreases quantal size at the frog neuromuscular junction.

AH5183 was studied because it inhibits acetylcholine transport into synaptic vesicles. The drug apparently is a slow-acting anti-cholinesterase, so further experiments were performed with this enzyme inhibited. Soaking for hours in AH5183 in Ringer does not decrease quantal size. However, a few minutes of tetanic nerve stimulation results in a marked decrease in quantal size. Quantal size also decreased after hours in a hypertonic Ringer containing the drug.

Acetylcholine↗
PubMed1986

Storage and release of acetylcholine in rat cortical synaptosomes: effects of D,L-2-(4-phenylpiperidino)cyclohexanol (AH5183).

A post-stimulation synthesis of acetylcholine (ACh), its incorporation into a 'stable-bound' (vesicular) compartment and subsequent release, were compared in K+-stimulated synaptosomes, in the absence and presence of 10 microM AH5183. The drug depressed by 16% the net intrasynaptosomal formation of ACh from 1 microM [3H]choline (Ch) in the medium, by competitively inhibiting (Ki approximately equal to 20 microM) the high-affinity Ch transport, but it had no direct effect on the intraterminal synthesis of ACh per se. The drug reduced incorporation of newly synthesized [3H]ACh into synaptic vesicles by 55% and subsequent K+-depolarization-induced release of [3H]ACh by 83%, although it had no effect on Ca2+ influx into synaptosomes. These results are consistent with the hypothesis that AH5183 blocks cholinergic neurotransmission presynaptically by interfering with recharging of synaptic vesicles with ACh. Since the reduction of ACh release in the presence of AH5183 had no direct effect on ACh synthesis, these results also suggest that the transmitter release is not prerequisite for enhancement of Ch uptake and ACh synthesis in stimulated nerve terminals.

Acetylcholine↗