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  • Title: Enhancement of meal-associated hypertonic NaCl intake by moxonidine into the lateral parabrachial nucleus.
    Author: Andrade CA, De Luca LA, Colombari DS, Menani JV.
    Journal: Behav Brain Res; 2007 Nov 02; 183(2):156-60. PubMed ID: 17629970.
    Abstract:
    alpha2-Adrenoceptor activation with moxonidine (alpha2-adrenergic/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) enhances angiotensin II/hypovolaemia-induced sodium intake and drives cell dehydrated rats to ingest hypertonic sodium solution besides water. Angiotensin II and osmotic signals are suggested to stimulate meal-induced water intake. Therefore, in the present study we investigated the effects of bilateral injections of moxonidine into the LPBN on food deprivation-induced food intake and on meal-associated water and 0.3M NaCl intake. Male Holtzman rats with cannulas implanted bilaterally into the LPBN were submitted to 14 or 24h of food deprivation with water and 0.3M NaCl available (n=6-14). Bilateral injections of moxonidine (0.5nmol/0.2microl) into the LPBN increased meal-associated 0.3M NaCl intake (11.4+/-3.0ml/120min versus vehicle: 2.2+/-0.9ml/120min), without changing food intake (11.1+/-1.2g/120min versus vehicle: 11.2+/-0.9g/120min) or water intake (10.2+/-1.5ml/120min versus vehicle: 10.4+/-1.2ml/120min) by 24h food deprived rats. When no food was available during the test, moxonidine (0.5nmol) into the LPBN of 24h food-deprived rats produced no change in 0.3M NaCl intake (1.0+/-0.6ml/120min versus vehicle: 1.8+/-1.1ml/120min), nor in water intake (0.2+/-0.1ml/120min versus vehicle: 0.6+/-0.3ml/120min). The results suggest that signals generated during a meal, like dehydration, for example, not hunger, induce hypertonic NaCl intake when moxonidine is acting in the LPBN. Thus, activation of LPBN inhibitory mechanisms seems necessary to restrain sodium intake during a meal.
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