Sign and goal tracker rats process differently the incentive salience of a conditioned stimulus

Abstract

Sign and goal tracker animals show different behavioral patterns in response to conditioned stimuli, which may be driven by different neural circuits involved in processing stimuli. Here, we explored whether sign and goal-tracker profiles implicated different brain regions and responses to incentive salience of stimuli. We performed three experiments using male Wistar rats. Experiment 1 showed that lesioning the medial prefrontal cortex increased the prevalence of the goal-tracker phenotype. Experiment 2 assessed the developmental trajectory of the salience incentive attribution to a conditioned stimulus, showing that increased incentive salience of stimuli increased the prevalence of the sign-tracker phenotype in mature, but not preadolescent rats. In experiment 3, the functional impact of the medial prefrontal cortex circuits was analyzed with a latent inhibition procedure. Sign tracker rats showed a reduced latent inhibition to stimuli previously exposed when compared to goal tracker or intermediate rats. The overall results of this study highlight a key role of the medial prefrontal cortex for sign tracking behavior. The expression of sign and goal tracker phenotypes changed after lesion to the medial prefrontal cortex (experiment 1), differed across development (experiment 2), and showed differences in the attentional processes to previously exposed stimuli, as preexposure to CS was ineffective in sign tracker animals (experiment 3). These data indicate that the responses to the incentive salience of stimuli in sign tracker and goal tracker profiles are likely driven by different neural circuitry, with a different role of prefrontal cortical function.

Fig 1

A. Reconstruction of the mPFC lesions displayed on standard coronal sections from the atlas of Paxinos and Watson [28]. The largest lesion is shown in pale shading and the smallest in dark shading. B. Photomicrograph showing a no lesioned coronal brain section. C. A coronal section after excitotoxic lesion of mPFC. Cg1: cingulate cortex, area 1; PrL: prelimbic cortex.

Fig 2

A. Entries to nose poke device in sham (open circles) and mPFC lesioned (black circles) animals. The figure includes the mean and standard error from session 1 to 4 for each group including all animals. Dotted lines show the limits between phenotypes. B. Mean of lever-press behavior and magazine entries (C) when CS was presented in ST (filled and white squares), GT (filled and white circles), and Int (filled and white diamonds) groups. Filled and open symbols indicate sham or mPFC groups, respectively. D. Approach Index Score of Sham and mPFC-lesioned rats. Asterisk indicate significant differences between sham and mPFC lesioned animals.

Fig 3. Distribution of GT, ST, or Int phenotypes in sham and mPFC-lesioned animals in session 4.

Black and open circles show data from all individual animals. Grey and white bars shows the percent of animals expressing each phenotype.

Fig 4

A. Approach Index Score of pre-adolescent (filled symbols) and Late adolescent (open symbols) groups. The figure includes mean and standard errors from session 1A to 4A, and 1B to 4B and 1A’ to 4A’ for each group. Dotted lines represent the limits among phenotypes. B. Mean of lever-press behavior and magazine entries (C) when CS was presented in ST (filled and open triangles), GT (filled and open circles), and Int (filled and open squares) groups.

Fig 5. Mean of freezing response in GT and ST groups exposed and non-exposed to the future CS in a LI test.

Asterisks indicate the conditioning after CS-US association (p < .05).