ingestive behavior...•psych 100: –a relatively long lasting change in behavior or potential...
TRANSCRIPT
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Ingestive Behavior
I. Physiological Regulatory Mechanisms
II. Drinking and Thirst
III. Eating and Metabolism
IV. Signals that Start a Meal
V. Signals that Stop a Meal
VI. Brain Areas Involved in Hunger & Satiety
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I. Physiological Regulatory Mechanisms
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3
Figure 11.1
An example of a regulatory system
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I. Physiological Regulatory Mechanisms
• Negative feedback: the effect of an action serves to stop that action
• Satiety: the feeling of fullness
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II. Drinking and Thirst
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Terminology
• Solutes: the substances that are dissolved in a solution
• Examples of solutes: ions such as sodium, chloride, & potassium dissolved in water
• Force of diffusion: molecules moving from areas of high concentration to areas of low concentration
• Molecules: ions and the water itself
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Interstitial Fluid Intracellular Fluid
Hypertonic: Solutes more concentrated
relative to outside
Which way will the water move?
Hypotonic: Solutes less concentrated
relative to outside
Hypotonic: Solutes less concentrated
relative to inside
Hypertonic: Solutes more concentrated
relative to inside
Isotonic: Solutes equally concentrated
inside & out
Isotonic: Solutes equally concentrated
inside & out
H2O
H2O
H2O
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Two fluid areas that our homeostatic system pays very close attention to:
1. Intracellular fluid
2. Intravascular fluid
• It’s possible for these fluid levels to vary independently, so it turns out that there are two types of thirst…
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Two Types of Thirst
• Osmometric/Osmotic thirst: loss of fluid from the cells
• Causes:
– Evaporation
– Eating a salty meal (pure osmometric thrist)
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Two Types of Thirst
• Volumetric/Hypovolemic thirst: loss of fluid from the blood
• Causes
– Evaporation
– Bleeding (pure volumetric thirst)
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Osmometric Thirst & Osmoreceptors near the AV3V
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Volumetric Thirst
• Baroreceptors in 1.) the blood vessels of the kidneys and 2.) the atria of the heart
• When they aren’t stretched out (due to lack of fluid in the blood), they send signals indicating that water levels are low
• One of these signals takes the form of a hormone…
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Volumetric Thirst
• … and the other signal takes the form of a “hard wired” neural connection
• Atrial baroreceptors send signals about lack of fluid up into the brain via neural connections
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III. Eating and Metabolism
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The Fasting Phase
• Defined: No nutrients in the digestive system (stomach and intestines are empty)
• Key hormones regulated by the pancreas: glucagon high and insulin low
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The Fasting Phase
• Short Term Store: the liver
• Stored energy: glycogen (animal starch)
• Energy: glucose (for CNS)
• Glucagon converts glycogen to glucose
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The Fasting Phase
• Long Term Store: adipose tissue (fat cells)
• Stored energy: triglycerides
• Energy: fatty acids (for PNS) & glycerol/glycerine (which can be converted into glucose for CNS)
• Glucagon converts triglycerides into fatty acids and glycerol/glycerine
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The Absorptive Phase
• Defined: Nutrients are available from the digestive system
• Key hormones regulated by the pancreas: glucagon low and insulin high
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The Absorptive Phase
• High levels of insulin allow all cells (CNS & PNS) to use glucose
• Insulin converts excess glucose into glycogen in the liver
• Insulin converts excess energy into triglycerides in the adipose tissue
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IV. Signals that Start a Meal
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Social/Environmental Factors that Effect Hunger
• Number of people present
• Time of day
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Physiological Factors that Affect Hunger
• Peripheral Nervous System (PNS)
– Lack of sugar (glucoprivation)
– Lack of fat (lipoprivation)
– Detected by the liver
• Central Nervous System (CNS)
– Lack of sugar (glucoprivation)
– Detected by neurons in area postrema and the nucleus of the solitary tract (NST)
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V. Signals that Stop a Meal
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Short-Term Satiety Mechanisms (act over the course of minutes)
• Head factors
– how food looks, smells, tastes, & feels
• Stomach
– distention and nutrient receptor activation
• Intestines
– Duodeenum & CCK
• Liver
• Insulin
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Long-Term Satiety Mechanisms (act over the course of days/weeks/months)
• Adipose tissue (fat cells) & the hormone leptin
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ob/ob mouse lacks leptin
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People sometimes lack leptin too (1 in 2,000)
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V. Brain Areas Involved in Hunger & Satiety
• Question: where in the brain would you expect hunger to be regulated?
• Answer: the hypothalamus
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Hunger in the Brain
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Ghrelin fluctuation during the day
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Satiety in the Brain: The Ventromedial Hypothalamus (VMH)
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Satiety in the Brain
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Learning & Memory
I. The Nature of Learning
II. Learning and Synaptic Plasticity
III. Perceptual Learning
IV. Stimulus-Response Learning
V. Relational Learning
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I. The Nature of Learning
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Definitions of Learning
• Psych 100:
– A relatively long lasting change in behavior or potential behavior that is due to experience.
• This Class:
– The process by which experience changes our nervous system and ultimately our behavior.
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Types of Learning
• Perceptual Learning • Stimulus-Response Learning
– Classical Conditioning – Operant Conditioning
• Motor Learning (special case of Stimulus-Response Learning?)
• Relational Learning – Spatial Learning – Episodic Memory – Observational Learning
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The Hebb Rule
• A synapse will be strengthened (more easily activated and/or produce larger depolarizations) if…
1. a synapse is repeatedly active when…
2. the post-synaptic neuron is firing.
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II. Learning & Synaptic Plasticity
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Long-Term Potentiation (LTP)
• Defined: A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activation of that input.
• In other words: if you use a synapse a lot in a short period of time, it will strengthen.
• Though found to occur in numerous brain areas, LTP was initially demonstrated in the hippocampal formation
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LTP Version 1.0
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LTP Version 2.0
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LTP Version 3.0: Associative LTP
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65
Figure 12.13
Chemistry of Long-term Potentiation. These chemical reactions appear to be triggered by the entry of an adequate amount of
calcium into the dendritic spine.
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Long Term Depression
• A long-term decrease in the excitability of a neuron to a particular synaptic input caused by stimulation of the terminal button while the postsynaptic membrane is hyperpolarized or weakly stimulated
• In other words, if you don’t use a synapse, with will weaken (“use it or lose it”)
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III. Perceptual Learning
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A
B C
A
B C
A
B C
A
B D
A B
C
Object-Memory Task
(inferior temporal lobe
more active)
Spatial-Memory Task
(parietal lobe more
active)
Target
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IV. Stimulus-Response Learning
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Debiec et al. (2002)
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Reinforcement Pathways
• Mesolimbic System: projects from the midbrain to parts of the limbic system, including the nucleus accumbens (NA)
• Mesocortical System: projects from the midbrain to the frontal lobes
• Both rich in dopamine • Originally thought dopamine release in the NA
was responsible for the experience of pleasure • Now many consider dopamine release to more
about desire, craving or wanting
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V. Relational Learning
• Amnesias
• Retrograde Amnesia: loss of ability to recall old memories
• Anterograde Amnesia: loss of ability to form new memories
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Anterograde Amnesia & the Case of H.M.
• Had hippocampi removed in an attempt to reduce seizures
• Surgery did reduce seizures but afterward, it appeared H.M. could form no new memories
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Initial Conclusions Reached
• Is the hippocampus the location of long term memory (LTM)?
• NO
• Is the hippocampus the location of short term memory (STM)?
• NO
• Is the hippocampus involved in moving new memories from STM to LTM?
• YES
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Revised Conclusions Reached
• Is the hippocampus the location of long term memory (LTM)?
• NO
• Is the hippocampus the location of short term memory (STM)?
• NO
• Is the hippocampus involved in moving new CONSCIOUS memories from STM to LTM?
• YES
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Anterograde Amnesia Redefined
• A failure of declarative/conscious/relational memory
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Spatial Memory & LTP
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Language & Communication
I. Speech Production
II. Speech Comprehension
III. Aphasias in the Deaf
IV. Reading Disorders
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I. Speech Production
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Broca & Patient Tan
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I. Speech Production
• Broca’s Area
• Broca’s Aphasia
– Anomia
– Articulation difficulties
– Agrammatism
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Broca’s Aphasia & Agrammatism
Though they primarily have production problems, people with Broca’s aphasia can also show minor comprehension problems.
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II. Speech Comprehension
• Wernicke’s Area
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Wernicke’s Aphasia
• Core symptoms:
• Fluent but meaningless speech
• Poor speech comprehension
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Two Aspects of Speech Comprehension
• Recognition: knowing that a sound you’ve heard is part of language you know
• Comprehension: understanding what a particular sound means
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A Recognition Deficit: Pure Word Deafness
• Poor auditory speech comprehension (reading is fine)
• Speech production is normal
• Produced by damage to Wernicke’s area
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A Comprehension Problem: Transcortical Sensory Aphasia
• Poor speech comprehension
• Fluent but meaningless speech
• BUT can copy speech they hear without understanding it (what differentiates it from Wernicke’s aphasia)
• Produced by damage to the posterior language area
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Putting It All Together
• Damage to what area would produce speech recognition problems?
• Wernicke’s area
• Damage to what area would produce speech comprehension problems?
• Posterior language area
• If you damage both of these areas, you get…
• Wernicke’s aphasia
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The Dictionary Analogy
• The way the brain accomplishes language can be likened to a dictionary
• Word entries (by sound):
• Wernicke’s Area
• Definitions of the Words:
• All over the cortex
• Evidence that this is so…
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The Dictionary Analogy
• Autotopagnosia/Autopagnosia
• The inability to name one’s one body parts
• Most common: finger agnosia
• Produced with damage to the left parietal lobe
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The Dictionary Analogy
• Anomic Aphasia
• Difficulty finding and using particular words
• Often use circumlocutions (they talk around the word they can’t remember)
• Lose nouns with damage to the temporal or parietal lobes
• Lose verbs with damage to… (anyone?)
• Frontal lobes
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Conduction Aphasia
• What differentiates TSA from Wernicke’s aphasia
• People with TSA can copy or parrot speech
• Suggests there is a copy circuit in the brain: the arcuate fasiculus
• Direct connection from Wernicke’s area to Broca’s area.
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Conduction Aphasia
• Own speech is fluent and meaningful (no problems)
• Show good comprehension much of the time
• BUT, they can’t copy what they don’t understand
• Struggle with nonsense speech sounds and “repeat after me” scenarios
• Produced by damage to the arcuate fasiculus
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III. Aphasias in the Deaf
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IV. Reading Disorders
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Alexia
• Defined: the complete inability to read
• Produced by brain damage
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The
The
The
The
cat
cat
cat
cat
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Dyslexia
• Defined: difficulty in reading
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Types of Reading
• Phonological reading (phonetic coding): recognizing and sounding out letter combinations
• Whole word reading: recognizing the entire word and pronouncing it from memory
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Aoccdrnig to a rscheearch at Cmabrigde Uinervtisy, it deosn't mttaer in waht oredr the ltteers in a wrod are, the olny iprmoetnt tihng is taht the frist and lsat ltteer be at the rghit pclae. The rset can be a toatl mses and you can sitll raed it wouthit porbelm. Tihs is bcuseae the huamn mnid deos not raed ervey lteter by istlef, but the wrod as a wlohe.
Can you read this?
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Acquired Dyslexias
• Surface Dyslexia
• Defined: difficulty reading via the whole word method
• Consider these words: may, disk, moon
• Now consider these words: cough, through, rough, bough
• Damage to visual word-form area (VWFA) in the left temporal lobe
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Damage to VWFA (left temporal lobe)
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Acquired Dyslexias
• Phonological Dyslexia
• Defined: difficulty reading phonetically
• Difficulty sounding out unfamiliar words
• If vocabulary is developed prior to damage, they can often read OK relying on whole word reading
• Damage to left temporparietal complex
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Damage to left temporoparietal complex
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Acquired Dyslexias
• Direct Dyslexia
• Can read but can no longer understand what they are reading
• Damage to left frontal and temporal lobes
• Some people reading via whole word method, others reading via phonetic reading
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Developmental Dyslexia
• Difficulty reading that appears to have a biological/genetic basis
• People with developmental dyslexia struggle with reading from the very beginning
• 5%-10% of the population of this country
• Concordance rates for MZ twins between 84% and 100%
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Developmental Dyslexia
• Poor phonological awareness
• Example: have a hard time hearing the three “duh”-”aw”- “n” sounds in the word Don
• Biological difference: magnocellular layer of the LGN doesn’t have uniformly large cells
• Magnocellular layer known to be involved in the processing of motion
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Developmental Dyslexia
• The handy man versus the plumber
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Developmental Dyslexia
• Other related behaviors
• Often have balance/coordination issues
• Hit major developmental milestones later (walking, riding a bike, etc…)
• Often don’t develop strong handedness
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V5/Occipitotemporal Complex