Adenosine receptor antagonism (caffeine's primary mechanism of action) indirectly promotes neurotransmitter release (i.e., monoamines and acetylcholine), which endows caffeine with its stimulant effects. This indirect promotion as a result of antagonism is because adenosine's biological purpose serves as an inhibitory regulator of the central nervous system. Specifically, adenosine suppresses activity when the body believes it is in need of rest.
Amphetamine is more stimulating than caffeine for two reasons.
(1) Amphetamine is a potent full agonist of trace amine-associated receptor 1. TAAR1 is a neuromodulator that, upon interacting with amphetamine, dose-dependently increases the activity of the neurotransmitters dopamine and norepinephrine in the brain. It also triggers the release of several other hormones (e.g., epinephrine) and neurotransmitters (e.g., serotonin and histamine) as well as the synthesis of certain neuropeptides (i.e., cocaine and amphetamine regulated transcript (CART) peptides, which are the result of increased dopaminergic activity in the nucleus accumbens)
(2) Amphetamine inhibits vesicular monoamine transporter 2 (VMAT2). In the absence of amphetamine, VMAT2 will normally move monoamines (e.g., dopamine, histamine, serotonin, norepinephrine, etc.) from the intracellular fluid of a monoamine neuron into its synaptic vesicles, which store neurotransmitters for later release (via exocytosis) into the synaptic cleft. When amphetamine enters a neuron and interacts with VMAT2, the transporter reverses its direction of transport, thereby releasing stored monoamines inside synaptic vesicles back into the neuron's intracellular fluid.
By interacting with both VMAT2 and TAAR1, amphetamine releases neurotransmitters from synaptic vesicles (the effect from VMAT2) into the intracellular fluid where they subsequently exit the neuron through the membrane-bound, reversed monoamine transporters (the effect from TAAR1). In summary, these two biological targets are the reason behind why Amphetamine is as 'potent' as it is with regard to central nervous system activity, at least when compared to caffeine.
Also, for the people mentioning caffeine tolerance, it was my understanding that tolerance to the effects of caffeine occurs for caffeine-induced elevations in blood pressure and the subjective feelings of nervousness. But for positive effects such as feelings of alertness and wellbeing,
sensitisation occurs instead and confers amplified effects with repeated use of the same dose.
It's also worth mentioning that amphetamine too causes sensitisation in low doses, like those used to treat ADHD, with respect to reward-related cognition (particularly incentive salience). This is probably one of the mechanisms that serves to improve establishment of routine and regular goal-driven behavior in people with ADHD who take amphetamine everyday, despite some physical and cognitive effects undergoing tolerance after dose titration (such as the anorectic effect, euphoria, noticeable increases in blood pressure/heart rate).