Here's a copy of a post I made at M&M long, long ago, with a few studies about the relationship between DA and motivation:
Dopamine and Motivation
A few papers (rat studies) examining the role of D1/D2 in making decisions based on effort, delayed reward, and risk.
19331447 (comment in 19331471): D1/D2 antagonism caused rats to choose lesser rewards requiring less effort. Amphetamine administration blunted this effect, and biased them toward greater effort/reward ("bidirectional modulation of choice behavior"). D3 agonists/antagonists had no effect.
17142306: Evidence that D1 receptors in the anterior cingulate cortex (ACC) encode whether or not an action is worth performing due to expected benefit/cost. Intra-ACC D1 antagonism reduced the tendency to expend effort for greater reward, while ACC D2 antagonism had no effect on this.
18668030: Activation of D1/D2 biased rats toward risking painful response for greater reward; antagonism blocked this, and producd risk aversion. D3 operated inversely.
15864561: D2 antagonism reduced tolerance for greater effort and delay to attain rewards, while inhibition of serotonin biosynthesis reduced acceptance of only delay.
17805307 echoes these results with dopamine generally, and notes effort and delay are modulated by NMDA as well (but with less direct receptor/behavior correlation). A result worth noting is that high doses of amphetamine caused rats to discount greater effort when seeking reward, while low doses allowed them to discount delay.
And one regarding food preference:
16549074: Selective D1 agonism enhanced the preference for high palatability (high-fat/sugar) food, while selective D2/D3 agonism eliminated this preference.
Here's one more, regarding additional impact of NE:
Prefrontal norepinephrine determines attribution of "high" motivational salience.
Ventura R, Latagliata EC, Morrone C, La Mela I, Puglisi-Allegra S.
Santa Lucia Foundation, European Centre for Brain Research (CERC)
Intense motivational salience attribution is considered to have a major role in the development of different psychopathologies. Numerous brain areas are involved in "normal" motivational salience attribution processes; however, it is not clear whether common or different neural mechanisms also underlie intense motivational salience attribution. To elucidate this a brain area and a neural system had to be envisaged that were involved only in motivational salience attribution to highly salient stimuli. Using intracerebral microdialysis, we found that natural stimuli induced an increase in norepinephrine release in the medial prefrontal cortex of mice proportional to their salience, and that selective prefrontal norepinephrine depletion abolished the increase of norepinephrine release in the medial prefrontal cortex induced by exposure to appetitive (palatable food) or aversive (light) stimuli independently of salience. However, selective norepinephrine depletion in the medial prefrontal cortex impaired the place conditioning induced exclusively by highly salient stimuli, thus indicating that prefrontal noradrenergic transmission determines approach or avoidance responses to both reward- and aversion-related natural stimuli only when the salience of the unconditioned natural stimulus is high enough to induce sustained norepinephrine outflow. This affirms that prefrontal noradrenergic transmission determines motivational salience attribution selectively when intense motivational salience is processed, as in conditions that characterize psychopathological outcomes.
PMID: 18725944 [PubMed - indexed for MEDLINE]
Most of the pharmaceuticals that enhance motivation significantly seem to do so through nonselective mechanisms. One of my long-term goals is to find something (maybe a D-something agonist) that will increase motivation without some of the side effects and concerns associated with adderall.
Edited by chrono, 13 October 2010 - 07:50 PM.
LongeCity
