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Written by Scott Merville
Connect Brain Cell Changes
to Reward Learning
— Neuroscientists have identified a brain cell that changes during
operant conditioning, which is a form of reward learning, providing
the first look at cellular processes involved in this major, but
poorly understood, form of learning.
at The University of Texas Medical School at Houston describe their
findings in the May 31 issue of Science. By pinpointing
a neuron that changes when a sea snail learns to bite to earn a
reward, the research team opened a new path for analyzing the cellular
and molecular processes underlying operant conditioning.
is a very big part of everything that we do. When you do something
and get a reward for doing it, you change your behavior,” said the
paper’s senior author, John H. Byrne, Ph.D., head of the UT-Houston
Medical School Department of Neurobiology and Anatomy. Scientists
have observed the behavioral aspects of operant conditioning in
animals and humans for decades.
“The big question
is how does it work, what are the underlying processes in the brain?”
Byrne said. “We’ve reduced the complex process of reward learning
down to the level of a single nerve cell. The promise here is that
we can use biochemical and molecular approaches to understand the
cellular processes in the neuron that gives rise to changes in behavior.”
Byrne and colleagues
drew on their extensive knowledge of the marine snail Aplysia
to design a project that tracked a learned behavioral change to
a change in a single neuron. The project focused on the snails’
feeding habits. Aplysia bite spontaneously in their search
for food. A successful bite that secures food sends a reward signal
to the brain via a nerve in the animal’s esophagus. The reward
signal is absent when the bite comes up empty.
By wiring an
electrode to this nerve, the scientists mimicked the food reward
signal with electrical stimulation. Similar to the virtual reality
depicted in the movie The Matrix, they now could “feed” the
snails with food that didn’t exist. A group of snails received such
a “virtual” food reward every time they bit. One control group
got no stimulation, and a second control group received stimulation
that was only randomly associated with biting. The rewarded group
learned to bite more often than the two control groups, even though
there never was any “real” food. In addition, just 10 minutes of
training induced a memory that lasted at least a day.
the brain activity from trained animals pinpointed changes in a
specific neuron, known as B51. Activity in B51 has been correlated
with the ingestion of food. The changes in B51 following conditioning
are such that the cell is more likely to be active. Thus, the animals
could be expected to increase their eating responses after conditioning.
other variables that might have influenced the results, the team
then removed the individual cell from the brain, placed it in culture,
and conducted an experiment using the neurotransmitter dopamine.
Previous research has associated dopamine with the brain’s reward
response in a variety of animals, including both snails and humans.
Cultured B51 cells changed their electrical properties when they
were “rewarded” with a puff of dopamine right after receiving an
electrical pulse that mimicked the cell’s activity during the biting
behavior. “The B51 neuron changes its properties to allow it to
get more dopamine,” Byrne said. “The changes resulting from conditioning
the single cell are the same changes found in the B51’s from the
thought to mediate the rewarding properties of drugs abused by humans.
One commonly used animal model in addiction research is to study
the brain of rats after they have self-stimulated reward centers
in their brains by pressing a lever. Apparently, self-stimulating
their brains by biting leads to dopamine-mediated changes in identified
Aplysia cells. If the similarities continue on the molecular
level, the single-cell approach introduced by Byrne and his colleagues
would be a very promising way to study the molecular mechanisms
on the paper are postdoctoral researcher Björn Brembs, Ph.D., and
Fred D. Lorenzetti, a doctoral student with the Graduate Neuroscience
Program in Byrne’s lab. Neuroscience doctoral student Fredy D.
Reyes and Douglas Baxter, Ph.D., associate professor in the department
of Neurobiology and Anatomy are also co-authors.