Fluzepam® binds to and modulates the GABA operated chloride channel. It thereby potentiates the inhibitory actions of GABA in the spinal cord, brain stem, cerebellum, limbic system and cerebral cortex. Potentiation of GABA inhibition diminishes the activity in ascending activating systems, particularly noradrenergic and serotonergic pathways, from brain stem and mid-brain to the cerebral cortex. Sedation and muscle relaxant actions are typical of benzodiazepines. 

Lofranil® is a potent inhibitor of norepinephrine reuptake at noradrenergic nerve endings. It is also an inhibitor of 5- hydroxytryptamine (5-HT) reuptake but these effects are less marked than those on norepinephrine. The relative activity of Lofranil® at the noradrenergic and 5-HT reuptake sites is 7:3. The active metabolite of Lofranil® (desmethylimipramine) is considerably less potent as an inhibitor of 5-HT reuptake. 

Lofranil® is a potent inhibitor of norepinephrine reuptake at noradrenergic nerve endings. It is also an inhibitor of 5- hydroxytryptamine (5-HT) reuptake but these effects are less marked than those on norepinephrine. The relative activity of Lofranil® at the noradrenergic and 5-HT reuptake sites is 7:3. The active metabolite of Lofranil® (desmethylimipramine) is considerably less potent as an inhibitor of 5-HT reuptake. 

Midazolex® binds to benxodiazepine receptors in various regions of the brain such as the spinal cord, brain stem, cerebellum, limbic system, and the cercbral cortex. Benzodiazepines like Midazolex® block EEG arousal from stimulation of the brain stemcticular formation. Midazolex® acts as CNS depressant on CNS reflexes via the brain stem reticular form tion. Midazolex® is an anxiolytic in animal test systems such as the fear of electroshock in rats or monkey. It is sedative as judged by reduction of fighting in n ice of monkeys. The hypnotic effects of Midazolex® hat are demonstrable in humans are difficult to show in animals even in very high doses. Midazolex® produces anterograde amnesia similar to that produced by diazepam but neither benzodiazepine produces retrograde amnesia. Midazolex® has a more rapid one et of action and shorter duration of effect than diazepam in most animal test systems. The antinociceptive effect of intrathecal Midazolex® inay involve interaction with a delta opiate receptor. Midazolex® has a marked anticonvulsant effect with a nonlinear relationship between concentration and effect without an apparent ceiling at higher concentrations. The EC350 was 0.067 ??? 0.01 mg l-1 for Midazolex®. Antagonism of the anticonvulsant effect of Midazolex® by flumazenil suggested that there might be two separate sites of action, of which only one is antagonized by flumazenil. This study concluded that the effect of benzodiazepines on seizures induced by cortical stimulation in vivo cannot be fully accounted for by an interaction at the GABA A receptor. At high concentrations, Midazolex® can inhibit calcium entry into cells by a non- GABA dependent mechanism and thereby relaxes bronchial and vascular smooth muscle, but the relevance of this finding to the concentrations achieved in humans is doubtful.