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Nadine Fresquet

Publications and source records attributed to Nadine Fresquet.

4 recordsLinked to original sources

Adrenergic drugs modify the level of noradrenaline in the insular cortex and alter extinction of conditioned taste aversion in rats.

We compared the effect of conditioned taste aversion in rats by measuring the amount of sucrose that they drunk after conditioning, which differed according to whether rats had drunk the sucrose freely (SD: self drinking) during the conditioning session, or had been forced to drink it (IO: intra-oral administration through a chronically implanted cannula). The SD procedure delayed the extinction of conditioned taste aversion. Enhanced arousal, alertness, awareness or attention in the SD condition may have strengthened the memory of the taste. Brain noradrenergic networks are involved in such processes. We administered two noradrenergic drugs that produce opposite effects on noradrenaline release in the brain, methoxy-idazoxan, RX821002 (1mg/kg, i.p.), and guanfacine (0.12mg/kg, i.p.). We evaluated their effect (i) on the level of noradrenaline in the gustatory cortex using microdialysis, (ii) on glycaemia that is an essential factor of taste learning and (iii) on the comparative SD versus IO conditioned taste aversion protocol mentioned above. Injecting RX821001 increased the level of noradrenaline in the gustatory cortex up to two-fold of the baseline. This effect lasted 1h. The same dose of RX821002 did not elicit any alteration of glycaemia. It enhanced extinction of conditioned taste aversion in the SD group of rats. Injecting 0.12mg/kg of guanfacine produced the opposite effect. The noradrenaline level of the gustatory cortex decreased, but only down to 20% of the baseline. This decrease lasted 2h. Guanfacine increased glycaemia. Extinction of conditioned taste aversion was only marginally decreased by guanfacine in the SD group of rats. These results fit with Aston-Jones' point of view that the role of the noradrenergic coeruleo-cortical system may be to enhance arousal, alertness, awareness or attention to an event by a transient increase of cortical noradrenaline.

Adrenergic Agents↗

Insular cortex lesions alter conditioned taste avoidance in rats differentially when using two methods of sucrose delivery.

The insular gustatory cortex may be essential for the evaluation of saliency and representation of the incentive values of tastes. Gustatory cortex lesions should interfere with conditioned taste avoidance according to these factors, which depend on the conditioned taste avoidance protocol used. The present study was aimed at investigating the effects of bilateral lesions of the gustatory cortex-focusing on electrolytic and excitotoxic lesions. Lesioned and sham-operated male Long-Evans rats were intoxicated using LiCl after drinking sucrose from a tube (SD) or having the same amount of sucrose fed directly into their mouths through a chronically implanted intra-oral (IO) cannula. Every aspect of the experiment was carefully counterbalanced between the experimental groups. In the control groups, the acquired avoidance towards sucrose was strongly preserved over eight extinction test days in SD rats but not in IO rats, in which a progressive decline was recorded. Electrolytic gustatory cortex lesions impaired but did not suppress conditioned taste avoidance in both protocols. Excitotoxic lesions tend to impair CTA also, but differentially according to the SD or IO protocols. Extinction of CTA was selectively impaired in the SD protocol by small lesions destroying the anterior insular cortex.

Animals↗

Frontal lesions do not alter the differential extinction of taste aversion conditioning in rats, when using two methods of sucrose delivery.

The frontal cortex is involved in the planning of behavioural responses and in the processing of their outcomes. Thus it contributes to several learning mechanisms, including those of conditioned taste aversion (CTA). A solution of sucrose drunk freely by a rat from a drinking tube-self-drinking protocol (SD)-was used as a conditioned stimulus in CTA. The intake of this solution was followed by gastric malaise. It produced an aversion to sucrose that withstood extinction over a week of repetitive tests. But, when the sucrose was perfused intra-orally (IO), i.e. not depending on any specific action by the rat, the extinction of aversion was much faster. Several factors may explain this differential extinction including the contribution of contextual factors linked to the achievement of an action and/or the enhancement of the attention towards the outcome of the action (the taste). The processing of such factors is usually believed to require the prefrontal cortex or the cingulate cortex (CgC). In our first experiment, the frontal cortex was totally transected. In the second experiment, the CgC was removed by aspiration. None of these lesions elicited any change in CTA, either in IO or in SD conditions, meaning that the differential extinction remained. The surprising absence of a frontal lesion effect was thought to indicate the low attentional demand required in both CTA protocols.

Animals↗

Conditioned taste aversion using four different means to deliver sucrose to rats.

A solution of sucrose either to be drunk from a drinking tube-self-drinking procedure (SD)-or perfused intraorally as a consequence of nose-pokes-self-administration procedure (SA)-or perfused as a consequence of licking an empty tube (LA)-was paired with an LiCl-induced malaise in rats. The effects were compared to those of a procedure consisting of intraoral administration (IO) of sucrose not contingent to any specific action of the rat. Similar levels of conditioned taste aversion (CTA) were obtained but extinction in the IO procedure was quicker than in the SA procedure, which was itself quicker than in the SD procedure. Extinctions in the IO and LA procedures resembled one another and were quicker than in the SD procedure. A step towards deciding between several explanatory hypotheses of these differences was made by conducting two more experiments. The third experiment was based on reinstatement, or not, of the conditioning procedure for the test after standard IO extinction. CTA was produced only when SD was used both at conditioning and test. A fourth experiment was based on latent inhibition where the procedure was changed, or not, between preexposure and conditioning. Latent inhibition was absent only when the rats had been preexposed to sucrose with the SA procedure and conditioned with the SD procedure.

Animals↗