Lecture 16: The Amygdala Complex
Key brain area for learning, motivation and emotion
On the other hand, it is a tricky brain area to discuss: (1) it is a very complex brain region; it is not
(probably) a single unitary functional piece of tissue (e.g. hippocampus and striatum), (2)
furthermore, behavioural neuroscience still has a long way to go in understanding what the
amygdala does
For a long time fear has been proposed as a main role of the amygdala
Actually, we understand a lot about one particular function of the amygdala – Pavlovian Fear
Condition – learning to be afraid of a neutral stimulus that signals an unpleasant stimulus(shock).
But there are multiple lines of evidence to suggest that the amygdala does more than just
supporting Pavlovian Fear Conditioning.
But what the amygdala does beyond that – what the amygdala’s role is as a whole – we still have a
lot to learn about this
In that sense, it is a tricky brain area to give a comprehensive and definitive overview on because,
with the exception of Pavlovian Fear conditioning, we seem to know disconnected facts here and
there that are difficult to draw into a coherent picture
Can tell you what we do know about the amygdala
Amygdala gross anatomy (early lesion and patient studies)
• In the human brain, the amygdala lies anterior to the hippocampus, underneath the
temporal lobes
• Smooth, round nucleus (almond-shape)
• In the rodent brain, the amygdala also lies at the end of the hippocampus but more
ventrally - not so much a round shape
• The amygdala is a complex structure, not one homogenous nucleus, but several nuclei
lying together – some are interconnected with each other, some of them are actually
quite separate from each other
• The amygdala is made up of 13 different structures, that can be classified into three sub-
groups:
o Basolateral nuclei
o Cortical nuclei
o Centro-medial nuclei
• Other structures are the intercalated cell masses and the amygdaloid-hippocampal area
,What were the first studies that gave us some idea of what the amygdala does?
Early lesion studies
(Brown and Schafer, 1888) (Kluver and Bucy, 1938) – both of these studies chopped off (temporal
lobectomy) the anterior parts of the temporal lobe to varying degrees, in Rhesus monkeys. The
psychological symptoms seen following this were:
• Marked changes in emotional behaviour – particularly hypoemotionality (consistent
symptom)
§ Flat affect – do not see any heightened reactions anymore, whether
positive (excitement) or negative (fear), nor engagement with stimuli
o On the other hand, you also see hypersexuality (atypical sexual behaviours)–
animals will make sexual advances to inappropriate conspecifics, humans,
inanimate objects
o Animals become very tame – essentially, a part of the flattened emotional
response – one of the emotions missing is that they are no longer aggressive
towards humans (Rhesus monkeys are normally very aggressive animals, difficult
to train)
• Some symptoms that seem to indicate that they can no longer respond appropriately to
particular objects and understand what they are
o One of the common symptoms is hyper-orality (oral exploration) and they will
also eat it à weight gain; they will eat anything that is even remotely palatable
even when they should be sated
o Visual defects – visual agnosia (a failure to recognise what a particular object
may be or what it might mean)
§ Psychic blindness - inability to recognise objects visually
§ For example, can no longer teach a simple conditioning between an
object and a reward
You could think of these visual defects in being linked to the emotional defects in the sense that they
are not producing the correct emotional response to an object anymore (they can’t make that
memory)
Or you could think of it as a memory defect in and of itself – remember, in primates, the temporal
number has a bunch of neocortex that is closely functionally linked to the hippocampus and involved
in processing memories – probably the anterior tip of the temporal lobe is the key area for
semantic memory
This visual agnosia could be thought of as a primate version of semantic memory deficits
(Weiskrantz, 1956) – did same thing; bilateral temporal pole/amygdaloid complex lesion à He
emphasised two things - results in tameness/emotional blunting and hyperphagia (eating)
• Suggested the effects of the amygdalectomy to make it difficult for positive or negative
reinforcing stimuli to become established or to be recognised as such (valence??)
, What happens to humans that damage their amygdalae?
(David Amaral – Living without Amygdala, 1992) – includes summaries of patients who have lost
their amygdala due to seizures or trauma
Adult acquired amygdala lesions (bilateral removal of amygdalae, psychosurgery) generally show a
much milder phenotype than the full blown Kluver-Bucy syndrome observed in macaques
If you look at the overall pattern of outcomes when you lose the amygdala in this way; two things
jump out in both of these two cases:
• Language problems Commented [IM304]: An aspect that is hard to characterise in
animal lesion models
• Loss of word meaning – the ability to coherently produce and understand words (In his
opinion, you could consider this a problem with semantic memory, caused by damage to
that anterior tip of the neocortex, close to the amygdala) Commented [IM305]: oWe are talking big brain lesions
here, thus you can have effects spreading from one brain
region to another – even if they have little functional
Other symptoms seen in adult human amygdala lesions include hyperorality (and hyperphagia?), similarities – physical anatomical closeness in the brain
inappropriate sexual advances - also ‘her affect was characterised by passivity and compliance’ means they can get damaged at the same time
Conclusion: In all of these cases we can see that damaged to the anterior tip of the temporal lobe
and amygdala in human patients can lead to symptoms reminiscent of Kluver-Bucy syndrome as
observed in macaque monkeys.
However, bear in mind that these are all traumatic injuries (i.e. involving generalised seizures or
traffic accidents) and the damage may not be specific to the amygdala.
Electrical stimulation studies in awake patients
Another way of looking at amygdala functions in humans is, rather than looking at cases where it
had been damaged, you can try to stimulate it (i.e. during awake surgeries with medical justification
to put electrodes in the human brain, stimulating the amygdala – can ask the patient what they feel
or what effect it has)
(Mullan and Penfield, reproduced from Gloor, 1997) First done by Wilder Penfield in the 1950s –
demonstrated that stimulation in/around temporal lobes in humans induces illusion of fear and Commented [IM306]: Stimulation in amygdala or adjacent
temporal lobes
nervousness (anxiety)
• This was one of the first pieces of evidence to propose the idea that the amygdala aids in
producing the sensation of fear and other negative emotions – this would explain a large
part of the Kluver-Bucy syndrome (i.e. animals without a sense of fear will show a flattened
emotional affect à tameness; no fear = lack of aggressiveness)
But more recent studies have broadened the potential function of the amygdala in that sense –
confirm and extend upon these earlier findings: both positive and negative feeling can be evoked
upon amygdala stimulation
Key brain area for learning, motivation and emotion
On the other hand, it is a tricky brain area to discuss: (1) it is a very complex brain region; it is not
(probably) a single unitary functional piece of tissue (e.g. hippocampus and striatum), (2)
furthermore, behavioural neuroscience still has a long way to go in understanding what the
amygdala does
For a long time fear has been proposed as a main role of the amygdala
Actually, we understand a lot about one particular function of the amygdala – Pavlovian Fear
Condition – learning to be afraid of a neutral stimulus that signals an unpleasant stimulus(shock).
But there are multiple lines of evidence to suggest that the amygdala does more than just
supporting Pavlovian Fear Conditioning.
But what the amygdala does beyond that – what the amygdala’s role is as a whole – we still have a
lot to learn about this
In that sense, it is a tricky brain area to give a comprehensive and definitive overview on because,
with the exception of Pavlovian Fear conditioning, we seem to know disconnected facts here and
there that are difficult to draw into a coherent picture
Can tell you what we do know about the amygdala
Amygdala gross anatomy (early lesion and patient studies)
• In the human brain, the amygdala lies anterior to the hippocampus, underneath the
temporal lobes
• Smooth, round nucleus (almond-shape)
• In the rodent brain, the amygdala also lies at the end of the hippocampus but more
ventrally - not so much a round shape
• The amygdala is a complex structure, not one homogenous nucleus, but several nuclei
lying together – some are interconnected with each other, some of them are actually
quite separate from each other
• The amygdala is made up of 13 different structures, that can be classified into three sub-
groups:
o Basolateral nuclei
o Cortical nuclei
o Centro-medial nuclei
• Other structures are the intercalated cell masses and the amygdaloid-hippocampal area
,What were the first studies that gave us some idea of what the amygdala does?
Early lesion studies
(Brown and Schafer, 1888) (Kluver and Bucy, 1938) – both of these studies chopped off (temporal
lobectomy) the anterior parts of the temporal lobe to varying degrees, in Rhesus monkeys. The
psychological symptoms seen following this were:
• Marked changes in emotional behaviour – particularly hypoemotionality (consistent
symptom)
§ Flat affect – do not see any heightened reactions anymore, whether
positive (excitement) or negative (fear), nor engagement with stimuli
o On the other hand, you also see hypersexuality (atypical sexual behaviours)–
animals will make sexual advances to inappropriate conspecifics, humans,
inanimate objects
o Animals become very tame – essentially, a part of the flattened emotional
response – one of the emotions missing is that they are no longer aggressive
towards humans (Rhesus monkeys are normally very aggressive animals, difficult
to train)
• Some symptoms that seem to indicate that they can no longer respond appropriately to
particular objects and understand what they are
o One of the common symptoms is hyper-orality (oral exploration) and they will
also eat it à weight gain; they will eat anything that is even remotely palatable
even when they should be sated
o Visual defects – visual agnosia (a failure to recognise what a particular object
may be or what it might mean)
§ Psychic blindness - inability to recognise objects visually
§ For example, can no longer teach a simple conditioning between an
object and a reward
You could think of these visual defects in being linked to the emotional defects in the sense that they
are not producing the correct emotional response to an object anymore (they can’t make that
memory)
Or you could think of it as a memory defect in and of itself – remember, in primates, the temporal
number has a bunch of neocortex that is closely functionally linked to the hippocampus and involved
in processing memories – probably the anterior tip of the temporal lobe is the key area for
semantic memory
This visual agnosia could be thought of as a primate version of semantic memory deficits
(Weiskrantz, 1956) – did same thing; bilateral temporal pole/amygdaloid complex lesion à He
emphasised two things - results in tameness/emotional blunting and hyperphagia (eating)
• Suggested the effects of the amygdalectomy to make it difficult for positive or negative
reinforcing stimuli to become established or to be recognised as such (valence??)
, What happens to humans that damage their amygdalae?
(David Amaral – Living without Amygdala, 1992) – includes summaries of patients who have lost
their amygdala due to seizures or trauma
Adult acquired amygdala lesions (bilateral removal of amygdalae, psychosurgery) generally show a
much milder phenotype than the full blown Kluver-Bucy syndrome observed in macaques
If you look at the overall pattern of outcomes when you lose the amygdala in this way; two things
jump out in both of these two cases:
• Language problems Commented [IM304]: An aspect that is hard to characterise in
animal lesion models
• Loss of word meaning – the ability to coherently produce and understand words (In his
opinion, you could consider this a problem with semantic memory, caused by damage to
that anterior tip of the neocortex, close to the amygdala) Commented [IM305]: oWe are talking big brain lesions
here, thus you can have effects spreading from one brain
region to another – even if they have little functional
Other symptoms seen in adult human amygdala lesions include hyperorality (and hyperphagia?), similarities – physical anatomical closeness in the brain
inappropriate sexual advances - also ‘her affect was characterised by passivity and compliance’ means they can get damaged at the same time
Conclusion: In all of these cases we can see that damaged to the anterior tip of the temporal lobe
and amygdala in human patients can lead to symptoms reminiscent of Kluver-Bucy syndrome as
observed in macaque monkeys.
However, bear in mind that these are all traumatic injuries (i.e. involving generalised seizures or
traffic accidents) and the damage may not be specific to the amygdala.
Electrical stimulation studies in awake patients
Another way of looking at amygdala functions in humans is, rather than looking at cases where it
had been damaged, you can try to stimulate it (i.e. during awake surgeries with medical justification
to put electrodes in the human brain, stimulating the amygdala – can ask the patient what they feel
or what effect it has)
(Mullan and Penfield, reproduced from Gloor, 1997) First done by Wilder Penfield in the 1950s –
demonstrated that stimulation in/around temporal lobes in humans induces illusion of fear and Commented [IM306]: Stimulation in amygdala or adjacent
temporal lobes
nervousness (anxiety)
• This was one of the first pieces of evidence to propose the idea that the amygdala aids in
producing the sensation of fear and other negative emotions – this would explain a large
part of the Kluver-Bucy syndrome (i.e. animals without a sense of fear will show a flattened
emotional affect à tameness; no fear = lack of aggressiveness)
But more recent studies have broadened the potential function of the amygdala in that sense –
confirm and extend upon these earlier findings: both positive and negative feeling can be evoked
upon amygdala stimulation
