Elsevier

Behavioural Brain Research

Volume 256, 1 November 2013, Pages 36-42
Behavioural Brain Research

Research report
Effects of nucleus accumbens core and shell lesions on autoshaped lever-pressing

https://doi.org/10.1016/j.bbr.2013.07.046Get rights and content

Highlights

  • Separate lesions of nucleus accumbens core or shell had no effect on sign-tracking.

  • Results contrast with the effects of whole accumbens lesions on sign-tracking.

  • Neural circuitry of sign-tracking depends upon conditioned stimulus modality.

Abstract

Certain Pavlovian conditioned stimuli (CSs) paired with food unconditioned stimuli (USs) come to elicit approach and even consumption-like behaviors in rats (sign-tracking). We investigated the effects of lesions of the nucleus accumbens core (ACbC) or shell (ACbS) on the acquisition of sign-tracking in a discriminative autoshaping procedure in which presentation of one lever CS was followed by delivery of sucrose, and another was not. Although we previously found that bilateral lesions of the whole ACb disrupted the initial acquisition of sign-tracking, neither ACbC or ACbS lesions affected the rate or percentage of trials in which rats pressed the CS+. In addition, detailed video analysis showed no effect of either lesion on the topography of the sign-tracking conditioned response (CR). These and other results from lesion studies of autoshaping contrast with those from previous sign-tracking experiments that used purely visual cues (Parkinson et al., 2000a,b), suggesting that the neural circuitry involved in assigning incentive value depends upon the nature of the CS.

Introduction

Environmental cues associated with food can become powerful elicitors of a variety of learned behaviors. For example, in an autoshaping procedure in which insertion of a lever conditioned stimulus (CS) in the chamber signals the delivery of a food unconditioned stimulus (US), the lever may control approach and contact responses directed to the lever (“sign-tracking”) and/or to the food delivery site (“goal-tracking”) [4], [5], [11], [16]. These conditioned responses (CRs) develop despite the absence of any explicit response-US response contingency [26]. Some investigators have argued that CS-directed sign-tracking behaviors reflect the acquisition of incentive salience to the CS, by which the incentive motivational value of the US is transferred to the CS [1], [2]. As a result of the attribution of incentive salience to a lever, rats may try to “consume” it by biting or chewing [1], [2], [30]. Moreover, the topography of the CR is also dependent on the type of US that is used: Rats given a food US tend to nibble and bite the lever CS, whereas rats given a liquid US (20% sucrose or 25% condensed milk) tend to lick the lever CS [8], [9]. Consistent with previous findings that implicate ACb and its midbrain dopamine (DA) projections from the ventral tegmental area (VTA) in the transfer of incentive value from the US to the CS [10], [15], [24], [25], Chang et al. [7] found that whole ACb lesions impaired the initial acquisition of sign-tracking, although not its terminal levels.

To further characterize the role of ACb and its subnuclei in incentive learning, here we investigated the effects of separate bilateral lesions of the nucleus accumbens core (ACbC) or medial shell (ACbS) on autoshaped lever-pressing in rats. Parkinson et al. [20] showed that bilateral lesions of ACbC, but not ACbS, disrupted the acquisition of conditioned approach to visual CSs (white rectangles displayed on a monitor). Although approach to a visual CS is considered a form of sign-tracking, we hypothesized that the neural circuitry involved in assigning incentive salience to a CS that can only be approached (white rectangle) may be different from that engaged by a CS that can be approached, manipulated, and “consumed” (lever). Specifically, autoshaping with lever CSs may allow for the transfer of hedonic properties from the US to the CS, referring to the pleasure associated with consuming a sweet and energy-rich reward (e.g. “liking”; [3]). Previous taste reactivity studies by Berridge and colleagues have shown that microinjections of the μ opioid agonist DAMGO ([D-Ala2, N-MePhe4, Gly-ol]-enkephalin) or the endogenous cannibinoid anandimide into particular “hotspots” into the medial ACbS can enhance the hedonic impact of a sweet US [18], [22], [23]. In contrast, no such hedonic enhancements were observed with comparable treatment in the ACbC. If autoshaping with lever CSs allows for the transfer of hedonic properties (e.g. conditioned “liking”; [1]), then we would expect ACbS but not ACbC lesions to alter sign-tracking, particularly in how rats interact with the lever CS. However, if sign-tracking with lever CSs is similar to sign-tracking with visual CSs, then ACbS lesions would have no effect and ACbC lesions would produce deficits in sign-tracking.

Section snippets

Animals

The subjects were male Long-Evans rats (Charles River Laboratories, Raleigh, NC, USA), which weighed 300–325 g on arrival. Rats were individually housed in a climate controlled colony room that was illuminated from 7:00 a.m. to 7:00 p.m. Rats were provided ad libitum access to food and water before and continuing until after two weeks of recovery from surgery. They were then placed on food restriction and were maintained at 85% of their ad libitum weights throughout the autoshaping procedure.

Histological results

Fig. 1, Fig. 2 show schematic representations of neural damage in accepted ACbC- (n = 13) and ACbS- (n = 8) lesioned rats. On average, 80.0 ± 3.1% (mean ± SEM) of ACbC was eliminated in ACbC-lesioned rats, whereas only 13.9 ± 2.6% of ACbS was damaged. In ACbS-lesioned rats, 70.3 ± 5.9% of ACbS was eliminated while only 13.3 ± 1.9% of ACbC was damaged. Data of rats with less than 48.9% damage to the intended lesion region were discarded. In addition, 33.13 ± 5.29% of lateral nucleus accumbens shell (lACbS) was

Discussion

We showed that bilateral lesions of either ACbC or ACbS alone did not disrupt the acquisition of sign-tracking, as indexed by conventional measures of the rate or probability of lever pressing. In addition, neither ACbC or ACbS lesions disrupted the number of consummatory behaviors made toward the CS+.

Our failure to find significant effects of separate lesions of ACbC or ACbS separately on the acquisition of autoshaped lever pressing contrasts with our previous observation that lesions that

Acknowledgement

This work was supported by NIH Grant MH53667.

References (33)

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