Reward sensitivity to faces versus objects in children: an ERP study

How children respond to social and nonsocial rewards has important implications for understanding social cognitive development. Adults find faces intrinsically rewarding. However, little is known about how children respond to face vs nonface rewards. We utilized event-related potentials (the stimulus-preceding negativity, SPN) to measure differences in reward anticipation during a guessing game in 6- to 8-year-olds. Children were presented with reward indicators accompanied by incidental face or nonface stimuli. Nonface stimuli were comprised of scrambled faces in the shape of arrows, controlling for low-level properties of the two conditions. Children showed an increased SPN when the reward stimuli were accompanied by faces, relative to nonface stimuli. This suggests that children find a face stimulus more rewarding than a nonface stimulus. The results have important implications for processing social vs nonsocial rewards in typically developing children, and allow testing of populations with deficits in social reward processing, such as autism spectrum disorder.     

Rash Impulsiveness and Negative Mood,but not Alexithymia or Reward Sensitivity,Differentiate Young to Middle-Aged Chronic Daily Smokers from Never-Smokers

Given the well-established associations of the personality traits alexithymia, impulsivity, and reward sensitivity with problematic use of a variety of substances, including alcohol and cannabis, the present study sought to determine whether daily tobacco smoking is similarly linked to these traits. Male and female adults aged 18 to 40 years were recruited from the local Australian community, allowing comparison of demographically similar samples of current daily smokers (n = 47) to never-smokers (n = 59) on the relevant self-report measures. Multivariate analysis of covariance revealed that current smokers scored significantly higher than never-smokers on indices of negative mood, impulsiveness, and risky alcohol use, after controlling for social desirability. No significant group differences were found on indices of alexithymia, reward sensitivity, or punishment sensitivity. Results suggest that chronic daily cigarette smoking may be an exception to the maladaptive behaviors associated with alexithymia, and is driven primarily by mood regulation and poor impulse control.     

Cortical and subcortical components of the conditioned saccharin aversion

Cortical mechanisms of the conditioned saccharin aversion were studied in 190 rats by the functional ablation technique. Water deprived animals had 15-min access to water on the familiarization Days 1 and 2. On Day 3 the rats were offered saccharin (0.1%, CS) followed 30 min later by LiCl injection (0.14 M, 2% body weight, UCS). The resulting intoxication caused marked conditioned saccharin aversion leading to reduced saccharin ingestion (by 60–80%) on Day 4. Unilateral cortical spreading depression (CSD) elicited on Days 3 and/or 4 by application of 25% KCl on the same or on opposite hemispheres does not diminish conditioned saccharin aversion in comparison with intact animals. Bilateral CSD elicited after saccharin administration, 15 min before or 5 min after LiCl injection on Day 3, does not prevent the development of conditioned saccharin aversion. On the other hand, forced feeding of saccharin under bilateral CSD elicits conditioned saccharin aversion neither with 30 min nor with 5 min CS-UCS delays although significant conditioned saccharin aversion was observed under forced feeding conditions in normal rats. It is concluded that cerebral cortex is necessary for the initial short-term storage of the indifferent gustatory trace but that the association of this engram with aversive gastrointestinal stimuli can be accomplished without cortical participation.     

Plasmalemmal mu-opioid receptor distribution mainly in nondopaminergic neurons in the rat ventral tegmental area

Opiate-evoked reward and motivated behaviors reflect, in part, the enhanced release of dopamine produced by activation of the mu-opioid receptor (muOR) in the ventral tegmental area (VTA). We examined the functional sites for muOR activation and potential interactions with dopaminergic neurons within the rat VTA by using electron microscopy for the immunocytochemical localization of antipeptide antisera raised against muOR and tyrosine hydroxylase (TH), the synthesizing enzyme for catecholamines. The cellular and subcellular distribution of muOR was remarkably similar in the two major VTA subdivisions, the paranigral (VTApn) and parabrachial (VTApb) nuclei. In each region, somatodendritic profiles comprised over 50% of the labeled structures. MuOR immunolabeling was often seen at extrasynaptic/perisynaptic sites on dendritic plasma membranes, and 10% of these dendrites contained TH. MuOR-immunoreactivity was also localized to plasma membranes of axon terminals and small unmyelinated axons, none of which contained TH. The muOR-immunoreactive axon terminals formed either symmetric or asymmetric synapses that are typically associated with inhibitory and excitatory amino acid transmitters. Their targets included unlabeled (30%), muOR-labeled (25%), and TH-labeled (45%) dendrites. Our results suggest that muOR agonists in the VTA affect dopaminergic transmission mainly indirectly through changes in the postsynaptic responsivity and/or presynaptic release from neurons containing other neurotransmitters. They also indicate, however, that muOR agonists directly affect a small population of dopaminergic neurons expressing muOR on their dendrites in VTA and/or terminals in target regions.     

Chronic bupropion attenuated the anhedonic component of nicotine withdrawal in rats via inhibition of dopamine reuptake in the nucleus accumbens shell

Bupropion, a dopamine reuptake inhibitor, is an effective therapy for smoking cessation, but the behavioral and neurochemical mechanisms mediating its antismoking properties are relatively unknown. To explore the hypothesis that bupropion ameliorates nicotine withdrawal partly by a dopamine-dependent mechanism, we investigated the effects of chronic bupropion on potassium-stimulated dopamine overflow in the nucleus accumbens shell in nicotine-withdrawing rats. We also assessed the effects of chronic bupropion on behavioral aspects of nicotine withdrawal measured by elevations in brain reward thresholds and somatic signs of withdrawal. Rats were treated with nicotine or saline for 7 days and then coadministration of bupropion or saline was initiated. After 14 days of coadministration of bupropion/saline and nicotine/saline, nicotine/saline administration was terminated, whereas bupropion/saline administration continued. These conditions mimic bupropion administration in human smokers. Cessation of nicotine administration in non-bupropion-treated rats elevated reward thresholds reflecting a reward deficit, increased somatic signs and diminished potassium-evoked dopamine overflow in the nucleus accumbens shell. Chronic bupropion lowered reward thresholds and increased potassium-evoked dopamine release regardless of previous nicotine exposure, possibly by inhibition of dopamine reuptake, and thus attenuated the anhedonic and neurochemical effects of nicotine withdrawal. Chronic bupropion blocked withdrawal-associated increased somatic signs. Finally, acute experimenter-administered nicotine enhanced brain reward function equally in all groups, indicating that bupropion does not alter the reward-facilitating effects of experimenter-administered nicotine. In conclusion, the bupropion-induced increase in extracellular dopamine in the nucleus accumbens shell may ameliorate the anhedonia associated with nicotine withdrawal, which in turn may facilitate smoking cessation.     

The nature of conditioned anti-analgesia: spinal cord opiate and anti-opiate neurochemistry

The central nervous system contains circuitry that inhibits pain sensitivity (analgesia), as well as circuitry that opposes pain inhibition (anti-analgesia). Activation of analgesia systems and anti-analgesia systems can each be brought under environmental control using classical conditioning procedures. Analgesia can be produced by cues present before and during aversive events such as electric shock, while active inhibition of analgesia comes to be produced by cues never present immediately before or during shock and therefore signal safety. We have recently reported that these analgesia and anti-analgesia systems interact at the level of the spinal cord. A series of 3 experiments were performed to examine how such interactions occur. First, potential opioid mediation of conditioned analgesia was investigated using systemic and intrathecal (i.t.) delivery of opiate antagonists. Conditioned analgesia was found to be mediated by activation of spinal μ and δ opiate receptors. Second, analgesia produced by each of these receptor subtypes was challenged by environmental signals for safety. Analgesias produced by μ and δ opiate agonists were each abolished by safety signals. Third, antagonists/antisera directed against several putative anti-opiate neurotransmitters were tested i.t. to identify which mediate conditioned anti-analgesia at the level of the spinal cord. A cholecystokinin antagonist abolished conditioned anti-analgesia. In contrast, neuropeptide FF antiserum and a κ opiate antagonist were without effect.     

Pre-treatment with high doses of cocaine decreases the reinforcing effects of cocaine in the conditioned place preference paradigm

The aim of the present study was to determine if pre-exposure to high doses of cocaine can subsequently alter the rewarding effects of this drug. Adult male mice received a pretreatment of physiological saline, or 12.5 or 25 mg/kg of cocaine (one injection a day for five days). After an interval of six days without injections, the rewarding effects of low doses of cocaine (0.5, 1 or 1.5 mg/kg) were evaluated in the conditioned place preference (CPP) paradigm. Doses of 1 and 1.5 mg/kg induced a clear CPP in animals pre-treated with saline but were ineffective in those pre-treated with 25 mg/kg of cocaine. Only the dose of 1.5 mg/kg induced CPP in mice pre-treated with 12.5 mg/kg of cocaine. Our results, which reveal a decrease in the conditioned rewarding effects of threshold doses of cocaine, demonstrate that exposure to high doses of this drug can alter the reward system.