Abstract
The effects of 2-phenylethylamine (PEA) and related compounds on the spinal monosynaptic reflex (MSR) were examined using Cl-spinalized rats. At low doses, PEA, S (+)-amphetamine, S (+)-methamphetamine and phentermine increased the amplitude of the MSR, whereas high doses of these drugs reduced it. p-Substituted PEA analogs (p-Cl-PEA, p-methoxy-PEA and (±)-p-Cl-amphetamine) only reduced the MSR. Low doses of PEA-related rigid compounds, R (+)-2-aminotetralin, (±)-N-methyl-2-aminotetralin and (±)-N, N-dimethyl-2-aminotetralin only reduced the MSR. S(-)-2-Aminotetralin did not affect the MSR. Depressions of MSR produced by PEA, S(+)-methamphetamine and R (+)-2-aminotetralin were antagonized by ketanserin and haloperidol which have 5-hydroxytryptamine (5-HT) antagonistic activity, and the MSR depression caused by S (+)-methamphetamine but not PEA and R (+)-2-aminotetralin was abolished by intracisternal 5, 6-dihy-droxytryptamine treatment or chronic spinal transection. These results suggest that PEA-related compounds cause MSR depression by direct and indirect 5-HT agonistic mechanisms, and support the proposal that the PEA moiety which exists in R (+)-2-aminotetralin is important for the direct 5-HT agonistic activity of some hallucinogens.
