GS: But I think that a lot of these studies are looking at changes in
> the VTA, NAcc, VP etc. as a function of extended exposure to drugs.
> No? I don't think the notion ever was "this is where the learning
> takes place." Indeed, I'm not sure most people regard "addiction" as
> primarily a learning phenomenon. Certainly, learning to
> self-administer a drug puts one on the road, and it is clear that
> (most) drugs of abuse (DOA) function as reinforcers in non-humans, but
> the notion is that the whole motivational system goes out of whack as
> a function of repeated self-administration (and the neurochemistry is
> different when the drug is self-administered - at least with cocaine).
B: No, I think a lot of people are looking at changes in the VTA being
responsible for the learning, they're not putting it forward blatantly
yet, but putting it as questions. For instance "It is not clear,
if these early alterations in VTA function act solely as a transient
to permit downstream changes or play a more significant long term role
the persistent changes that underlie drug-craving"..."Enhanced
glutamatergic transmission at VTA synapses may also produce long-term
changes in the VTA itself that contribute to relapse to drug use."
Both from Annu Rev Physiol. 2004;66:447-75
..what you have quoted here seems to support my interpretation
of the way the field is viewed. The term "craving" clearly indicates a
motivational function, and relapse is thought to occur because this
alleged motivational cause simply becomes too powerful to resist. But,
of course, the trouble with "craving" is that "it" doesn't exist. It
is NOT the same as a gene or a receptor.
But, anyway, my point was not to defend this notion strenuously but,
rather, to suggest that we are far from having some complete picture
of what is happening when a food-reinforced (or drug-reinforced)
response is acquired. And it is because *we* cling to old explanatory
> GS: Hmmm...yes, I suppose that recording from cells while an animal is
> behaving is worthwhile, but the problems with much of behavioral
> neuroscience, IMO, is largely its conceptual structure. My guess is
> that "goal cells" will eventually be seen as a silly notion, as will
> representation (but not "mapping") and a host of other things borrowed
> from our folk-psychology vernacular. No offense intended.
B: Well it all gets rather philosophical doesn't it. I mean, science
never worked like how philosophers would like it to, and it never
Research asking the 'wrong' questions should still come up with useful
GS: What you have just said IS the naïve philosophical view, and it is
precisely what doesn't work. Progress is not the result of mindless
application of some simplistic rules about testing hypotheses if the
concepts underlying the theories are stupid, then the theories are a
dead-end and painstaking analysis of the concepts can reveal this. But
this can only happen if conceptual analysis is afforded the importance
]so in my mind, even if someone is experimenting on the brain
with completely a whack hypothesis, the results shouldn't care what he
GS: Obviously, I disagree.
B: Meanwhile, whether or not "goal cells" make any sense, or whether
should be talking about "goal arrays" or "goal recursive neuronal
circuitry", if you find a correlation between two things (cell spiking
and behavior) whether its causative or not, it is going to tell you
GS: Only once it is placed in some particular context. And it is
likely that when it is done, the meaning of the fact will not be the
same as the original mentalistic meaning. Mentalism breaks up the
world into parts in the wrong way fueled by centuries of
BilZ0r <BilZ0r at TAKETHISOUThotmail.com> wrote in message news:<Xns950D87456D5FCBilZ0rhotmailcom at 18.104.22.168>...
>gmsizemore2 at yahoo.com (Glen M. Sizemore) wrote in