The Neural Bases of Operant Conditioning
By Brian Urmanita
	
For many students, exposure to operant conditioning is limited to its 
uses in learning new behaviors in human applications.  Behavior 
modification, in a social context, can be described as teaching 
individuals new ways of doing things based on four basic categories of 
increasing wanted behavior or decreasing unwanted behavior.  Positive 
reinforcement is the method that shows the best results and can be used 
in almost any learning situation.  But operant conditioning is also 
used in the laboratory to study the brain and the role it plays in 
learning and memory.  By teaching animals to learn tasks and rewarding 
them for doing those tasks correctly, we can observe how learning 
actually takes place in the brain and the structures that are involved 
in that process.  We can also introduce different chemicals into the 
brain that can impede or enhance learning which also provide clues as 
to which structures of the brain participate in this development or 
decay.
One such experiment uses a substance called losartan to offset the 
effects of ethanol on male Sprague Dawley rats (Tracy, Wayner & 
Armstrong, 1997).   The authors cite Walker and Freund (1971) as 
discovering that ethanol disrupts the ability to obtain operant 
behaviors.  By teaching rats to navigate an eight arm radial maze using 
operant conditioning techniques using food as the reward, the 
researchers discovered that despite the effects of ethanol, the rats 
were able to retain their reference and working memory that gave them 
the ability to choose the correct maze arm for the reward of food rats 
when injected with Losartan (Tracy, Wayner & Armstrong, 1997).  This 
supports the authors' conclusion that Angiotensin II (Ang II) and the 
AT 1 receptor are involved with decreased performance caused by ethanol 
(1997).  Losartan appears to block the inhibition of long term 
potentiation (LTP) in the medial perforant path of the dentate gyrus 
granule cells (1997).
Another study found that ethanol inhibits the NMDA receptors of 
juvenile rats to a greater degree than in adult rats cited by (Pyapali 
et al., 1999).  The age of the rats was given in Tracy, Wayner and 
Armstrong's (1997) study and apparently was not considered in 
performance tasks whereas the focus in the Pyapali et al. (1999) 
research hinged upon the age as a contributing factor of inhibition of 
LTP in hippocampal slices.  They propose as age increases from 
adolescence to adulthood in animals, the effect of ethanol changes in 
its ability to inhibit LTP.   
By observing operant conditioning on a different cellular level we 
further understand what chemicals are involved in the learning process.  
Injecting dopamine, cocaine or the dopamine D2 agonist N 0437 locally 
to the CA1 area of the hippocampus has provided the necessary or 
sufficient reinforcement for operant conditioning to take place (Stein, 
Zue, & Belluzzi, 1993).  But the rate of increased firing was found to 
be dependent on whether bursting had taken place before the injection 
(1993).  This work confirmed a previous study done by Stein and 
Belluzzi in 1988 and 1989, which also found that dopamine or cocaine 
could reinforce CA1 bursting in vitro. Work also conducted with 
crickets has shown that nitric oxide is critical in creating long term 
memory (Jaffe & Blanco 1994; Rickard & Gibbs, 1994). In order for LTP 
to occur, the NMDA receptors must be involved and nitric oxide must be 
released.
Another surprising discovery has revealed that there is actual new 
growth of neurons in the hippocampus.  This has also been discovered in 
a few mammals including adult mice, rats, marmosets, macaque monkeys, 
tree shrews and even humans (Gould et al., 1999).  A closer inspection 
has shown that a few thousand new hippocampal cells are generated per 
day occurring in the dentate gyrus but their function is believed to 
contribute minimally to increased function (1999).  The authors suggest 
enriched environments and learning increase the survival of new cells 
which would, in turn, augment hippocampal dependant learning tasks but 
question to what extent they play in performance in another type of 
learning (1999).  Conversely, stress, glucocorticoids, and aging can 
decrease performance based on hippocampal dependant learning (1999).  
In conclusion, the use of certain chemicals injected or introduced into 
particular areas of the hippocampus can be shown to influence operant 
learning.  By taking place at a cellular level and being able to see 
those changes through various methods of measurement we begin to see 
that operant conditioning isn't just a social mechanism of change.  
It's also a physical change that is demonstrated at a microscopic level 
previously unknown in neuroscience research.





References
	Gould, E., Tanapat, P., Hastings, N.B., & Shors, T.J., (1999). 
Neurogenesis in adulthood: A possible role in learning. Trends in 
Cognitive Sciences. 3, 186-192.
	Jaffe, K., & Blanco, M.E., (1994). Involvement of amino acids, 
opioids, nitric oxide, and NMDA receptors in learning and memory 
consolidation in crickets. Pharmacology Biochemistry and Behavior. 47, 
493-496.
	Rickard, N.S., Ng, K.T., &Gibbs, M.E., (1994). A nitric oxide 
agonist stimulates consolidation of long term memory in the 1 day old 
chick. Behavioral Neuroscience. 108, 640-644.
	Stein, L. & Belluzzi, J.D., (1989). Cellular investigations of 
behavioral reinforcement. Neuroscience & Biobehavioral Reviews. 13, 69-
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	Stein, L., Bao, L.G., & Belluzzi, J.D., (1993). A cellular 
analogue of operant conditioning. Journal of the Experimental Analysis 
of Behavior. 60, 41-53.
	Wenrich, D., Lichtenberg Kraag, B., & Rommelspacher, H., (1998). 
G protein pattern and adenylyl cyclase activity in the brain of rats 
after long term ethanol. Alcohol. 16, 285-293.

Copyright © 2001, Dr. John M. Morgan, All rights reserved - This page last edited March 12, 2001
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