Dopamine: Learning, Memory and Motivation
Dopamine is about more than just pleasure. It’s also central to learning. When the brain is rewarded unexpectedly, dopamine surges, prompting the Limbic “reward system to take note in order to remember how to replicate the positive experience. In contrast, negative encounters deplete dopamine as a signal to avoid repeating them. This is a key learning mechanism which is also involves memory-formation and motivation.
Scientists believe the brain establishes a new temporary neural network to process new stimuli. Each repetition of the same experience triggers the identical neural firing sequence along an identical neural journey, with every duplication strengthening the synaptic links among the neurons involved. Neuroscientists say, “Neurons that fire together wire together.”
If this occurs enough times, a secure neural network is established, as if imprinted, and the brain can reliably access the information over time. A discrete act of learning has been initiated, reinforced, and embedded, a process called “Long-Term Potentiation” (LTP). Most people have experienced this model of learning when memorizing facts and figures or a foreign language’s vocabulary.
Drug use affects LTP. In one experiment involving rats, Julie Kauer, a professor at Brown University, found that morphine disrupted LTP in the ventral tegmentum area (VTA), a key part of the brain’s Limbic system, and that it continued for about 24 hours thereafter; morphine blocks an enzyme (guanylate cyclase) that limits the release of dopamine, as if removing a brake on it. Kauer explains, “We’ve shown here that morphine makes lasting changes in the brain by blocking a mechanism that’s believed to be the key to memory making. So these findings reinforce the notion that addiction is a form of pathological learning.”1
It has long been observed that alcoholics have memory problems. This may be due to the negative impact alcohol has on the hippocampus, the center of new-memory formation.2 Adolescent rats given alcohol were found to have significant damage to their hippocampi.3 In another study involving rats fed alcohol over a four-day period to simulate alcoholism, researchers found that the rats’ ability to grow new cells in the hippocampus was substantially slowed. In a possible sign of the brain’s innate ability to recover, however, they experienced a growth spurt in hippocampal cells after they stopped drinking.4 On the other hand, extremely small amounts (repeat, extremely small amounts) of alcohol given to rats actually helped memory-formation by increasing expression of a memory-related receptor dubbed NR1.5
Damage to the hippocampus in humans can cause amnesia, and that’s not all. In a study reported in the January 2002 Proceedings of the National Academy of Sciences, researchers asked subjects with damaged hippocampi to imagine future situations like meeting a friend or attending a Christmas party: they couldn’t. “We found that the role played by the hippocampus in processing memory was far broader than merely reliving past experiences,” Dr. Eleanor McGuire said in a statement. “It also seems to support the ability to imagine any kind of experience including possible future events. In that sense, people with damage to the hippocampus are forced to live in the present.”6
Talk about one day at a time.
Temporary amnesia, what alcoholics call “blackouts,” can also be caused by drinking too much. During a blackout, a drunk person continues to do things like have a conversation or, more dangerously, drive a car, but has no memory of it. Many alcoholics who suffer blackouts report that they have found themselves (and their cars) either at home or in an unfamiliar place after a night of drinking but have no recollection of how they got there. Blackouts can last a few minutes or stretch into hours. It was once thought that these episodes resulted from neuron death caused by over-indulgence. However, the July 6, 2011 issue of The Journal of Neuroscience reported that rather than brain-cell death, blackouts are caused by disruption of LTP — too much alcohol prevents memory formation in the hippocampus.7
Because of the significant impact drugs have on learning and memory, addiction researchers describe the disease, in part, as a memory disorder. Treatment, they say, is a lengthy process during which the motivational power of those toxic memories diminishes. The longer one is sober, the more the power of those memories wanes and cravings become less robust and compelling.
1. Morphine Causes Lasting Changes In The Brain, April 30, 2007; Addictive drugs harm brain’s natural brake, CNN.com, April 26, 2007.
2. Memory Often a Victim of Ecstasy, New York Times, April 10, 2001.
3. The Grim Neurology of Teenage Drinking, New York Times,July 4, 2006.
4. Beating Alcohol Addiction Gives Brain a Boost, WebMD Medical News, Nov.9,2004.
5. Moderate Drinking May Boost Memory, Study Suggests, medicalnewstoday.com, Oct. 28, 2006.
6. Cause of Amnesia Curbs Ability to Imagine Future, Wall Street Journal, January 16, 2007.
7. The Biology Behind Alcohol-Induced Blackouts, mdecalnewstoday.com, July 7, 2011.
I think the blackouts in the drinking issue is because the alchool somehow indirectly affects the signaling through the brain, especially in memoring the events.
Dopamine it must be well known that has a very strong relationship with serotonin, when dopamine ( http://www.neuralpedia.com/neurotransmitters/dopamine/ ) levels go up serotonin ( http://www.britannica.com/EBchecked/topic/535741/serotonin ) levels goes down. So alchool addiction and other addictions should be researched with both neurotransmitters in mind.
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