Biomedical subjects

Marie-Josée Angst

Publications and source records attributed to Marie-Josée Angst.

4 recordsLinked to original sources

PubMed2006

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↗

PubMed2004

Prenatal exposure of Long-Evans rats to 17alpha-ethinylestradiol modifies neither latent inhibition nor prepulse inhibition of the startle reflex but elicits minor deficits in exploratory behavior.

Prenatal administration of synthetic estrogens in humans as well as lower mammals was reported to alter behavior in adulthood. The alterations remain to be characterized according to specific pathophysiological hypotheses. In this study, three common behavioral models of schizophrenia were tested, i.e., latent inhibition (LI), prepulse inhibition of the startle response (PPI) and hyperlocomotion under amphetamine. Female Long-Evans rats were injected i.p. with a solution of 17alpha-ethinylestradiol (15 microg kg(-1)) everyday from day 9 to 14 of pregnancy, and behavioral characteristics of their offspring, raised by Wistar foster mothers, were compared to those of rats born from dams injected with the vehicle only, over the same gestation period. LI was tested in a conditioned taste aversion and a conditioned passive avoidance paradigm followed by a parametric study of PPI and an evaluation of locomotion in an open field under saline or amphetamine (1.5 mg kg(-1)). Histological brain measurements were also carried out in a subset of the same rats. Neither LI nor PPI was altered using methods that had proven sensitive in previous pharmacological studies. Treated rats' locomotion was impaired, but amphetamine did not elicit a differential enhancement. A thinner Amon's horn layer was observed in their hippocampus. This indicates that standard models of schizophrenia did not fit to the behavioral abnormalities found by others and confirmed in this study. They were not due to the abnormal maternal care to pups elicited by the treatment.

Amphetamine↗

PubMed2004

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↗

PubMed2002

Effect of a nonsedative dose of propofol on memory for aversively loaded information in rats.

BACKGROUND: The effects of propofol on memory for aversive information are not well determined. The authors evaluated the effects of a minimal nonsedative dose of propofol or midazolam on memory in rats, using an apparatus composed of two compartments: a large bright anxiogenic one and a small dark neutral one. METHODS: Groups of rat received propofol (9 mg/kg, intraperitoneally) or midazolam (3 mg/kg). Anxiety was assessed in rats placed in the anxiogenic compartment as the time before the animals entered the neutral compartment. Memory for an aversive event was assessed in rats placed in the anxiogenic compartment as the time to enter the neutral one where they previously experienced foot shocks (fear conditioning). To assess the memory for a nonaversive event, rats were placed in the neutral compartment with no shocks (preexposure). The following day, rats were placed in it and they experienced foot shocks. As a result of the preexposure, rats exhibit less fear to enter it. RESULTS: Propofol and midazolam increased the time to enter the neutral compartment. Propofol or midazolam was given to rats before experiencing foot shocks in the neutral compartment. When later tested, the time to enter it was decreased. Propofol or midazolam was given to rats before the preexposure to the neutral compartment. When later tested, the latency to enter it was not modified by the preexposure. CONCLUSIONS: Propofol and midazolam impaired memory for aversive and for nonaversive experiences at equianxiolytic doses that do not produce locomotor impairment in rats.

Anesthetics, Intravenous↗