Recent evidence suggests that rewarding and aversive stimuli affect the same brain areas, including medial prefrontal cortex and nucleus accumbens. Although nucleus accumbens is known to respond to salient stimuli, regardless of their hedonic valence, with selective increased dopamine release, little is known about the role of prefrontal cortex in reward-and aversion-related motivation or about the neurotransmitters involved. Here we find that selective norepinephrine depletion in medial prefrontal cortex of mice abolished the increase in the release of norepinephrine by prefrontal cortex and of dopamine by nucleus accumbens that is induced by food, cocaine, or lithium chloride and impaired the place conditioning induced by both lithium chloride (aversion) and food or cocaine (preference). This is evidence that prefrontal cortical norepinephrine transmission is necessary for motivational salience attribution to both reward-and aversion-related stimuli through modulation of dopamine in nucleus accumbens, a brain area involved in all motivated behaviors. motivation ͉ norepinephrine ͉ prefrontal cortex ͉ dopamine ͉ place conditioning
Intense motivational salience attribution is considered to have a major role in the development of different psychopathologies. Numerous brain areas are involved in “normal” motivational salience attribution processes; however, it is not clear whether common or different neural mechanisms also underlie intense motivational salience attribution. To elucidate this a brain area and a neural system had to be envisaged that were involved only in motivational salience attribution to highly salient stimuli. Using intracerebral microdialysis, we found that natural stimuli induced an increase in norepinephrine release in the medial prefrontal cortex of mice proportional to their salience, and that selective prefrontal norepinephrine depletion abolished the increase of norepinephrine release in the medial prefrontal cortex induced by exposure to appetitive (palatable food) or aversive (light) stimuli independently of salience. However, selective norepinephrine depletion in the medial prefrontal cortex impaired the place conditioning induced exclusively by highly salient stimuli, thus indicating that prefrontal noradrenergic transmission determines approach or avoidance responses to both reward- and aversion-related natural stimuli only when the salience of the unconditioned natural stimulus is high enough to induce sustained norepinephrine outflow. This affirms that prefrontal noradrenergic transmission determines motivational salience attribution selectively when intense motivational salience is processed, as in conditions that characterize psychopathological outcomes.
The Wechsler Adult Intelligence Scale (WAIS) has been used extensively to study intellectual abilities of special groups. Here, we report the results of an intellectually gifted group on the WAIS-IV. Gifted individuals are people who obtained scores equal to or greater than 2 standard deviations above the mean on an intelligence test. Hence, the current study aims first, to examine mean group performance data of gifted individuals on the WAIS-IV; second, to revalidate the pattern of performance identified in this special group in previous studies (i.e., verbal skills higher than all other abilities); third, to compare scatter measures across intellectual domains with a matched comparison group. A total of 130 gifted individuals (79 males) were administered the full battery and their performance was compared with a matched comparison group. Analyses revealed that gifted group displayed higher scores in all intellectual domains. Contrary to expectations, they showed the highest scores in perceptual reasoning tasks. A multivariate approach revealed that this ability was statistically different from all other domains within the gifted group. Moreover, gifted individuals showed higher discrepancies across intellectual domains than average-intelligence people. Findings have important practical implications to detect intellectual giftedness in adulthood.
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