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CHAPTER 14 Feeling, Smelling, andTasting 281
Tasting with the Brain
Each taste bud has ve to ten taste receptor cells (Figure14-5 shows only three),
with most taste buds having at least one of each of the ve basic receptor types.
Taste information projects to the rostral part of the nucleus of the solitary tract
(nucleus tractus solitarius; NTS) in the medulla. Two nerves carry this information:
»
The chorda tympani (a branch of the facial nerve) carries signals mostly from
fungiform papillae in the anterior two
-thirds of the tongue.
»
The glossopharyngeal nerve sends information from foliate and circumvallate
papillae, and a few rearward fungiform papillae in the posterior third of the
tongue.
These sections explain how taste information is transmitted from the NTS to the
thalamus, other brain areas, and the primary taste cortex.
Projecting taste to the thalamus
The NTS projects to the thalamus, but also to the reticular formation, hypothala-
mus, and parasympathetic preganglionic neurons. Neurons projecting from the
NST of the medulla mediate gag and cough reexes. Figure14-6 shows the pro-
jections for taste.
SUPERTASTERS: SUPER SENSITIVE TO TASTE
Some people are far more sensitive to taste than others and are called supertasters.
About one third of women but only 10 percent to 20 percent of men are supertasters,
and they’re less common in Caucasians than in other ethnic groups. Besides having
lower taste thresholds and better taste discrimination generally, supertasters have a
heightened taste response to bitterness. This makes some supertasters picky eaters,
but many picky eaters aren’t supertasters.
The supertaster ability is associated with several factors:
•
An increased number of fungiform papillae
•
The TAS2R38 gene that codes for bitter taste
•
The ability to taste substances called PROP (propylthiouracil) and PTC (phenylthio-
carbamide) that have no taste to non-supertasters
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282 PART 3 Understanding Perception and Cognition
The taste region of the thalamus to which the NST projects is the ventropostero-
medial thalamus (VPM). Reciprocal connections between this thalamic area and
the cortical processing areas for taste mediate conscious awareness of the taste
sensation. Lesions in the VPM cause ageusia, the loss of the sense of taste.
Discriminating taste in the cortex
The VPM thalamus projects to the insula and frontal operculum cortex (refer to
Figure14-6), both of which are primary cortical taste areas. The insular lobe is
hidden behind the temporal lobe at the junction of the parietal, frontal, and tem-
poral lobes. The opercular cortex (operculum means “lid”) is located just above
the insula. The insula and operculum cortex are evolutionarily old and participate
in cortical circuits that are also aected by olfaction and vision. These cortical
areas are involved in satiety (feeling full), pain, and some homeostasis functions.
Food texture, which is communicated by mechanoreceptors while chewing, is an
important component of eating. Even people who congenitally lack both taste and
smell still enjoy eating. Careful attention to food texture is part of the fare of all
high-quality restaurants.
Combining taste and smell for avor
The insula and opercular cortices project to the orbitofrontal cortex where some
neurons receive inputs from the olfactory system as well. Neurons receiving both
taste and smell information mediate the perception of avor, the complex percep-
tion derived from a combination of taste and smell. Much of the sense of taste is
FIGURE14-6:
Central
projections
for taste.
© John Wiley & Sons, Inc.
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CHAPTER 14 Feeling, Smelling, andTasting 283
derived from odors emitted while chewing food that reach the nasal mucosa. Most
people are unable to identify the tastes of chocolate or coee with their noses
blocked, for example.
The insula and opercular cortices also project to the amygdala, which mediates
memory for emotionally salient experiences. The amygdala projects back to the
orbitofrontal cortex. This pathway allows you to associate the sight, smell, and
taste of foods with your experience before and after ingesting them.
Losing taste through injuries
Although some people are born without a sense of taste (ageusia), total lack of the
taste sense is very rare. A very poor sense of taste (hypogeusia) is more common.
This may arise from damage to the olfactory mucosa, which is an anosmia leading
to hypogeusia because of the involvement of smell with taste. Hypogeusia is rare
as a congenital condition, but it may occur as a result of disease or injury to the
chorda tympani nerve. Temporary hypogeusia often occurs during some cancer
chemotherapies. Aging tends to reduce sensitivity to bitter tastes, which explains
why children nd some vegetables strongly bitter that are much less so to their
parents.
Feeling full
Eating is partly controlled by satiety mechanisms that modulate the sense of taste.
An adaption mechanism in the taste receptors themselves and a central brain
mechanism mediate satiety:
»
Sensory-specic satiety: This occurs in taste and olfactory receptors
themselves. It tends to suppress your appetite specically for the taste of
what you’re consuming, acting on a fast time scale.
»
Alliesthesia: This name refers to the central satiety mechanism. As you eat
and grow full, what you’re eating loses its desirability because of the brain
mechanism that indicates you’re getting full. The mechanism for this is seen in
the reduced ring of orbitofrontal taste/smell neurons to the specic odor of
a food after you’ve eaten a lot of it.
Several gastrointestinal hormones regulate appetite via their actions on the brain.
These hormones mediate hunger and satiety that aren’t linked to specic foods.
Gut-derived hormones include ghrelin, insulin, CCK, pancreatic polypeptide (PP),
and peptide YY (PYY). They stimulate specic areas of the hypothalamus and
brainstem and modify sensations transmitted by the vagus nerve to the NTS.The
hypothalamus and brainstem control appetite via interactions with brain centers
such as the amygdala and cortex.
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284 PART 3 Understanding Perception and Cognition
Glucagon-like peptide 1 (Glp-1) receptor agonists are an exciting topic in obesity
research and modern culture. Developed to treat Type 2 diabetes, Glp-1 agonists
reduce food intake, appetite, and hunger,and promote fullness and satiety with
the result of promoting weight loss. These drugs slow the transit of food from the
stomach into the small intestine, making you feel full faster and longer.In addi-
tion, Glp-1 works on receptors in the brain, with receptors located in the PVN,
dorsomedial and arcuate hypothalamic nuclei, NTS and area postrema. The race is
on to identify the mechanism of Glp-1 induced appetite suppression and develop
oral delivery for these drugs. Intriguingly, Glp-1 agonists seem to have benecial
eects on other organs including the heart and brain, with potential neuroprotec-
tive eects.
Monitoring Body Functions with
Internal Chemoreceptors
Olfaction and taste involve chemoreception, the detection of substances that enter
the body. The body has receptors that detect concentrations of many important
substances within it, such as glucose and CO
2
. Many of these receptors are in the
hypothalamus where the blood-brain barrier is weak, allowing them to access
neuronal receptors there. Other internal chemical detection sites include the sub-
fornical organ and the organum vasculosum of the lamina terminalis. These are
called circumventricular organs where neurons can sense chemicals from both
blood and CSF.
Examples of substances detected by internal chemoreceptors include osmolarity
and sodium concentration for uid balance. A host of other receptors exist for
peptide hormones, such as endothelin and relaxin, angiotensin, steroids, gluco-
corticoids, and monoamine neurotransmitters noradrenaline, dopamine, and
serotonin (5-hydroxytryptamine).
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CHAPTER 15 Learning to Remember 285
Chapter15
Learning to Remember
T
he good thing about making mistakes is the opportunity to learn from them.
Throughout a person’s lifetime their nervous system can learn through
experiences and store experiences as memories to maintain and improve
behaviors. Learning and memory inuence thinking, planning, and decision
making.
For millennia, philosophers and scientists have wondered about memory. Some of
the mysteries about memory processes began to be solved in the last half of the
20th century. It’s now known that memory involves multiple brain systems that
function at dierent time scales and dier by the type of information being stored
and retrieved. In addition, research has identied actual cellular and molecular
mechanisms underlying memory. Memory can be improved with practice and
repetition, while loss of neurons in memory regions can lead to amnesia or a slow
decline in memory as seen with dementia. This chapter delves into the world of
learning and memory.
IN THIS CHAPTER
»
Adapting your behaviors according to
environment
»
Separating implicit and declarative
memory
»
Keeping memories for the short and
long term
»
Looking at brain structures for
learning and memory
»
Uncovering synaptic mechanisms
underlying memory
»
Improving your memory
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286 PART 3 Understanding Perception and Cognition
Dening Learning and Memory
Memory can be dened in dierent ways. Exposure to the environment, experi-
ences, or even just thinking can cause changes in the nervous system. Meanwhile,
learning is dened as the acquisition of skills or knowledge. Memory is the expres-
sion of what you’ve acquired, or a behavioral change caused by an experience.
Memory involves the encoding, storage, and recall of information and past expe-
riences. Here we incorporate both behavioral and mechanistic views to describe
learning and memory.
During development, the brain undergoes massive changes in neurons, synapses,
and circuits as babies and young children interact with the environment, and their
sensory, motor, and cognitive systems are built and rened (Chapter2 discusses
developmental processes). Here we keep our focus on learning and memory after
the early developmental stages. Many of the same mechanisms and genes are
involved in both.
ARRIVING AT MEMORY MODELS
WITH THE HELP OF H.M.
Some of the most important studies for understanding human memory were con-
ducted for many years on one individual, Henry Molaison, a subject known widely
before his death as patient H.M.After a bicycle accident at age 9, H.M. developed epi-
lepsy as an adolescent, with intractable seizures, (that didn’t respond to medications). In
1953 when H.M. was in his late 20s, he underwent surgery to treat his epilepsy. The sur-
geon removed both hippocampi and surrounding cortical areas in the medial temporal
lobe, which is where H.M.’s seizures were originating before spreading to other brain
areas.
After the surgery, H.M.’s seizures were better controlled, but he was left with a devastat-
ing decit. He was completely unable to permanently store new information, in a decit
called anterograde amnesia. Although H.M. couldn’t form new memories, he could recall
many previously stored memories and his short-term memory was intact. In addition,
H.M. could still improve his performance on motor tasks such as mirror writing, even
though he had no memory of doing or practicing these tasks. Science owes a great of
gratitude to H.M. for his willingness to be tested for so many years and for donating his
brain to science.
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CHAPTER 15 Learning to Remember 287
The studies of Henry Molaison (see the nearby sidebar) were revolutionary because
they showed that memory can be classied along two attributes:
»
The time course of storage
»
The characteristic of the information stored
The studies demonstrated that the hippocampus is required for laying down
memories of facts, words, and events. However, the hippocampus isn’t the site of
permanent memory storage and isn’t needed for short-term memory or motor
memories.
Human memory systems involve information processing and storage with
distinct time courses. This idea was rst described by the psychologist Henry
James in 1890, who wrote about primary and secondary memory. In 1968, Richard
Atkinson and Richard Shirin published the multistore memory model based on
this concept (see Figure15-1). The model proposes three separate memory stores.
Each store diers in the way information is processed, how much information can
be stored, and for how long. Information is transferred between the stores in a
sequence, so subsequent stores depend on earlier stores.
In the model, information enters into the sensory memory register for a very brief
time. If you focus attention on specic sensory information, it can be transferred
to short-term memory for a minute or less. If information in the short-term store
is important, it can be transferred or encoded into a long-term memory store. We
describe the features of these stores in the section “Focusing on Declarative
Memory” later in the chapter.
FIGURE15-1:
A memory
taxonomy.
© John Wiley & Sons, Inc.
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288 PART 3 Understanding Perception and Cognition
The Atkinson Shirin model was groundbreaking, but it didn’t incorporate stud-
ies showing hippocampal independent long-term memory. In 1976 Dr. John
Anderson divided long-term memory into declarative (explicit) and procedural
(implicit) memory (see Figure15-1).
Examining Implicit (Nondeclarative)
Memory
The rst type of memory we describe is implicit or nondeclarative memory that
can be acquired consciously or unconsciously and typically aects behavior.
Implicit memory includes a group of learning process for particular perceptual,
motor and cognitive skills that are unconsciously retrieved.
Procedural memory is a form of implicit memory used every day. It lets you per-
form actions such as writing, tying a shoelace, or riding a bike, even if you aren’t
consciously thinking about it. Procedural memory involves the cerebellum and
basal ganglia. Other implicit memory types include non-associative and associa-
tive learning and priming.
Starting with sensation: Sensory memory
In the multi-store model, the process by which a stimulus from the environment
becomes a memory starts with the initial neural image registered by your sensory
system, called sensory memory. If you see someone waving a sparkler against a
dark sky on a Fourth of July evening, you can, for a split second, see the light fol-
lowing the moving sparkler. This is called iconic memory. Other sensory modali-
ties, including sound, touch, smell, and taste are registered in sensory memory.
Sensory memory is closely linked to the perceptual domain in which it was ini-
tially registered, such as seeing the sparkler. The image that you see in your
mind’s eye fades very rapidly, within seconds. That’s because of the decrease in
activity of the neurons in the sensory system after the stimulus stops. Sensory
neurons and systems can also change their responses with constant or repeated
stimulation.
Getting used to habituation
Most sensory receptors adapt to a constant or continually repeated stimulus. For
example, when you rst sit down in a chair, you’re aware of your body touching
the chair seat and back, but after a few minutes, your awareness of the chair fades.
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CHAPTER 15 Learning to Remember 289
Habituation is a type of non-associative learning dened as a decrease in a behav-
ioral response that results from repeated stimulation and that doesn’t involve
sensory adaptation or motor fatigue.
Habituation allows you to be sensitive to changes in the environment and not dis-
tracted by a constant stimulus that’s no longer important. Habituation can occur
at lower levels of sensory processing or in higher brain areas.
High-level habituation can also be reversed, which is then called dishabituation.
Dishabituation typically results from the eect of another novel stimulus that
reverses some of the habituation to the rst, habituated stimulus.
Responding to sensitization
Sometimes your brain can learn to react to a stimulus very quickly. When you’re
outside on July 4th, you may not notice the rst few mosquitoes that land on and
touch your legs. But after one bite, you become hypersensitive to mosquitoes and
swat at them quickly, before they bite. This is called sensitization.
Habituation and sensitization both occur unconsciously, although the behavior
they provoke can be realized consciously. They’re types of non-associative learning:
a change in behavior due to repetition of specic stimuli, and they occur in all
animals.
Classical conditioning
Associative learning involves behavioral change caused by associating temporal
relationships between stimuli and responses or motor behavior. Classical
conditioning is a type of associative learning famously studied by Ivan Pavlov in his
dog experiments. The experiment depends on that fact that a known pleasant or
noxious stimulus, called the unconditioned stimulus (US), produces an appropriate
response (approach or avoidance), called the unconditioned response (UR). For
Pavlov, the presentation (sight and smell) of food (US) produced salivation in
dogs (UR).
A NOBEL PRIZE FOR MEMORY RESEARCH
Non-associative learning was studied extensively by Eric Kandel and colleagues with the
gill withdrawal response in the mollusk Aplysia californica. They demonstrated that syn-
aptic and neuronal plasticity underlie the changes in behavioral responses. Dr. Kandel
was awarded a Nobel prize for his memory research.
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290 PART 3 Understanding Perception and Cognition
In the experiment, a neutral stimulus such as a tone or light is presented about the
same time as the US (or slightly earlier). This new, initially neutral stimulus is
called the conditioned stimulus (CS). Pavlov paired a tone (CS) with the presentation
of food.
The US always produces the UR.When the CS is repeatedly paired with the US, it
also comes to predict the UR. After this conditioning, the CS elicits the same
response that the US elicited, and the response is now called the conditioned
response (CR).
Classical conditioning occurs naturally throughout our lives. If you answer cell-
phone calls while driving and you often almost get in accidents, you learn (hope-
fully) to associate answering phone calls with negative consequences and begin to
avoid this behavior.
Fear conditioning
The amygdala enables you to acquire and retain lasting memories of emotional
experiences, including fear. Some fears are innate, but fear can also be learned.
Learned fear prepares you for behavioral, autonomic, and endocrine responses
when a potentially dangerous situation is present.
Implicit emotional memoryhas been assessed in rodent experiments using Pav-
lovian fear conditioning. The presentation of an initially neutral stimulus such as
a tone (CS) is followed by an aversive or mildly painful stimulus, such as electrical
stimulation (US) that results in behavioral fear responses such as freezing (UR).
Following repetitions of this pairing, the tone (CS) will elicit behavioral fear
responses (CR-conditioned fear response).
Fear conditioning is rapid and persistent, occurs in all animals tested, and involves
similar neural circuits in all vertebrates. Thus fear conditioning is useful for
investigating mechanisms of implicit memory. In the amygdala, fear conditioning
leads to modication of synaptic transmission through synaptic plasticity, which
we discuss in section “Looking at synaptic plasticity in implicit memory” later in
this chapter.
Operant conditioning
Operant conditioning is associative learning that involves the pairing of rewards or
punishments with some antecedent behavior. Edward Thorndike rst described it,
and B.F. Skinner coined the term. Operant conditioning is based on spontaneous
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