Introductory
Psychology 85-102 Exam I Review Notes The following things would be good
knowledge to have. Be able to identify each topic and feel comfortable writing
a short essay on it. Your notes and the book have everything you need to know.
This is only a review or guide. It is intended to help you organize your notes
and study for the exam and is in no way a substitue for your attending class
and taking a good set of notes for yourself.
I. Sleep and Dreaming (Ch. 6, Ch. 15-pp606-615.
+ Related readings) (Note: pages
Why do we sleep? Is it biologically necessary in some restorative sense, or
merely a useful-adaptive behavior (see your notes). There are many
arguments/pieces of experimental evidence that bear on this issue (strength of
the motivation, correlation with some psychological disorders, the fact that we
make up some lost sleep (or lost dream time), hallucinations when deprived,
wide disparity in amount of sleep, animal sleep deprivation studies, people who
sleep very little, and people who thru training learn to sleep much less). A
consensus (sort of) is that sleep is a biologically adaptive behavior--ie. it
is sleep itself that is useful, rather than allowing some function to occur
within sleep that is "life-necessary". This doesn't deny that there
are some metabolic and possibly memory enhancement (consolidation) processes
that are enhanced during sleep, as well as a few studies showing deleterious
effects of sleep loss.
Theories of Dreaming:
Freud (know about the whole "wish fulfillment" expression of id
desires idea; latent dream, manifest dream, remembered dream); his theory was
all about mental conflict. The result is 2 forces in dreaming: one trying to
express and one trying to repress; the dream is a compromise between these two
forces (see your notes and ch. 15 pages) and functions, according to his
theory, to prevent the repressed impulses from disturbing sleep. Dreamwork
(symbolization, etc.) converts latent or "real" dream into manifest
dream that you actually dream, and together with a second mechanism,
forgetting, helps maintain the "repression".
Aserinsky, Dement, & Kleitman: discovered REM; found they occurred with
dreaming; stages of REM regular periodicity of sleep cycles and of dreaming.
How does this work on dream regularity and also that of Hall on dream series
and Cartwright on the emotional content of dreams collected in dream series
support or modify the Freudian theory?
Physiology: Hobson-->initially, dream only a physiological event, random
neural activity--no function whatsoever (very radical stand!); Has now shifted
to the view that dreams do have content that exhibits regularity in subject
shifts and in other aspects as well; i.e. they do have content and even meaning.
The view is
that they are generated by waves that start in the brainstem and travel up to
the visual cortex--thus causing visual hallucinations, and easier/greater
spreading of activation from ideas to other ideas--accounting for the jumps of
subject/time/place that occur in dreams. His Activation-Synthesis hypothesis
states that while the dream generation process might be more or less random or
non-meaningful, the higher brain centers impose meaning on the activity, with
the result that the dream can be randomly generated but still meaningful!
Others say we dream to purge unwanted neural connections; some say it's for a
sorting function (integrate important days events into memory and discard the unimportant
ones) or simply to make permanent (consolidate) important learnings from the
day. This latter view of consolidating or making permanent the days' learning
of important information has received support from recent studies of the
pattern of neural activity during dreams mimicking the patterns found during
initial learning in studies with rats learning mazes. There are also
neuroimagining studies of dreaming that are broadly consistent with Freud���s
view viz a viz emotional content of dreams���see your notes.
How could you put all of this together/use it, as for example by the Senoi and
other dream focused cultures?
II. Methodology: Ch. 1
The material on scientific method and data representation was mainly covered in
your testbook and/or in recitation and a reasonable expectation is that an
overview of the material (your having read it and understood the major points)
is the most that will be expected. Specific issues that are of importance are:
III. Biology of Behavior (Ch3 + Related
readings & Film)
The basic model here is a mechanistic
(be aware of mechanist-vitalist debate and the respective positions of each
side). The view is of a small set of physical forces that give rise to
electrical and chemical (concentration) processes that can be assembled into
increasingly complex behavior.
Simple behaviors: kinesis (undirected movement), taxis (directed movement as in
phototaxis of the moth), simple reflex (unlearned behavior --stimulus--sensory
nerve--interneurons (sometimes) --motor nerve--effector (usually
muscle)--response). Also Braightenberg's artificial examples: "vehicles"
that exhibit behavior based on very simple mechanisms are a nice analogy to the
argument that behavior can emerge from mechanistic processes.
Cephalization is a principle that was talked about a lot. What is it? What
implication does it have for us? (increased effect of learning on behavior,
longer development (due to large head); increased flexibility/adaptability in
behavior--> for example, humans can learn to do more than frogs, such as
talk, think, etc). The question: "Why is the brain in the head?" is
part of this.
The neuron. Major parts (dendrites, axons, etc) Resting potential established
by chemicals (ions)? These ions are located, inside and outside the neuron.
Remember: inside of neuron negative with respect to the outside. Mostly
potassium (K+) inside, mostly sodium (Na+) outside. Large anions (A-) are
inside and can't get out; they outnumber the K+ (that's why the inside is
negative--because some of the K+ can leak out). Also, chloride ions (Cl-) are
mostly outside but some leak in so it is outnumbered outside by the positive
Na+. Know the forces that act on the ions (answer: concentration forces or
gradients and electrical forces; see your notes) Action potential: Na+ rushes
in to cause rising phase; K+ then leaves to cause fall. AP goes from -70 or -75
to around +35 to +40 millivolts; threshold is around -55 millivolts. Resting
potential is around -70 to -75 millivolts. Be able to draw an action potential
and label all of the major parts. How fast does the electrical signal move?
(answer: about 40 meters per second (m/sec.) Helmholtz's discovery in the frog
leg experiment, but can vary from less than 1 m/sec.. to more than 120
m/sec.--varies widely across neurons & species). How long does action
potential take? --about a millisecond or slightly less.
The synapse & neurotransmitters. Excitatory and inhibitory synapses; know
about some of the main neurotransmitters (such 'as acetylcholine, dopamine,
etc. ). Remember that virtually all drug effects are occurring at the level of
the synapse. What is a reflex and how does it work? Who came up with the
concept of the reflex and why is it important to the idea of mechanism or the
mechanist position in the mechanist-vitalist debate?
Brain: cephalization again; dichotomies in the nervous system: Central nervous
system (brain and spinal cord) and Peripheral nervous system (everything
outside CNS); also, sensory (inputs to the spinal cord and up to brain) and motor
(signals to muscles so action can occur).
Know the trip from the spinal cord to the cerebral cortex (see your notes):
hindbrain (brainstem--> biological functions such as heart beat and
breathing), midbrain (includes some control of sleep and waking); forebrain
(includes hypothalamus--brain area controlling endocrine system via the
pituitary, sleep, many motivations); thalamus (a relay station--it relays sensory
inputs to the cortex); limbic system (emotion--> Also formation
of long term memories--> hippocampus); cerebral cortex-->higher mental
functions.
���Organizing principles��� of nervous system: localization of function (see your
notes): Localization is a major organizing principle, but the phrenologists who
started it made a scam out of it, remember? Know where some functions are
localized (for example, vision in the occipital lobe, language in the left
hemisphere, somato- (body) sensory in the parietal lobe, motor control and
consciously directed and higher level thinking in the frontal lobe, etc. How do we know
about localization of function? Begins with Phineas Gage who lost
frontal lobe and with it executive functioning, stimulation of motor cortex results in
movement of limbs, etc. The connections
between brain regions are also important, review how we know this. Also
review the split brain material in the text--a high level example of interesting
localization that is visible under very special (split brain) conditions.
Another principle of the brain: topographic projections (the idea that things
close to each other on the body are close to each other in the brain--remember
the sensory and motor maps. Also remember how it is
distorted--some areas more sensitive than others, require more brain
representation. Understand why sensation can be felt in a removed limb
(neurons from face area will remap to
tissue previous devoted to hand because of their proximity - shows neuroplasticity).
Neurons that formerly carried signals to/from the missing limb can still activate
the brain. Know why pain (particularly clenching) can
be felt in a phantom limb (to function properly the brain needs feedback, when the
hand is missing but brain tissue still devoted
to the hand, the brain will send a signal to clench hand but will not get feedback
from the hand unclench). The mirror box
helps alleviate the pain by providing false visual input that the hand
is unclenching.
Other principles to recall: All or none law for action potentials with result
that size of action potential can't encode intensity of stimulus, it's the
frequency that codes intensity (the idea that the rate at which a neuron fires
codes how intense the stimulation is-- along with recruitment of other neurons
into the set that is firing). ; also, doctrine of specific nerve energies (how
the brain knows about the outside world--> brain knows by way of what area
of the brain is active (or what inputs are active)). Other generalizations are
genetic determination of neural organization vs. many types of adaptiveness/modifiability
of nervous tissue with experience (remapping of neural tissue or
neuroplasticity): both play a role.
IV. Motivation (Ch 12 + Related
readings) We will be covering
mostly motivation material at this time rather than the end of the chapter
material on emotion.
The basic model here is a mechanistic
one of organisms needing to adapt to highly volatile environments by means of
homeostatic mechanisms and motivational systems that have evolved to maintain a
degree of inner constancy in the face of a changing external environment. (It
is also the case that not all motivations fit the basic model (ex. hunger only
partially fits--there are also non-homeostatic influences on our hunger).)
Maslow's hierarchy and what it implies (answer: need to satisfy lower level
needs before progressing: you wouldn't worry about love if you were in a
burning building. (but his critics might say you're likely to run back in and
try to save one you love!) While not totally accurate it expresses an
interesting generalization about there being at least a partial priority
ordering of motivations while recognizing that at any one time, we can be
motivated by multiple motives, even from different levels,
with each exhibiting different strengths.
The basic model: Primary drives are
those that take care of our biological self (things like thirst and hunger).
Their operation can be described as a negative feedback loop. Walter
Cannon/Claud Bernard view of dual output regulation; physiological and
psychological (motivational) as an adaptation to living in a highly variable
environment. Idea of general control systems (the negative feedback systems, including
regulators and setpoints,
that accomplish homeostasis and other forms of control).
Autonomic nervous system (parasympathetic and sympathetic divisions that have
somewhat opposing actions.) Prepares body (long term--energy storage) and short
term--arousal/emergency response (Cannon-flight-fight-fright).)
Motivation has two consequences: makes us move more (increases our activity)
and makes us goal oriented (remember the "cold" example from
class--> what happens when we get cold? remember that cells in the
hypothalamus are temperature sensitive and start the whole process of adjusting
when we get cold by shivering, goose bumps, etc.) Another example of
motivation: dehydration. Hypothalamus, in response to osmotic
pressure changes, causes pituitary to release anti-diuretic
hormone that acts on kidney reabsorbtion of water. Also pressure receptors that
respond to overall fluid volume.
Here the physiology can't solve the problem itself because water will always be
lost. As a result we need to invoke motivation--motivation to go find something
to drink. (Also, if we lose water via sweat, we need to replace both salt &
water.)
Hunger: Role of the hypothalamus in the homeostatic control of hunger.
Two parts (1) lateral hypothalamus (2)
ventromedial hypothalamus. Ventromedial called "satiety center" and
seems to move the set point for how much you'll eat. Rats who have this part
destroyed will over eat, but they are not hungrier than normal rats. Lateral
hypothalamus has feeding centers. Rats won't eat and may actually starve if
this area is destroyed (see notes).
Final example of motivation: Eating (and obesity- a problem of
"plenty" coupled with inactivity (although inactivity might have
genetic component--and remember, correlation doesn't prove causation! Potential causes of
obesity:
1. Fat cell storage hypothesis: Fat is stored in fat cells. Fat cells are
established during infancy and mainly through heredity. In order to satisfy
hunger in the long run you want to fill up the fat cells. If you have more fat
cells, you have more room to fill up with fat and so you're obese. So, if you
diet to lose weight, you reduce the fat in the fat cells. However, there is
pressure to keep the fat cells full (to reach homeostasis), so there is
pressure to eat. The fat cell hypothesis then predicts that diets will fail in
the long run because of this. Probably genetically determined. Leptin release signals
that fat cells are full and reduces hunger/feeding.
2. Glucose/Glycogen: Glucose turned into glycogen for storage; glycogen turned
into glucose for fuel. When the reaction in your body is going from glycogen to
glucose there is hunger; but when it's going the other direction there is no
hunger. This suggests that you become hungry before you need food--and thus have
the energy needed to go look for or capture it! Insulin and the accompanying
movement of glucose between blood and storage role.
3. Stomach distention plays some role in regulating eating. although not the
exclusive role people used to assign to it.
4. Schacter: Externality Hypothesis: Some people are more sensitive to bodily
cues than others. Obese people turn out to be less sensitive to bodily cues
than non-obese people (non-obese people are more "plugged into" their
body). Evidence for this: Lab experiment with an inaccurate clock (found obese
people would eat when it was noon, regardless if they were hungry or not). Also
the liquid diet in hospitals: obese people reduced their caloric intake because
of the change in food; non-obese people were less affected by these external
changes. Finally, the fasting study looking at people fasting during Yom
Kipper. When inside the synagogue without any external cues, non-obese people
found it harder to fast than obese people (because their bodies told them they
were hungry). However, outside the synagogue, obese people had a harder time
because all of the external cues to eat (such as being near normal dinner
time).
5. Another interpretation is that of distinction between restrained and
non-restrained eaters, with the former eating vast amounts once they
"break" through some inhibition of eating--i.e., the first milk shake
might be might be resisted, but once eaten, there will be four more. The idea
is that many people are strongly inclined to look thin in this culture and
spend lots of effort and time trying to control their food intake in various
ways.
6. Other phenomena that have to do with motivation. Olds and Milner: Pleasure
centers (dopamine into the nucleus accumbuns). Rats bar-pressing for electrical
stimulation plus related lab (dopamine) showing chemical mechanism for
pleasure. Also, the Yerkes-Dodson Law--there is a "best" level of
arousal for performance--too low or too high reduces performance. As the task
becomes easier (or equivalently, you become more expert/practiced at it) the
optimum level of performance occurs at higher arousal levels. (The neophyte
actor may get overwhelmed on openng nite but the experienced (and highly
practiced actor) doesn't. Think cockroaches!
A. Audition (Ch. 4): normal range 20-20,000 Hz; transduction from physical signal into neural signal occurs in the ear at the basilar membrane with the membrane vibrating against the hair cells. Know the parts of the ear.
Two theories: Frequency theory states that the frequency of the action potentials tells the actual frequency in the real world (problem is that we could only hear to 1000 Hz since neurons can only fire about 1000 times per second). Place theory says that where on the basilar membrane hair cells are depolarized (firing) tells the frequency of the sound in the real world (different parts of the basilar membrane have different points of maximum vibration and this gets neurally sharpened via lateral inhibition).
Recall that we do not hear all sounds equally well. We are more sensitive to the central range than the low or high ends, and that is the range where most speech sounds occur. This effect decreases with volume (remember the "loudness control" issue in your stereo.)
B. Vision (Ch. 4):(low level stuff); how do you focus on objects? Change the shape of your lens. Recall the responses to looking at something close: (1) lens gets fat (2) eyes converge (point in--cross-eyed), and (3) the pupil gets smaller. Also remember what the eye looks like: where is the lens, pupil, retina? Where does vision (or at least the portion or the process that goes on in the eye) really take place? (answer: retina)
Retina: Rods and Cones: rods very sensitive to light; cones sensitive to color and have high acuity (acuity = how sharp you can see something). These two different systems lead to the duplex theory of vision: The center of the retina (fovea) is good for processing fine detail and color. There are mostly cones here, and each cone connects to one ganglion cell, which connects to one cell in the visual cortex. Because of this the fovea has a very direct path to the brain. Peripheral part of the retina is predominantly rods. Because of this you have poor color vision in the periphery (very few cones), but you are very sensitive to light (consider looking at stars at night--you can not see them if you look directly at them--i.e., with your fovea, but you can see them by looking to the side of them using the more peripheral retina). The peripheral system is however not sharp (low acuity).
Other things to remember about vision: very wide intensity range from candle at 12 miles to noonday sun (ratio of intensities is 1:10,000,000,000,000 ); we can also see things that are very small (1 second of arc, which is 1/60 of 1/60 of 1/360 of a circle--very small indeed--under optimal conditions a bar the thickness of a thumb at 15 miles!).
Vision and the brain: Lateral (or sideways) inhibition: (originally studied with Limulus, the horseshoe crab) when cells that are next to each other inhibit their neighbors; this is good for detecting changes in the visual world (such as borders or edges). The visual system (and other sensory systems as well) seem to be specialized for picking up changes rather than steady state stimulation. Remember the lateral inhibition lab that dealt with this issue and what it showed/how it works. Another important issue is the separation of the visual stream into different brain areas, summarized as a "what" system and a "where" system.
Feature detectors--a major mechanism of bottom up perception: Cortical Simple cells (Hubel & Wiesel): Simple cortical cells respond to bars of light (or darkness) surrounded by darkness (or light; see above) in a particular orientation. They seem to be made up of a line of circularly oriented retinal ganglion cells connecting to a brain cell These are good examples of feature detectors--detectors that "look out" at the world for particular, organized features rather than simply responding to the level of light (or sound). Remember the study by Riggs, Ratliff, Cornsweet & Cornsweet where they presented the word BEER and held it on the same place on the retina (i.e., they did not let the subjects move their eyes to different parts of the word). The word faded along feature lines, e.g., PEEP, BFFR, PEER etc.
C. Perception (Ch. 5): Top down processing: Remember the Muller-Lyer illusion and the top-down explanation for it. One factor involved in that explanation (and in many other aspects of our perceptual processing) is our having a perceptual constancy, in this case, size constancy that helps us interpret the distal stimulus correctly (in most cases). This is the tendency to see a stimulus as having a constant size even though the retinal image varies greatly depending how far away it is. There are other constancies as well. Remember the "we are not from Missouri" argument-that the eye-brain does not take a photograph of the world, but rather actively extracts information from it and reaches a decision about the stimulus. Top-down processes allow this to happen more effectively but this introduces the possibility of the wrong conclusion being reached. Think about top down effects found in the illusion lab. An overiding issue is that in order to perceive the world correctly we have to potentially distort it--top down perception is necessary! Review text treatment of depth perception and the type of cues (binocular and monocular) that accomplish it. Binocular cues includes convergence (the two eyes converge on the same point/object) and monocular include linear perspective (far objects cast a smaller retinal image than near ones--picture railroad tracks running off to the horizon), relative size (also far objects cast a smaller retinal image than near ones), texture gradiant (like the "tunnel" walls in the big monkey/small monkey chase illusion shown in class), and interposition (far objects are usually blocked by near ones). These depth cues also show importance of top-down proc. as we construct a three dimensional image of the world from the two-dimensional image on our retinas.
Good Luck!!!