Evaluation of food intake and Fos expression in serotonergic neurons of raphe nuclei after intracerebroventricular injection of adrenaline in free-feeding rats.

Previous studies indicate that the modification of adrenergic neurotransmission in median raphe nucleus (MRN) enhances or removes an inhibitory influence on food intake, possibly serotonergic, due to a presence of serotonin-producing neurons in that nucleus. Therefore, the aim of this study is evaluated whether the activity of neurons in the MRN and dorsal raphe nucleus (DRN) are affected by intracerebroventricular injection of adrenaline (AD) in free-feeding rats. Male Wistar rats with guide cannulae chronically implanted in the lateral ventricle were injected with AD followed by evaluation of ingestive behavioral parameters. Behavior was monitored and the amount of food ingested was assessed. The highest dose (20 nmol) of AD was the most effective dose in increasing food intake. Subsequently, AD 20 nmol was injected to study neuronal activity indicated by the presence of Fos protein and its co-localization with serotonergic neurons in the MRN and DRN of naive rats with or without access to food during the recording of behavior. The administration of AD 20 nmol increased Fos expression and double labeling with serotonergic neurons in the DRN in rats with access to food, but not in animals without access. No statistically significant changes in Fos expression were observed in the MRN in any of the experimental conditions tested. These results suggest that DRN serotonergic and non-serotonergic neurons are activated by post-prandial signals. In contrast, the absence of Fos expression in the MRN suggests that this nucleus does not participate in the circuit involved in the control of post-prandial satiety.

Ingestive and locomotor behaviours induced by pharmacological manipulation of -adrenoceptors into the median raphe nucleus.

The present study evaluated the involvement of α-adrenoceptors of the median raphe nucleus (MRN) in satiated rats, in food and water intake and motor behaviour. Control groups were treated with saline (SAL) or adrenaline (ADR), injected into the MRN seven minutes after injection of the vehicle used to solubilize the antagonists, propylene glycol (PLG) or SAL. Experimental groups were treated with an α-adrenoceptor antagonist, prazosin (α1, 20 or 40 nmol) or yohimbine (α2, 20 or 40 nmol) or phentolamine (non-selective α, 20 or 40 nmol), followed (later) by injection of ADR or SAL. Behaviour was recorded for 30 min. The injection of ADR and the blockade of α1 receptors resulted in hyperphagia whereas blocking α2 or α1 and α2 simultaneously did not change feeding behaviour. Pre-treatment with prazosin, followed by injection of ADR was not able to cause an increase in the amount of food ingested, while the higher dose of the α1 antagonist reduced the latency to start feeding. Pre-treatment with prazosin also caused hyperactivity. However, pre-treatment with phentolamine or yohimbine was able to block ADR-induced feeding. The present study supports the hypothesis that there is a tonic activation of α1-adrenoceptors in the MRN in satiated rats, which activates an inhibitory influence in areas that control food intake. Injection of ADR seems to activate α2 receptors, resulting in a decrease in the availability of endogenous catecholamines, which reduces the release of the signal that inhibits food intake, leading to hyperphagia.

The microinjection of a cannabinoid agonist into the accumbens shell induces anxiogenesis in the elevated plus-maze.

This study investigated the effect of a cannabinoid agonist injected into the shell region of the nucleus accumbens (nAcb shell) on anxiety-related behaviors. The animals (male Wistar rats) were unilaterally microinjected with either ACEA (arachidonyl-2'-chloroethylamide a CB1 receptor agonist) at doses of 0.005, 0.05 or 0.5 pmol, or vehicle (ethanol 0.04% in saline 0.9%) and submitted to the elevated plus-maze (EPM), a pre-clinical test of anxiety. The data showed that rats microinjected with ACEA (0.05 pmol/0.2 µl) into the nAcb shell exhibited decreased % open arm time and open arm entries in comparison with the control group, which is compatible with an anxiogenic-like effect. To rule out the hypothesis that spread of the drug into the ventricle was responsible for the observed anxiogenic effect, 0.05 pmol ACEA was injected into the lateral ventricle and shown not to alter the responses representative of fear/anxiety and locomotion. The locomotor activity was not changed at the dose of 0.05 pmol ACEA microinjected into the nAcb shell. The present data suggest that activation of cannabinoid receptors in the nAcb shell may modulate fear/anxiety in the EPM.