Wie im Formelschema angegeben, werden auf der Basis von Phenylcyclohexenen (I) die Aralkylamino‐ketone (XI) hergestellt.

1 (+ )-Amphetamine mimicked the intermittent and sustained electrocortical desynchronization produced by (-)-noradrenaline (NA) when perfused directly into the dorsal raphe nucleus of cat encephale isole preparations. 2 The effects of amphetamine or NA were abolished or significantly attenuated by prior application of (-)-propranolol. 3 The effect of amphetamine, but not that of NA, was blocked by prior applications of guanethidine or chlorpromazine (CPZ). 4 Desmethylimipramine (DMI) produced dose-related changes in electrocortical activity which were similar to those induced by NA when applied to the same sites within the dorsal raphe nucleus. 5 DMI potentiated the effects of both amphetamine and NA, but guanethidine only abolished the DMI-induced potentiation of the amphetamine response. 6 (-)-Propranolol, guanethidine and CPZ produced a short period of electrocortical desynchronization at the beginning of the perfusion period before antagonism of the amphetamine response was apparent.7 The results suggest that CPZ and amphetamine have an action within the dorsal raphe nucleus possibly related to noradrenergic terminals.

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