If we were to look at all of the steps of emotional learning, it 
would quickly become apparent that all parts of the brain have a role 
in the process, from perception to response.  There are however certain 
systems in the brain which play a major part in the formation of 
emotional memories, the foundation of emotional learning.  A 
description of these systems and their functions in emotional learning, 
as well as the cellular activities associated with the systems, will 
follow.




Neural Systems Underlying Emotional Learning
Stephaney M. Cox


	The limbic system plays a major role in emotional learning and is 
comprised of the limbic cortex (including the cingulate gyrus), the 
hippocampus, the mammillary body, and the amygdala (Bradley & Lang, 
2000; Cahill et al., 1995; Carlson, 2001; De Amaral & De Oliveira, 
2000; Plutchik, 1994).  The cingulate gyrus of the limbic cortex is 
located dorsal to the corpus callosum.  It is thought that the 
cingulate gyrus connects the emotional brain with the thinking brain 
(Johnston, 1999).  What little else is known about the gyrus suggests 
that it associates smells and sights with pleasant emotional memories 
and that it has some role in the emotional reaction to pain (De Amaral 
& De Oliveira, 2000).  The hippocampus, located just posterior to the 
amygdala, is especially important in emotional learning because it 
allows for the creation of long term memory.  That long term memory 
holds emotional experiences that can be compared to present emotional 
experiences to determine any potential threat (De Amaral & De Oliveira, 
2000).  Lucas et al. (1974) found that emotionally unstable dogs showed 
reduced hippocampal theta energy at all times, while emotionally stable 
dogs only had that response while orienting and avoiding.  This seems 
to suggest that the dogs were unable to store the emotional memory that 
would allow them to feel comfortable in what should have been a 
somewhat familiar environment. 
Much work has been done on the role of the amygdala in emotional 
learning.  It is thought that the amygdala, an acorn shaped structure 
located in the medial temporal lobe, is a major relay station for 
emotional information.  It receives information from all sensory 
modules in the brain and has extensive connections to other brain 
structures affecting or affected by emotion (Adolphs & Damasio, 2000), 
such as the hippocampus and the frontal, temporal, and occipital 
cortices, including the anterior cingulate, ventral striatum, and 
nucleus basalis, to name a few (Aggleton & Young, 2000; Dolan & Morris, 
2000; Emery & Amaral, 2000).  The lateral nucleus of the amygdala acts 
as the input system and the central nucleus acts as the output pathway 
(Aggleton & Young, 2000). These connections suggest that the amygdala 
can categorize the early stages of sensory processing, laying the 
groundwork for emotional memory and learning.  Reiman et al. (2000) 
proposes that the amygdala organizes emotional experience in terms of 
the potential, not actual, effect, indicating that the brain is 
recalling the effect of learned emotional consequence.  When the 
amygdala is damaged, animals are more likely to approach an unknown 
person or animal, demonstrating a lack of learning about potentially 
harmful consequences (Aggleton & Young, 2000). There is an interesting 
theory on the lateralization of the amygdala during conditioned 
learning.  Dolan and Morris (2000) showed that when test subjects were 
shown pictures of fearful faces there was increased activity seen in 
the left amygdala.  When the subjects were conditioned to display an 
acquired fear response to previously unfearful faces there was 
activation of the right amygdala (Lane 2000).  The amygdala seems to 
play a large part in the formation of fear memories, including aversive 
or fear conditioning (Johnston, 1999; Maren, 1999). Lesions of the 
central nucleus can disturb some of the components of fear conditioned 
behavior in nonhuman animals, but damage to the amygdala generally 
produces no such response in humans (Aggleton & Young, 2000).  There is 
still much work to be done to discover the full contributions of the 
amygdala to emotional learning, but most of the groundwork has been 
laid, with new information arising constantly.  For instance, just 
recently long term potentiation has been identified in the basolateral 
ganglia of the amygdala (Maren, 1999).  
The thalamus is associated with changes in emotional reactivity, 
predicting responses in subcortical structures associated with 
emotional learning (De Amaral & De Oliveira, 2000; Dolan & Morris, 
2000).  It is one of the key structures in a neural system including 
the basal forebrain, amygdala, and brainstem (Dolan & Morris, 2000).  
It is important in interpreting stimuli so that other structures may 
evaluate what emotional reaction is called for (Heilman, 2000).  The 
thalamus, like the amygdala, is an important relay station for 
perceptual information, sending axons into the hypothalamus (Carlson, 
2001). This thalamic hypothalamic amygdaloid emotion circuit is 
essential in fear conditioning; ablation of the thalamus and amygdala 
disrupt behavioral emotional response to conditioned stimuli (Heilman 
et al., 2000).   Recall generated emotion shows activity in medial 
prefrontal cortex and thalamus (Reiman et al., 2000).  
	The hypothalamus is believed to be involved with aversion, a 
result of emotional learning (De Amaral & De Oliveira, 2000).  Its most 
important role in emotional behavior is in the expression of emotions 
as deemed appropriate by prior association, as well as serving as a 
neural pathway for information related to emotion.  The brainstem has a 
similar function in the generating of emotional response to emotionally 
learned events.
	It is interesting to note that throughout the intense evolution 
of the mammalian brain the older areas involved in emotional response 
and learning have remained relatively unchanged (De Amaral & De 
Oliveira, 2000).  The fact that these areas have not been selected out 
of mammalian brain structure signifies the importance of emotional 
learning and response to the ultimate survival of an organism.



References

Adolphs, R., & Damasio, A. R. (2000).  Neurobiology of emotion at a 
systems level.  In J. C. Borod (Ed.), The neuropsychology of emotion 
(pp. 194_213).  New York: Oxford University Press.
Aggleton, J. P. & Young, A. W. (2000). The enigma of the amygdala: On 
its contribution to human emotion.  In R.D. Lane & L. Nadel (Eds.), 
Cognitive neuroscience of emotion (pp. 106_128).  New York: Oxford 
Press.
Bradley, M. M. & Lang, P.J. (2000).  Measuring emotion: Behavior, 
feeling, and physiology.  In R.D. Lane & L. Nadel (Eds.), Cognitive 
neuroscience of emotion  (pp. 242_276). New York: Oxford Press.
Cahill, L., Babinsky, R., Markowitsch, H. J., & McGaugh, J. L. (1995).  
The amygdala and emotional memory.  Nature, 377, 295_296.
Carlson, N. R. (2001).  Psychology of behavior.  Allyn & Bacon: Boston
De Amaral, J. R., & De Oliveira, J. M. (2000). Limbic system: The 
center of emotions. Internet address 
www.epub.org.br/cm/n05/mente/limbic_i.htm  
Dolan, R. J. & Morris, D.J. (2000).  The functional anatomy of innate 
and acquired fear: Perspectives from neuroimaging. In R.D. Lane & L. 
Nadel (Eds.), Cognitive neuroscience of emotion (pp. 225_241). New 
York: Oxford Press.
Emery, N. J. & Amaral, D.G. (2000).  The role of the amygdala in 
primate social cognition.  In R.D. Lane & L. Nadel (Eds.), Cognitive 
neuroscience of emotion  (pp. 156_191). New York: Oxford Press.
Heilman, K. M. (2000).  Emotional experience: A neurological model.  In 
R.D. Lane & L. Nadel (Eds.), Cognitive neuroscience of emotion  (pp. 
328_344).  New York: Oxford Press.
Heilman, K. M., Blonder, L. X., Bowers, D., Crucian G. P. (2000).  
Neurological disorders and emotional dysfunction.  In J. C. Borod 
(Ed.), The neuropsychology of emotion (pp. 367_412).  New York: Oxford 
University Press.
Johnston, V. S. (1999). Why we feel. Reading: Perseus Books.
Lane, R. D. (2000) Neural correlates of conscious emotional experience.  
In R.D. Lane & L. Nadel (Eds.), Cognitive neuroscience of emotion  
(pp.345_370).  New York: Oxford Press.
LeDoux, J. E. (1995). In search of an emotional system in the brain: 
Leaping from fear to emotion and consciousness.  In M. S. Gazzaniga 
(Ed.), The cognitive neurosciences (pp. 1049_1061). Cambridge: MIT 
Press
Lucas, E A., Powell, E. W., & Murphree, O. D. (1974). Hippocampal theta 
in nervous pointer dogs.  Physiology and behavior, 12 413_418
Maren, S. (1999). Long term potentiation in the amygdala: A mechanism 
for emotional learning and memory.  Trends in neuroscience, 22(12), 
561_568.
Plutchik, R. (1994). The psychology and biology of emotion.  New York: 
Harper Collins College Publishers.
Reiman, E. M., Lane R. D., Ahern, G. L., Schwartz, G. E., & Davidson, 
R. J. (2000).  Positron Emission Tomography in the study of emotion, 
anxiety, and anxiety disorders.  In R.D. Lane & L. Nadel (Eds.), 
Cognitive neuroscience of emotion  (pp. 389_406).  New York: Oxford 
Press.







Neurological Bases for Emotional Learning
Jennifer Benzle

Investigating the neural mechanisms such as neurogenesis, 
synaptic plasticity, and axonic circuits as underlying aspects of 
emotional learning and memory calls for some brief clarification. There 
is endless speculation on emotions from both the scientific realm and 
the non-scientific realm. While non-scientists might react with raised 
hackles at the prospect of objectifying emotions, some scientists, 
including neurologists believe that emotional experience is absolutely 
a measurable aspect of existence and can be directly correlated with 
certain structures and neural phenomena in the brain. 
Most theoretical models of emotional learning emphasize the 
circuitry and inter-relatedness of several structures and cell 
assemblies in the brain. Generally described as the limbic system, the 
fundamental neural structures necessary for emotional learning and 
memory are found here. The amygdala, hippocampus, dendate gyrus, 
olfactory bulb, septum, and parts of the thalamus and cerebral cortex 
are some important centers of the limbic system (Kalat, 1995). While 
this system has generally been thought of as the seat of emotions, it 
would be an err of oversimplification to exclude other parts of the 
brain, physical environment, chemicals, and genetics (to name a few) 
that each have their own niche in the dynamics of emotional learning 
and memory. 
One model of emotional learning and memory, presented by Paul 
MacLean, is that the spinal chord represents Freud's ID, and that rage 
and unchecked desire is manifested in this old brain. The limbic system 
then acts as Freud's ego, and the cerebral cortex represents the ever 
rational, objective and perhaps moral superego (Greenfield, 2000). 
Although this model may seem far-fetched, it is somewhat analogous to a 
pervasive theme found in the study of human emotions. The body sends 
physical signals as an immediate reaction to an event, a few examples 
are changes in breathing, heart rate, pupil dilation, sweating, and 
muscle tension. A behavioral reaction is manifested as a consequence to 
the physiological signals. These reactions can range from first order 
emotions such as fear, rage or sexual drive, to second order emotions 
such as grief and love. The cerebral cortex then explores the emotion 
and establishes a way of dealing with it at that moment and also may 
check it in to long term storage for possible future reference.  
It is this interesting interplay of body and brain in regards to 
emotion that is analyzed from a neurologist's perspective in a book 
titled "Descartes Error" written by Antonio Damasio (1994). Damasio 
contends that Descartes was mistaken when he established his philosophy 
of the absolute duality of the mind and the physical body. Damasio 
calls the physiological influence on emotions a somatic marker and 
describes this marker as a conditioning tool for normal social behavior 
(Damasio, 1994).   
Now that the theoretical background has been briefly described, 
it's time to delve into some of the biological neurology that may be a 
basis for emotional learning. Among the important factors of this 
process of learning are the "pattern of connections among neurons and 
the strength of the synapses constituting those connections (Damasio, 
p. 108, 1994), also referred to as neuronal plasticity, it is 
apparently affected by neural phenomena such as neurogenesis and cell 
death. The descriptions I will provide of neural phenomena are related 
to neurological theories of learning in general.  
	Neurogenesis in the adult hippocampus and dendate gyrus has been 
linked to learning. In an article by Gould, Tanapat, Rydel, and 
Hastings (2000) instances of learning that were shown to enhance the 
number of new neurons in certain structures of the limbic system were 
cited. Among them were environmental stimulation and the consequent 
growth of new neurons in the hippocampus. Gould et al. (2000) found 
that "Evidence suggests that both learning and physical activity 
enhance the number of new granule neurons, apparently through different 
mechanisms" (p.716).  Learning also seemed to increase the survival of 
these new cells.
In a different article by Gould, Tanapat, Hastings and Shors 
(1999) the research showed that when new cells were generated, it took 
time for them to "become functionally integrated into existing 
circuitry. Chronic changes in cell production and survival might be 
capable of exerting additive effects throughout the continual 
production, differentiation and integration of adult generated 
neurons." (Gould, et al. P.187, 1999).  
An article that explores some of the mechanisms that influence 
survival and growth of new neurons is by Duman, Malberg, Nakagawa, and 
D'Sa. They list three possible factors for neurogenesis and cell 
survival. "First, an increase in the number of synaptic connections and 
neuronal activity could elevate the expression of neurotrophic factor 
in the post synaptic cells. Second, an increase in the number of 
synaptic connections could result in increased supply of neurotrophic 
factor from presynaptic terminal. Third, depolarization or activation 
of the cAMP cascade in postsynaptic neurons could increase the neuronal 
responsiveness to neurotrophic factor stimulation" (Duman, et al, p. 
733, 2000). As evidence for these factors, Duman et al. explain that 
"antidepressant treatment upregulates the cAMP-CREB cascade and 
expression of BDNF" (p.735, 2000) And that "Antidepressant treatment 
increases hippocampal neurogenesis"(Duman, et al., p. 736, 2000).  
	As opposed to neurogenesis, there is also cell death. While 
environmental stimulation, estrogen, and running have all been linked 
with the creation and survival of new cells, depression and chronic 
stress have been linked with cell degeneration and death.  Duman et al. 
(2000) describe that there have been both basic and clinical studies 
that have provided evidence of neuronal atrophy and loss in response to 
stress and depression. There were found a decreased number and size of 
neurons in the cerebral cortex of depressed patients.
The survival of cells is linked with nutritional conditions. 
Duman et al. write "In the absence of neurotrophic factor the neurons 
undergo a process of programmed cell death" (p.733, 2000).  "The 
survival of a neuron may also be dependent on its synaptic connections 
with a target cell as well as other cells" (Duman, et al, p.733, 2000).
It is evident that there are many influences that determine 
neurogenesis, cell death and cell atrophy. The main themes are that 
chronic and clinical depression, stress, and lack of environmental 
stimulation seem to correlate with the degeneration of cells. Factors 
that correlate with neurogenesis and cell survival are physical 
activity and increased environmental stimulation.   
In conclusion, it is important to acknowledge that the underlying 
neural mechanisms for emotional learning and memory systems in the 
brain are just beginning to be explored, observed and measured. Many 
scientists and theorists believe that the dynamic circuits and 
phenomena underlying emotions extend way beyond the limbic system and 
that humans are decades away from completely understanding them.



References:

Damasio, A.R., (1994). Descartes' error, emotion, reason, and the human 
brain. New York, NY: G.P. Putman Sons.

Duman, R.S., Malberg, J., Nakagawa, S, D'Sa, C. (2000). Neuronal 
plasticity and survival in mood disorders. Biological Psychiatry, 
48,732-739.

Gould, E., Tanapat, P., Hastings, N., Shors, T.J. Neurogenesis in 
adulthood: a possible role in learning. Trends in Cognitive Sciences, 
3(5), 186-192.

Gould, E., Tanapat, P., Rydel, T., Hastings, N. (2000). Regulation of 
hippocampal neurogenesis in adulthood. Biological Psychiatry, 48(8), 
715-720.

Greenfield, S. (2000). The private life of the brain. New York, NY: 
John Wiley & Sons, Inc.

Kalat, J. W. (1995). Biological psychology. Pacific Grove, CA: 
Brooks/Cole Publishing Company.








Emotional Learning caused by synaptic changes
Ponciano Hernandez

Many systems influence the formation of emotional memories, which 
leads to learning. Carlson defines learning as the process by which 
experience changes our nervous system and as a result our behavior 
(410). One major system is the limbic. 
The limbic system is concerned with motivation and emotion. It is 
composed of the limbic cortex (also cingulated gyrus_ an important 
region), hippocampus, amygdala, fornix, mammillary bodies, and parts of 
the hypothalamus (Carlson,71-2). 
We know that emotional learning occurs in the limbic system, but 
to be more precise, it occurs at the synapse. Changing the structure of 
the synapse implies learning. By doing so, the synapse becomes 
specialized to a particular stimulus. One method of altering the 
structure of the synapse is long-term potentiation (LTP). 
LTP is an increase in the excitability of a neuron to a 
particular synaptic input caused by repeated exposure (Carlson, 1998). 
According to Durand, Kovalchuk, and Konnerth, LTP is the foundation of 
learning and memory (1996). In Durand et al experiment, LTP caused a 
change in synaptic function. They demonstrated this by applying a +40mV 
or –70mV to a NMDA-mediated synaptic contact and identifying non-NMDA 
components, resulting from electric current, as glutamergic synapses by 
using cyclothiazide (1996). 
Another method of altering the structure of a synapse is by 
experience. Jones, Klintsova, Kilman, Sirevaag, and Greenough examined 
the experience-related changes that occur in the multiple synaptic 
boutons (MSBs) by placing rats in a stimulating environment and 
comparing them to a control group, who were individually caged (1997). 
Results showed rats in the stimulating environment had an increase in 
density of the axon-spine-shaft bouton and number of MSBs per neuron 
that form contacts with dendritic spines and dendritic shafts (1997). 
It is believed that the role of the dendritic spines is to protect 
parent dendrite from accumulating toxic levels of calcium(II) ion 
(Segal, 1995).
In another experiment by Friedlander (Comerey, Stamoudis, Irwin, 
Greenough, 1996) multiple synaptic contacts were changed by experience. 
In their experiment, they deprived kittens of sight in one eye. As they 
developed, the non-deprived eye showed an increase in the size of 
presynaptic bouton and number of synaptic contacts made with each 
bouton of axons (Comery, et al., 1996).
Although the limbic system is the area associated with formation 
of memory and learning, it appears that the synapse is the site of 
learning. This is achieved by changing the number of synaptic contacts, 
shape, length, or density of synapse. Changes in the synapse are 
brought about by experience or LTP.

References

Segal, M. (1995). Dendritic spines for neuroprotection: a 
hypothesis. Trend Neuroscience, 468-71.
Durand, M., Kovalchuk,Y., & Konnerth, A. (1996). Long-term 
potentiation and functional synapse induction in developing 
hippocampus. Nature, 381, 71-4.
Hosokawa, T., Rusakov, D.A., Bliss, T., & Fine, A. (1995). 
Repeated confocal imaging of individual dendritic spines in the living 
hippocampal slice: Evidence for changes in length and orientation 
associated with chemically induced LTP. The Journal of Neuroscience, 
15(8), 5560-73.
Comery, T., Stamoudis, C., Irwin, S., & Greenough, W. (1996). 
Increased density of multiple-head dendritic spines on medium-sized 
spiny neurons of the striatum in rats reared in a complex environment. 
Neurobiology of learning and memory, 93-6.
Jones, T., Klintsova, A., Kilman, V., Sirevaag, A., & Greenough, 
W. (1997) Induction of multiple synapses by experience in the visual 
cortex of adult rats. Neurobiology of learning and memory, 13-20.
Carlson, N. (1998). Physiology of Behavior. Boston; Allyn and 
Bacon.






Intracellular mechanisms involved in emotional learning
Greg Rickel

	To understand the intracellular mechanisms involved with 
emotional learning, one must use a reductionist perspective and break 
the phenomena down into the specific structures that mediate its 
existence.  Previously thought to be associated with the entire limbic 
system, current research suggests that the glutamate, NMDA, AMPA, and 
GABA receptors within the basolateral, basomedial, and central nuclei 
of the amygdala are the key mechanisms of emotional learning (LeDoux, 
1992). This paper will discuss the relationship these mechanisms have 
and the subsequent synaptic plasticity (long term potentiation) 
produced when emotionally relevant stimuli are presented to them.
	When an action potential is sent to the amygdala, from a variety 
of brain structures, glutamate is released from various pre_synaptic 
neurons. The growing body of research on this topic suggests that 
excitatory amino acids, such as glutamate, play a major role in the 
synaptic plasticity within the amygdala (Farb, Aoki, Milner, Kaneko, 
LeDoux, 1992).  Depending on where the stimuli were sent from will 
determine which of the aforementioned structures of the amygdala will 
be enacted.  Glutamate is one of the more common excitatory synaptic 
transmitters within the brain.  Of particular interest are the effects 
that glutamate has on the NMDA and AMPA receptors within the brain.  
Glutamate releases the magnesium ligand molecule that blocks the 
NMDA and AMPA receptors.  Once this is accomplished, calcium 2++ is 
allowed to enter the cell.  The calcium interacts with enzymes known as 
protein kinases, specifically calmodulin_dependant_protein kinase II 
(CaMKII).  It is these enzymes, which appear in high concentrations at 
post_synaptic thickening sites, which may be the molecular basis for 
the process of emotional learning (Maren, 1999).  It has been known 
that both NMDA and AMPA receptors sites are necessary in the mediation 
of emotional memory.  This has recently been discovered to only be 
necessary for thalamic input to the basolateral amygdaloid, whereas 
cortical input may only require the activation of AMPA receptor sites 
(Armony, Servan-Schreiber, Cohen, LeDoux, 1997).  The summation of the 
excitatory potentials of the AMPA receptors directly influences the 
synaptic plasticity of NMDA receptors.  Mainly thought to be due to a 
reverse flow of the electrical current of the original action 
potentials.  This causes the slow kinetic characteristics of NMDA 
receptors to be sped up by increasing the surface area of the receptor 
site (LTP).  The combination of these actions are thought to be related 
to emotional memory due to inhibition of the normal functioning of GABA 
inhibitory systems.
	 When the glutamate_enacted system is functioning collateral 
projections to GABA interneurons cause them to fire (LeDoux, 1992).  
Normally GABA acts as an inhibitory neurotransmitter causing the 
glutamate enacted NMDA and AMPA receptors to deactivate.  Current 
theories have hypothesized that this is the specific basis of emotional 
memory.  When the inhibitory effects of GABA are reduced the summation 
of the excitatory potentials allows a stronger exertion of excitatory 
influence onto specific areas within the amygdala.  This stronger 
exertion seems to mediate a greater rate and production of synaptic 
plasticity when emotionally relevant stimuli are presented.
	Various areas of the brain process information that is relevant 
to emotional learning, but the actual structural basis seems to be the 
amygdala.  On the intracellular level, the NMDA and AMPA receptor sites 
in conjunction with an inhibition of GABA inhibitory systems have been 
named as relevant to emotional learning.  On a molecular level it is 
being discovered that calcium dependant enzymes, such as CaMKII, are 
important for the mediation of long_term potentiation of emotionally 
relevant stimuli.  There are many research ventures that are trying to 
discover the basis for this type of learning.  As the technology 
involved in research methodology improves, the understanding of the 
systems and molecular basis for emotional learning will become clear.




REFERENCES

Armony, J.L., Servan-Schreiber, D., Cohen, J. D., LeDoux, J. E., 
(1997). Computational modeling of emotion: explorations through the 
anatomy and physiology of fear conditioning. Trends in Cognitive 
Sciences. Vol. 1 (1).

Farb, C., Aoki, C., Milner, T., Kaneko, T., LeDoux, J., (1992). 
Glutamate immunoreactive terminals in the lateral amygdaloid nucleus: a 
possible substrate for emotional memory.  Brain Research.  V.593, 145-
158.

Ledoux, J., (1993) Emotional memory systems in the brain.  
Behavioral Brain Research.  V.58, 69-79.

Maren, S., (1999).  Long_term potentiation in the amygdala: a 
mechanism for emotional learning and memory.  Trends in Neuroscience.  
V.22, 561-567. 
	
	
	  

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