Modulation of daily water intake by dopamine in caudate and accumbens nuclei in rats

Pal, G K; Bharathi, B.; Thombre, D P

doi:10.1016/0031-9384(92)90126-m

Cited by 17 publications

(17 citation statements)

References 31 publications

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“…This DA release is believed to be important in appetitive responding for ethanol, as well as in facilitating food intake and drug self-administration (Baldo et al, 2002; Czachowski et al, 2001; Gonzales et al, 2004; Pal and Thombre, 1993; Samson et al, 1999). Projections from the PVN extend rostrally to the NAc, possibly via lateral hypothalamic projections, where they can excite DA nerve terminals (Barone et al, 1981; Brog et al, 1993; Korf, 1984).…”

Section: Discussionmentioning

confidence: 99%

Opioids in the Hypothalamic Paraventricular Nucleus Stimulate Ethanol Intake

Barson

Carr

Soun

et al. 2010

Alcoholism Clin & Exp Res

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Background Specialized hypothalamic systems that increase food intake might also increase ethanol intake. To test this possibility, morphine and receptor-specific opioid agonists were microinjected in the paraventricular nucleus (PVN) of rats that had learned to drink ethanol. To cross-validate the results, naloxone methiodide (m-naloxone), an opioid antagonist, was microinjected with the expectation that it would have the opposite effect of morphine and the specific opioid agonists. Methods Sprague-Dawley rats were trained, without sugar, to drink 4% or 7% ethanol and were then implanted with chronic brain cannulas aimed at the PVN. After recovery, those drinking 7% ethanol, with food and water available, were injected with two doses each of morphine or m-naloxone. To test for receptor specificity, two doses each of the μ-receptor agonist [D-Ala2,N-Me-Phe4,Gly5-ol]-Enkephalin (DAMGO), δ-receptor agonist D-Ala-Gly-Phe-Met-NH2 (DALA), or k-receptor agonist U-50,488H were injected. DAMGO was also tested in rats drinking 4% ethanol without food or water available. As an anatomical control for drug reflux, injections were made 2 mm dorsal to the PVN. Results A main result was a significant increase in ethanol intake induced by PVN injection of morphine. The opposite effect was produced by m-naloxone. The effects of morphine and m-naloxone were exclusively on intake of ethanol, even though food and water were freely available. In the analysis with specific receptor agonists, PVN injection of the δ-agonist DALA significantly increased 7% ethanol intake without affecting food or water intake. This is in contrast to the k-agonist U-50,488H, which decreased ethanol intake, and the μ-agonist DAMGO, which had no effect on ethanol intake in the presence or absence of food and water. In the anatomical control location 2 mm dorsal to the PVN, no drug caused any significant changes in ethanol, food, or water intake, providing evidence that the active site was close to the cannula tip. Conclusions The δ-opioid receptor agonist in the PVN increased ethanol intake in strong preference over food and water, while the k-opioid agonist suppressed ethanol intake. Prior studies show that learning to drink ethanol stimulates PVN expression and production of the peptides enkephalin and dynorphin, which are endogenous agonists for the δ- and k-receptors, respectively. These results suggest that enkephalin via the δ-opioid system can function locally within a positive feedback circuit to cause ethanol intake to escalate and ultimately contribute to the abuse of ethanol. This is in contrast to dynorphin via the k-opioid system, which may act to counter this escalation. Naltrexone therapy for alcoholism may act, in part, by blocking the enkephalin-triggered positive feedback cycle.

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Section: Discussionmentioning

confidence: 99%

Opioids in the Hypothalamic Paraventricular Nucleus Stimulate Ethanol Intake

Barson

Carr

Soun

et al. 2010

Alcoholism Clin & Exp Res

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“…However, a plentiful supply of energy brings the risk of obesity; the stimulation of the ventral striatum rewards undesirable behaviour. Both dopamine (Pal & Thombre, 1993) and opioid peptides (Kelley et al 2000) modulate the ventral striatum and in this area stimulate the intake of palatable foods.…”

Section: Reward Mechanismsmentioning

confidence: 99%

Can artificial sweeteners help control body weight and prevent obesity?

Benton

2005

Nutr. Res. Rev.

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The possible role played by artificial sweeteners in the long-term maintenance of body weight is considered. Although artificial sweeteners can play a role in a short-term energy-controlled diet, the evidence that they are helpful over a longer period is limited. In those in the recommended weight range there is evidence of compensation; that is, the consumption of low-energy foods is followed by an increased energy intake to make up the lost energy. Energy compensation is more likely in those not displaying dietary restraint. The desire to remove sugar from the diet reflects an assumption that its intake is associated with obesity. However, the consumption of energy-dense food, that almost entirely reflects a high fat and low water content, is the best predictor of obesity. Diets offering a high proportion of energy in the form of carbohydrate tend to contain low levels of fat. There are several reports that the use of artificial sweeteners leads to an increased consumption of fat. The weak ability of fat to satisfy hunger makes it easy to overeat fatty foods; in contrast, carbohydrates promote a feeling of 'fullness'. Various short-term studies have found that carbohydrate consumed as a liquid, rather than a solid, is more likely to result in weight gain.

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“…The electrolytic lesions of the nuclei were produced in six experimental rats (lesion group) by passing an anodal current of 2 mA for 15 s with the help of a lesion maker (INCO). Details of lesion and cannulation are described in our earlier work [7]. After surgery, animals were allowed 2 days for recovery before the different experiments were performed.…”

mentioning

confidence: 99%

“…One microlitre (concentration: 4 g/l) of the above drugs was injected through the cannulae placed in caudate nucleus. These doses were selected because at these levels, feeding and dipsogenic behavior were found to be altered [7]. On seventh day of SRBC injection, the animals were anaesthetized with chloralose and 3-4 ml of blood was collected by cardiac puncture for estimation of anti-SRBC titer and serum proteins.…”

mentioning

confidence: 99%

“…Stained brain sections of rats were made on transparent papers and were overlapped on each other to mark the maximum extent of lesion in both groups. The area to which the tip of cannulae were limited and the extent of lesion were determined in a similar way as described earlier [7]. One-way ANOVA with Tukey HSD as post-hoc test was used for comparison of data.…”

mentioning

confidence: 99%

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