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[A1CR]

Does CR potentiate drug abuse? The paper below would
possibly have us
believe that the answer is in the affirmative.
Specifically, "food restriction ... increases the reward
magnitude and locomotor-activating effects of abused drugs"?
This quote was
from the below, bottom paper. Did not the previously
described in
http://tinyurl.com/y69k57 find the reverse effect of CR?

According to http://tinyurl.com/y69k57:

Table 1. Effect of food restriction on DAT function in rat
striatum
=====================================
Ad-lib fed Food-restricted
=====================================
http://en.wikipedia.org/wiki/Dopamine#Motivation_and_pleasure
[dopamine]
uptake Km (nmol/l) 121±18 (6) 93±9 (6)
[Dopamine] uptake Vmax (pmol/mg/min) 10.2±1.7 (6) 6.92±1.09
(6)*
Cocaine Ki (nmol/l) 135±68 (4) 146±46 (4)
d-Amphetamine Ki (nmol/l) 206±55 (4) 260±109 (4)
=====================================
Values are mean±SEM for the number of animals as
indicated between
parentheses. Each rat striatum was analyzed in duplicate in
an experiment
that lasted 3 days; each day, 2 food-restricted and 2 ad-lib
fed rats were
examined.
* P = 0.015 compared with ad-lib fed (2-way ANOVA with
factors food
regimen [F(1,18) = 7.199] and experimental day [F(2,18) =
20.37]).
[Km = http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=km ;
Vmax =
http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=vmax ; Ki =
http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=ki ]

Carr KD.
Chronic food restriction: Enhancing effects on drug reward
and striatal cell
signaling.
Physiol Behav. 2006 Oct 31; [Epub ahead of print]
PMID: 17081571

Chronic food restriction (FR) increases behavioral
sensitivity to drugs of
abuse in animal models and is associated with binge eating,
which shares
comorbidity with drug abuse, in clinical populations.
Behavioral,
biochemical and molecular studies conducted in this
laboratory to elucidate
the functional and mechanistic bases of these phenomena are
briefly
reviewed. Results obtained to date indicate that FR
increases the reward
magnitude and locomotor-activating effects of abused drugs,
and direct
dopamine (DA) receptor agonists, as a result of
neuroadaptations rather than
changes in drug disposition. Changes in striatal DA
dynamics, and
postsynaptic cell signaling and gene expression in response
to D-1 DA
receptor stimulation have been observed. Of particular
interest is an
upregulation of NMDA receptor-dependent MAP kinase and CaM
Kinase II
signaling, CREB phosphorylation, and immediate-early and
neuropeptide gene
expression in nucleus accumbens (NAc) which may facilitate
reward-related
learning, but also play a role in the genesis of maladaptive
goal-directed
behaviors. Covariation of altered drug reward sensitivity
with body weight
loss and recovery suggests a triggering role for one of the
endocrine
adiposity hormones. However, neither acute nor chronic
central infusions of
leptin or the melanocortin 3/4 receptor agonist, MTII, have
attenuated
d-amphetamine reward or locomotor activation in FR rats.
Interestingly,
chronic intracerebroventricular leptin infusion in ad
libitum fed (AL) rats
produced a sustained decrease in food intake and body weight
that was
accompanied by a reversible potentiation of rewarding and
locomotor-activating effects of d-amphetamine. This raises
the interesting
possibility that rapid progressive weight loss is sufficient
to increase
behavioral sensitivity to drugs of abuse. Whether weight
loss produced by
leptin infusion produces the same neuroadaptations as
experimenter-imposed
FR, and whether any of the observed neuroadaptations are
necessary for
expression of increased behavioral responsiveness to acute
drug challenge
remain to be investigated.