Has anyone utilized DA agonists long term(>2 weeks)? What has been your experience with their effects on mood?

That's a complex answer. So first, I am going to assume you mean D1 agonists when you ask to compare them with releasers or re-uptake inhibitors. So methylphenidate is a dopamine reuptake inhibitor. It binds to the DAT, and prevents synaptic dopamine from being re-uptaked into neurons to be broken down by MAO. So it make levels of DA higher in the synapse, but does not directly cause the release of extra dopamine into the synapse. Amphetamine (Adderall) is a dopamine releaser/reuptake inhbitor. It actually enters the neuron and activates TAAR1, which is what inhibits the DAT. So it is not binding directly to the DAT and blocking it. It's actually activating TAAR1, which inhibits the DAT. In addition, amphetamine inhibits VMAT2, which causes the vesicles to dump dopamine into the neuron, which then get dumped into the synapse by reversal of the DAT itself. So while methylphenidate blocks the DAT, preventing DA from being re-uptaked into the neuron, and causing extra-synaptic levels to rise, amphetamine actually dumps stored DA out into the synapse, while also blocking its re-uptake. That extra-synaptic dopamine then goes on to bind to various dopamine receptors, causing cascading signal releases.

D1 receptor agonists mimic dopamine at the D1 receptors themselves. So they have an affinity for the D1 receptors, and bind directly to the site, causing the cascading signal releases directly. In all reality, most D1 receptor agonists also have affinity for the D2 receptor. It's just that they have a certain affinity for the D1 over D2. Take Doxanthrine for example. It has a 168 fold higher affinity for D1 than D2. However, it still binds to D2 a little bit. D1 receptor agonists are usually used for things like Parkinson's disease.

Now the D1 receptor and D2 receptor kind of have opposite effects. Activation of the D1 receptor stimulates adenylate cyclase, which indirectly activates cAMP-dependent protein kinase. Activation of the D2 receptor actually inhibits adenylate cyclase activity. Adenylate cyclase catalyses the conversion of ATP to cAMP. So D1 agonists increase cAMP and D2 agonists decrease cAMP. D2 receptor agonists are used as anti-psychotics. Memantine does agonize the D2 receptor, along with antagonizing the NMDA receptors, and agonizing the sigma receptors. So its effects on tolerance are actually multi-fold.