Neuroscience and CR

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Hi All,

There are four papers (1-4) below on the neuroscience of CR. Three (1-3) seemed

to

be of sufficient potential interest to include the abstracts from Medline not

pdf-available reports.

The first paper (1) reported that the brain region affecting food intake, energy

balance and opioid addiction are not involved in the exploration levels of the

mice

or their body temperatures. In light of CRed animals appearing to increase

their

exercise in what may motivated by food-seeking intention and having decreased

body

temperature, the results seem to differentiate the neurophysiology of CR.

The second paper (2) reported that rats that were CRed look forward to eating

tasty

food more than the fully fed rats, although both tend to overeat the tasty food.

When the food was regular food, only CRed rats again looked forward to eating.

The third paper (3) apparently reported on the attributes of binge eating with

respect to how tasty foods were affects food intake. The roll of opioid

pathways in

the binge eating are manifest in the animals not needing the food when fed and

are

simply seeking the opioid system-related reward of food. CRed animals were used

to

induce the bingeing behavior. Therefore, the paper may examine what can go

wrong in

yo-yo type dieting, with bingeing causing the weight gain?

Paper (4) is an apparent neuroanatomical examination of CR-related behavior.

1. Weitemier AZ, Ryabinin AE.

Lesions of the Edinger-Westphal nucleus alter food and water consumption.

Behav Neurosci. 2005 Oct;119(5):1235-43.

PMID: 16300431

The Edinger-Westphal nucleus (EW) produces several neuropeptides, including

urocortin 1 and cocaine-amphetamine-regulated transcript, which regulate

feeding,

energy balance, and anxiety. Additionally, the EW projects to feeding and

anxiety-regulatory brain areas. The authors tested the effect of lesions of the

EW

on the consumption of food, water and flavored solutions, metabolic indices, and

exploratory behavior on the elevated plus maze in male C57BL/6J mice. EW lesion

significantly reduced basal and deprivation-induced food and fluid consumption

compared with sham and placement controls, but it did not alter behavior on the

elevated plus maze. EW lesion had no effect on indices of basal metabolic

activity,

including plasma glucose level and body temperature. These effects suggest that

the

peptidergic neurons of the EW regulate food consumption.

1. Barbano MF, Cador M.

Various aspects of feeding behavior can be partially dissociated in the rat by

the

incentive properties of food and the physiological state.

Behav Neurosci. 2005 Oct;119(5):1244-53.

PMID: 16300432

The authors investigated the role of food incentive properties and homeostatic

state

on the motivational, anticipatory, and consummatory aspects of feeding.

Behavioral

tests were carried out on food-sated and food-restricted rats that were

presented

with 2 kinds of food differing in their palatability level. Both food-sated and

food-restricted rats consumed large quantities and were highly motivated when

presented with very palatable food. In contrast, only food-restricted rats

developed

anticipatory responses, regardless of the kind of food presented. These data

suggest

that food incentive properties play a key role in the control of consummatory

and

motivational components of feeding but seem less involved in the regulation of

anticipatory behavior.

3. Boggiano MM, Chandler PC, Viana JB, Oswald KD, Maldonado CR, Wauford PK.

Combined dieting and stress evoke exaggerated responses to opioids in

binge-eating rats.

Behav Neurosci. 2005 Oct;119(5):1207-14.

PMID: 16300427

The authors developed an animal model of binge eating where history of caloric

restriction with footshock stress (R + S) causes rats to consume twice the

normal

amount of palatable food. The authors tested the hypothesis that binge eating is

mediated by changes in opioid control of feeding by comparing rats' anorectic

and

orexigenic responses to naloxone and butorphanol, respectively, and by testing

the

ability of butorphanol to elicit binge eating of chow when palatable food was

absent. Mu/kappa opioid-receptor blockade and activation had exaggerated

responses

in the R + S rats with naloxone suppressing binge eating to control levels, and

although butorphanol did not trigger chow binge eating, it enhanced binge eating

of

palatable food. These responses in sated normal-weight rats strengthen evidence

that

reward, over metabolic need, drives binge eating.

4. Baldo BA, Alsene KM, Negron A, Kelley AE.

Hyperphagia induced by GABA-sub(A) receptor-mediated inhibition of the nucleus

accumbens shell: Dependence on intact neural output from the central amygdaloid

region.

Behav Neurosci. 2005 Oct;119(5):1195-206.

PMID: 16300426

Al Pater, PhD; email: old542000@...

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