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 RosenfeldOn list that GOOGLE brings up , you’ll see

Rosenfeld Lab Home PageFind 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 non-text 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 312-1You 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 (classical-automatic and instrumental), deceptions (altruistic and self-serving), 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’sWe 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 variedwithin a bell curve, and F&Rrewarded deviant samples inthe blue tail at left. They chose rare but occasionallyoccurring samples with a finiteprobability (.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 thecriterion 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/non-associative 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 (170-190 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 concludedThe 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 x-

irradiation, 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.