Download Psychology312-2_000 - Northwestern University

Useful information:
 The readings are from 2 text
books: 1) Carlson “Physiology of
Behavior” latest (10th) edition
(2009) and 2) Andreassi
“Psychophysiology” 5th edition
(2007).
 Other readings and most class
notes are on my web site:
To get to web site….
 Google J Peter Rosenfeld
 On list that GOOGLE brings up , you’ll see
Rosenfeld Lab Home Page
Find out about current research in the Rosenfeld lab.Get
information on
groups.psych.northwestern.edu/rosenfeld/home.html
*Click it. You’ll see:

Note the buttons
 Clicking “publications” or
“classes” gets you where you
need to be for this course.
If you took 312-1…..
 Then clicking “classes” then “312-2”
and “Publications” gets you to all nontext assigned readings. That’s all you
need to know.
 Otherwise, you may want to
click”classes”, then “312-1” and go to
bottom of page for powerpoint
presentations, and review the one
called, “2. EEG,ERPs, & relation to single
neuronal activity.” and check out the first
29 slides.
If, from “Classes,” you go to the
312-2 site…
….You’ll see the texts, the syllabus,
lists of papers, chapters and
powerpoint presentations
(including this very presentation!)
which go with this course. Let’s do
for real…
Topic 1: Continuation of Neural
Coding from 312-1
 You may recall that we previously
subdivided this topic into 3
subtopics:
 1) Sensory coding, 2) Motor coding,
3) Coding of Psychological Events.
 We saw that the brain represents
sensory events in terms of neuronal
firing patterns. Remember the
following?
Or what about this?
These are neural representations
of somatic sensory sensations…
 Of course you read in 312-1 about
neuronal representation of visual
and auditory events. These are
sensory codes. There are also codes
for motor events, that is, firing
patterns in the motor cortex and
elsewhere that correlate with
muscle action leading to body
movements. These are motor codes.
Now for the almost unmanageably complex
and largely unknown neural representations
of “pure” psychological events….
 ….such as cognitions associated
with emotions(love, hate, sexual
arousal, perceptions), memories
(real and false), learning (classicalautomatic and instrumental),
deceptions (altruistic and selfserving), and so on… This giant topic
started out with the title, “Neural
Coding of Behavior” in the 1950s.
We now refer to this effort also as
“Neural Correlates of Behavior.”
 Note that word, “Behavior…”
(rather than “cognition” which is a
much broader and more sensible
term). That’s because the 1950s
was the heyday at most
universities of the Psychological
Movement known as
“Behaviorism” that dominated
academic Psychology.
In case you forgot, here is the
Wikipedia definition:
 Behaviorism (or behaviourism), also called the learning
perspective (where any physical action is a behavior), is a
philosophy of psychology based on the proposition that all
things that organisms do—including acting, thinking and
feeling—can and should be regarded as behaviors.[1] The
behaviorist school of thought maintains that behaviors as
such can be described scientifically without recourse either
to internal physiological events or to hypothetical
constructs such as the mind.[2] Behaviorism comprises the
position that all theories should have observational
correlates but that there are no philosophical differences
between publicly observable processes (such as actions)
and privately observable processes (such as thinking and
feeling).[3]
Now this was crazy, and has been largely
replaced by Cognitive Psychology…
 But a convenient thing about
behaviorism was its simplification of
psychological things to observable
behavior (omitting invisible thoughts
and such). So if you wanted to study
the neural substrates of learning, all
you had to do was study the “neural
correlates of observable behavior,”
which is where that term came from.
So the typical experiment in Neural
Correlates of Behavior went like this:
 OK, you are interested in learning,
so pick a standard learning protocol
(paradigm): Training animals like
cats to run down a maze to get food.
1. Get them hungry via food
deprivation. 2. Put them at the ‘start’
end with the food many feet away at
the ‘goal’. 3. Define ‘learning’ as the
state obtained when they can run
through the maze at top speed 5
times in a row with no wrong turns.
How do you study the neural
coding of this process?
 What neural events do you study?
That was easy to answer: There was no
method back in the 50s to record action
potentials from single neurons in freely
moving animals. (It is still not so easy to
do.) So you have to study population
neural activity such as EEG (spontaneous
brain waves) recorded from “chronically
implanted” animals.
From Carlson
OK, so back in 50’s we could record
EEG from freely moving animals…
 But a bigger question is: “From
where do you record the EEG?”
Well this is a learning experiment
so just put the electrodes in the
learning center(s). Where’s that?
There’s the problem: In the 50’s
 We didn’t know what or where the
learning center(s) is (are) and how
they connect or how they interact. If
we knew that we wouldn't need to
do these experiments. So how did
the neural correlators in the 50s
proceed? They used reason. They
reasoned that learning must involve
association (ala John Stuart Mill and
the British Associationists)..
So clearly, one needed record from
places where associations are formed.
 Such as association cortices…2-3
in each side?
The special thing about association
areas are that in those places…
 Different sensory pathways come
together and “talk to each other”
(synapse on the same neurons), so
that one can form an association
between say the tone CS and the
smell of food as in Pavlovian
conditioning—or between bar press
and food in Skinnerian conditioning.
Any other such places? (Class?)
Yes, reticular formation, so we should
put a few electrodes up and down the
r.f. too, maybe 4 or 6? (So far, 16 sites)
 But learning also involves motivation
and reinforcement, so we probably
need 2 more on each side of
hypothalamus. (total now 20.)
 Animals have to see & hear stimuli
and smell food, so in those sensory
systems, figure to add 12 more to
cover thalamus and cortex,
bilaterally. We might be now up to
40! Why the exclamation point?
Well 40 wires coming from the
animal’s recording socket is a lot.
 Rats like this with just 6 wires are not big enough, one
must use a cat or dog. In 50’s these head preamps were
unavailable. One had to use wires
embedded with mercury powder.
Very Heavy. A cat with 40 of them
would “run” down the maze with
head tilted over. But that’s what
they did! (Not terribly natural.)
Besides the question of how many
electrodes and where to put them..
 ..was
the question of what neural
events to analyze from the
ongoing EEG.
 What would a page of ongoing
EEG look like, taken from a live
subject like a cat?
Here’s page of 14 site’s worth in
about 30 sec…
This actually is
unusually pretty
This is more realistic---but I digress
In the old days, there were no FFTs
etc..
 Just amplitude and frequency.
 So the old neural correlators of the
1950s would plot amplitude and
frequency for each of the 40 brain
sites during, say, pre-learning, early
learning, mid-learning, asymptote
learning, and extinction. The results
read like this: “In early learning, the
visual cortex amplitude is high but
the frequency is low, but the …..etc”
It was like the stock market:
“In January, Boeing was up but…
Microsoft was low, but Apple was
up, but GE was middling while
Exxon and ATT were
recovering…etc, etc…. In Spring,
however, Boeing and Exxon
crashed, while Microsoft and GE
reached new historic highs….etc
etc…”
If every lab got the same results,
no matter how complex, well OK.
 But in 1961, there were 2 well-known
review papers that summarized the
neural correlates literature: One:
High nervous functions: brain functions
and learning ER John - Annual Review of
Physiology,
 The other:
Electrophysiological contributions to the
neural basis of learning F Morrell Physiological Reviews, 1961
These papers both summarized
over a thousand studies….
 They both should have ended the
neural correlates literature,
because both essentially noted
the same thing, namely, that no
labs replicated themselves, let
alone others!!!
 The literature did taper off,
producing 2 reactions, and 2 new
literatures:
The reactions:
 1) The Operant Controlled Neural Event
(“OCNE”) approach: Operant
Conditioning of ERP components.
 2) The Cognitive Psychophysiology
literature: The less radical and longer
lasting carefully controlled scientific
study of ERP indicators of psychological
events.
 (We’ll start with the first reaction now)
The “OCNE” approach began with a
paper* outlining this first reaction. The
paper involved 3 things:
 1. A systematic critique of the
neural correlates literature.
 2. The rather ambitious program
outlined in reaction (Note title):
3. An empirical description and
demonstration of the method.
*The paper was by Fox & Rudell (1968)
Science, and is on 312-2 web page, article 9
1. The critique:
 A) F&R cited the replicability issues as noted
by John and Morrell in the ‘61 reviews.
 B) problem of choosing electrode sites and
neural parameters for study.
 C) Correlation approach: let animals do their
own thing and see what neural events from
what sites correlate. That’s not controlled
science.
 D) Time base issues: Learning takes days vs.
EEG, ERPs, action potentials that are
measured in milliseconds. One cannot make
laws connecting things measured in such
different units. (The “reduction problem”—see
Bergmann, “The Philosophy of Science.” 1966
The OCNE approach was supposed
to solve all these problems…
 We’ll see if it did (and how) later,
after we consider OCNE’s empirical
approach, which went something
like this: “The old neural correlators
wanted to see systematic & reliable
brain wave changes by training
behavior and looking for brain wave
correlates. Why bother? If you want
see a brain wave change, TRAIN IT
DIRECTLY.”
That is, specify a brain wave variable from
some brain site, and operantly condition it
like a bar press, by rewarding its occurence.
 The following figure, from the F&R
‘68 paper, shows 2 sets of
superimposed photic erps (visual
eps) elicited by a light flash,
recorded from chronically
installed electrodes in a freely
moving Cat’s visual area 19
(tertiary visual cortex). (Why
there? It’s convenient on top.)
The cats had been operated on and
electrodes as well as a milk tube
…had been installed. They were
recovered and each one was run
in a chamber (former hollowed out
‘fridge) as the strobe lights
flashed every 3 seconds, evoking
the eps.
The 2 sets of waves shown next are
during baseline (A) and training (B)
within one day:
The area between the lines had been
pre-selected as the critical area, i.e.,
 F&R had decided that the cat was to
lower the amplitude of the EP
amplitude between the lines. (They
saw that in the naïve cat, this was a
variable amplitude.) Every time the
cat did so, a computer (6’x3’x3’)
detected this and caused a relay to
close, delivering ~ 1cc milk through
the tube implanted that ended in the
roof of the hungry cat’s mouth.
So F & R decided to treat a deviant ERP
amplitude like a bar press and give the
cat a reward for making them.
 These EP amplitudes varied
within a bell curve, and F&R
rewarded deviant samples in
the blue tail at left. They
chose rare but occasionally
occurring samples with a finite
probability (.16) of occurrence.
Of course the cats were able to do
it, increasing negativity:
Of course the naysayers said, “well, it’s
simply the effect of milk on the EP…”
 i.e., the non-contingent or non-
associative or unconditional effect
of reinforcement. It isn’t learning.
 There was evidence. Others had
shown that food or shock affects
ERPs. I did myself with
Routtenberg. But then how do you
explain the following?
Now the cats are making the
criterion segment go UP. they are
increasing positivity
The naysayers can’t have it both
ways….
 If the unconditional/non-
associative effect of milk is
making wave go up then the down
effects are learning
 If the unconditional/nonassociative effect of milk is
making wave go down then the up
effects are learning
So we do have the learning of
something going on here…
 But what, exactly? In other words, the
naysayers were not done complaining. Before
we get there, however, what did Fox say was
the importance of the demonstration?
 1. OCNE solves problem of choosing
electrode sites and neural parameters for
study. Well that’s sort of true. You pre-specify
what brain wave variable you train, and from
where you record it. In this first
demonstration, convenience and common
sense guided the choice….(continued)
In other words,
 As noted, site was chosen for surgical
convenience and familiarity to Fox, who
knew that at the segment chosen (170190 ms post stimulus), the EP amplitude
was typically variable, high to low
values. He intuited that the variability
was tied to some behavioral state which
he hoped could be operantly conditioned.
(The tricky, slippery part is identifying
that state. We never have. We still don’t
know the significance of the effect.)
Fox also concluded
 The neural correlate approach was not
controlled science. The OCNE
approach makes the neural event the
independent variable, not the
dependent variable.
 This was bogus. It is the reinforcement
contingency which is directly
manipulated as the independent
variable. As just noted, we still don’t
know its behavioral correlate.
He also stated:
 OCNE solves the time base
incompatibility problem that learning
takes days, as opposed to EEG, ERPs,
action potentials that are measured in
milliseconds.
 Not exactly. The OCNE method simply
calls an EP segment a behavior but
since it is already neural, it is force on
to a compatible time base. It’s not a
behavior like a CR paw lift is.
There are some incontrovertible
benefits of OCNE that Fox didn’t
mention (& maybe didn’t appreciate!):
 1. Replication was not a problem:
Hundreds of cats, rats, humans have
been trained to self-control all sorts of
ERPs as we’ll see.
 2. Obvious clinical applications? (If you
change a visual EP, do you change
vision? We’ll come back to this.
 3. OCNE uniquely can work out neural
code/mechanisms of voluntary
movement in an unrestrained animal (vs.
Mountcastle’s curarized,sedated cats).
This too is shown later…(continued)…
A final, most important benefit:
 4. Operant neural conditioning offers a
method of testing the generality of
putative laws of learning, (of which there
are precious few known). This because it
may be a new response system. (Laws
Theories that account for phenomena
like learning.)
 A fellow named John Garcia showed
how critical novel response systems are
in his now classical taste aversion
conditioning studies in dogs.
From the 40s to the 60s, the king of
learning theory was not Skinner (who
opposed theories), but Kenneth Spence
 …the head of Psychology at Iowa
(one reason I went there).
 Spence had found what he regarded
as a law of classical conditioning (a
learning protocol), stating that the
ideal CS-UCS interval was about ½
second. This was developed with
human blink conditioning, rat eye-lid
conditioning, and rabbit nictitating
membrane conditioning in rabbits.
Here was the typical supportive
datum:
Then Garcia showed that if you
exposed a dog to a food….
…followed immediately by xirradiation, 3-5 hours later he got
terribly sick and vomited the day
away (radiation sickness).
Thereafter, the dog would never
touch that particular food again.
Other dogs could be similarly
trained to avoid different foods.
Which are CS, UCS, UCR, CR ?
Well here is a classically
conditioned avoidance response…
 Involving a 3-5 hour CS-UCS
interval. Not = .5 sec.
 Garcia showed that the response
system determined the optimal
CS-UCS interval, and that
Spence’s putative learning law
was not general. Physiological
explanations based on .5sec
would be wrong.
OCNE could also be a novel
response system …
 …with which to test putative
operant conditioning laws
(magnitude of reinforcement
effect, acquisition/extinction law,
etc.)
 BUT…first you have to show that
operantly conditioned learning
laws were not trivially mediated
by known motor systems.