Place cells and addictive drugs

Glen M. Sizemore gmsizemore2 at yahoo.com
Wed Jun 16 18:16:35 EST 2004


B: So what do you guys think of an experiment like this:
You have a set-up much like a conditioned place preference box, a two 
compartment case, where a rat can walk from one comparment to the
other.
You then record from several hippocampal place cells, and find ones
that
corispond roughly to the the either of the 'rooms'.
Then you give the rat maybe, a microinfusion of methampehtamine into
the
hippocampus, or electrically stimulate the ventral tegmental
dopaminergic
neurons, only when the rat is in the right room.
So behaviourally, we would expect to see the rat spend its time in the
conditioned room, the right room, because that is where it recieves
the
reward. But your also recording from the place cells. Now will you see
an
increased rate of firing of the place cell?

GS: Do you really think it is that simple?

B: My idea basically stemed from the fact that people always look at 
synaptic placsticity in the VTA or the Nucleus Accumbens when they are
interested in drugs of abuse..

GS: Do they look for "plasticity?" People, no doubt look at the NAcc
after exposure to self-administered drugs (or drugs administered
response-independently), but you almost seem to be implying that it is
this site where "learning takes place." I think that the role of the
NAcc is thought to be more of the place where "reinforcement signals"
are generated. Certainly, though, changes in the NAcc after extended
exposure to the drug might be thought to reflect the change from
"recreational use" to "addiction."

B:  I don't really know why, I wouldn't have 
thought palsticity there would have explained addiction very well. I 
always thought that plasticity in the cortex would have far more 
interesting, i.e. when the reward coincides with a stimuli, then the 
cortical cells which code/interpret/are activated by that stimuli will
strengthen there synapses with other downstream neurons, increases the
attentional weighting of the stimuli. But it would be very hard to
find a
neuron which is strongly activated by a particular stimuli (I assume).
So
I thought, place cells seem easy enough to find...

GS: Perhaps the NAcc, and other parts of the basal ganglia and VTA
etc., produce a diffuse release of neurotransmitter into the PFC,
association cortices etc., and this produces LTP in the synapses
between sensory related neurons and motor related neurons. Here, the
"plasticity" could be "in the cortex," in the sense that that it is
here that a crucial step is occurring, and changes in NAcc function
(another kind of plasticity) would drive the "cortex system." I'm not
really advocating this, I'm just pointing out the ambiguity of your
question.

B:  I don't know, this stuff is really quite neurosciency for me, and
a bit
out of my neuropharmacology background, but I don't want to get stuck 
working in cultured neurons my whole life, and I'm thinking about a
PhD
or something...

GS: Fortunately or unfortunately, if you can drive a 20-electrode
gizmo into a rat's head and find orderly relations between behavior
and physiology, you can pretty much make up any silly story you want
to, and it'll be called "science."


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