I'm not surprised, being on that nasty ass haldol. Your psych is the mental case, he's right where he needs to be if hes in a nut ward, but only if he's in a room with rubber walls, combining haldol, amphetamine and a fucking MAOI, even a RIMA-type. I'm quite sure I know more than a few pharmacologists and bees both that would want to drop him out of a plane without a parachute into an area notorious for its high population of fire ant nests for that.
Amphetamines work by, in a simplified way of putting it, causing the vesicles that contain monoamine neurotransmitters (noradrenaline, dopamine, most importantly the latter) (and in the case of methamphetamine it also has effects on serotonin to a degree although dex doesn't afaik or if it does not until you'd reach millimolar plasma levels (which would be saturation bombing more or less, and take some surviving most likely, if dex does at all then it's the sort of thing you'd observe by patch-clamp or cell-clamp studies (where microelectrodes are poked into a cell or a patch of cell wall is excised, an amplifier to boost the signal hooked up and various drugs applied to the nutrient bath the cell is in to evoke electrophysiological responses, such as to a nerve, in a petri dish, but not in a human)
And taking a dopamine antagonist and a releaser like amphetamine (the monoaminergic stimulants fall into two major categories where dopamine is concerned, likewise noradrenaline and serotonin) the releasers, which do exactly what they sound like they do, forcing the dumping of neurotransmitter stores, these can cause a much higher peak level of synaptic neurotransmitter 'content' as stores are effectively turned inside out and whats in there dumped into the synapse from the neurotransmitter vesicles in the presynaptic terminals (usually) and then there are the reuptake inhibitors, which are thought to block DAT (dopamine transporter) the cellular entity responsible for sucking back up the dopamine which is not metabolized and repackaging it into vesicles for reuse, although it does seem like it may be more complex with certain DAT inhibitors, some are euphorigenic stimulants, like cocaine, methyl/ethylphenidates and other ritalinic acid esters (no joke, awful name or what, for the acid parent:P) whilst some tropane-based DAT inhibitors, like IIRC, troparil are apparently not euphoric, despite similarity chemically to cocaine. So there appears to be at least two different binding modes, perhaps an open channel block and preventing the channel opening, although I'm conjecturing there.
Along with two atypical compounds, really atypical in their mode of action in that they do not directly cause monoamine release, but when the body NATURALLY does so, I.e it was going to do it anyway, there is a phasic increase rather than the tonic increase in monoamine levels, with, per action potential received by the neuron, more monoamine is released per stimulatory event to that neuron.
Could be compared to, rather than increasing rate of fire of an old blackpowder cannon, packing a larger charge in before firing, but continuing to fire at the same rate it would do anyway, in the case of those two weird ones, BPAP and PPAP. Been meaning to make those a priority to have a look at myself when I can find the time, since they really are quite unique in their mode of action, and AFAIK it is just these two compounds thus far known that do this. Just the kind of oddball activity that screams 'project, lestat, project dammit and hurry up about it'
