There are a lot of theories about what dopamine transmission encodes. The "general salience" theory is not in favor right now, primarily because of electrophysiological data which show that dopamine neurons do not burst fire in response to aversive stimuli, and that their firing is indeed suppressed. Fast-scan cyclic voltammetry (electrochemical) recordings of dopamine concentration in the nucleus accumbens and more dorsal regions of striatum have shown greater dopamine release in response to appetitive rather than aversive stimuli, but as of yet there are no studies examining aversive stimuli, so the jury's still out on this one. Microdialysis and slower forms of voltammetry have shown elevations in dopamine in response to aversive stimuli; however, the temporal resolution of these methods is much lower than either single unit-recording or FSCV, so it's hard to directly attribute the rise in dopamine to the aversive event and not to some slower, underlying change in the behavioral state of the animal. Nonetheless, there is clearly a disconnect between the electrophysiological and microdialysis/slow voltammetry data. This can potentially be explained by neural activity in the terminal fields of dopamine neurons acting directly on the axon terminals to cause release of dopamine independent of cell body firing.
I must reiterate,
dopamine≠reward. While dopamine release may be necessary for signaling some forms of reward, for naturalistic stimuli it is probably not sufficient. It's interacting with incoming patterns of activity from other neurotransmitter systems and regions of the brain, and it's the interplay of these activity patterns that determines whether the experience is rewarding. One thing that has come to be well supported by evidence is that phasic dopamine release serves as a signal for unexpected reward.
samadhi_smiles said:
How can dopamine release encode salience for emotional stimuli (even unpleasurable stimuli) yet still be an extremely pleasurable monoamine when released in larger amounts (with a releaser such as methamphetamine)?
There are five different dopamine receptors, and each has a different affinity for dopamine. Thus, a small quantity of dopamine will preferentially activate the high-affinity receptors, whereas a larger quantity will activate them all. There is considerable evidence that D1 receptor activation in the NAcc plays a major role in the hedonic and reinforcing effects of natural and drug rewards. D1Rs have a lower affinity for dopamine than D2Rs, providing an appealing potential mechanism for reward signaling by massive dopamine release.
Another possibility is that the response to dopamine also depends on the signals coming from other brain systems.
