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Self administration cues as signals (Experiments (1 (Design --> …
Self administration cues as signals
Experiments
1
results
Design
-->
pretraining
: rats sweetened water 7*30mins each
---> teams balanced by how much the drank, then one of the team became SA the other Yoked (within each triad randomly assigned across the groups A YE AND YC
--> intragastric cannule in all rats
-->
SA-E rat licked sweet ethanol (increased by day 3, 6, 12%):
-->
lickometer detect
and administer same amount of sweetened sweetened ethanol through intragastric cannule to
Y-E rats
-->
Y-C received only sweetened water
3 groups
--> 42 rats
--> 14 per group
Y- E
--> yoked ethanol
Y- C
--> yoked control
SA-E
--> self administration ethanol
ataxia measure
--> tilting plane
--> board they can elevate at one end
--> angle of elevation where mouse slipped = correlated with how strong the ataxia
--> measured before and after each trial (three post trial every 5 minutes)
**--> impairment score = previous slip angle - smallest angle (after probs)
--> the more ataxia the smaller the angle needed for slipping
2
--> same as 1 but this time all intragastic cannule administration
--> cause different route of administration in experiment 1
--> they estimated how much SA-E rats had (some might have spilled)
Design
--> same as before
--> SA rat now also sugar water
--> but when driving sugar water ethanol administered intragastrically
20 sessions
conditioned response testing
5 or 6
and 15 or 16
contingency testing one day after last tolerance trial
3 phases
tolerance development
--> normal stuff like experiment 1
--> Sa rats less ataxia than YE rats
conditioned response test
--> day 5 or 6
and
--> 15 or 16
basically tolerance has developed
—> then the yonly inject sweet water and see who does better on the plane its usper duper easy actually :3!!
--> SA rats = higher hypertaxia (ability to stay on tilting plane longer) than YE rats
--> YE rats = higher hypertaxia than YC rats
contigency reversal =
SA rats become yoked and vice versa
—> because SA rats now no self sdminster cues there shoul dbe less tolerance cause no cue triggers the compensatory response :3 !!
--> Former SA rats (now YE) = higher ataxia than before because internal cues of self administration missing for first time!
--> YE rats tendency to be less ataxia but NO significance !!
3
--> because taste might have influenced
--> because calories of alcohol might have influenced
rats similar design just now with a lever press
and control group = saline production
and administration = intravenous
results
--> SAh = no ataxia but continued hypertaxia trial 3 and 4 statistically significant from YH and YS
--> YH first trial ataxia, second trial onward no difference to YS
Why ?
external cues can trigger conditioned compensatory response
So is the mere act of self administering/taking the drug oneself also a cue that can trigger the conditioned compensatory response ?
what is a conditioned compensatory response ?
if you take a drug certain cues are present internal or external (CS)
The effect the drug has on your body serves as an unconditioned response (UR)
--> this drug effect leads to a reaction in the body that tries to negate this drug induced changes in your body (compensatory response) --> reason why drug effects don't last forever!
after she time when you've take the drug just the cues that are present at the time you're taking the drug (internal / external) are enough to trigger the now conditioned response of starting this compensatory action --> now called conditioned compensatory response! (because even in the absence of the drug itself it already tries to counteract the effect of the drug
in this case its about internal cues (those that lead to self administration )
How?
Yoked design
shows difference between a rat that knew it would receive the drug because it was self administering --> which could serve as a cue for conditioned compensatory response
and rats that didn't know when they were to receive the drug thus had no external / internal cues when they would receive the drug
to make sure it was compensatory response
--> because there are other theories out there for example that focus on the biphasic effect of a drug
self administered drug rats that had full control thus knew when they would receive the drug if giving them the drug (not self administered) they would show greater ataxia thus no compensatory response could dampen the effect of alcohol / heroin
presenting the self administration cues (the lever) to the self administration rats but no actual drug, would lead to
hypertaxia (ability to stay in tilting plane longer!!)
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