***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Appetitive aggression occurs in the context of re source /dominance disputes in a wide variety of species . Hence , the possibility arises that a specific neural system may have evolved to detect and coordinate responses to this specific form of challenge or threat . The dopamine system has been implicated in the processing of signals of aggression in social-agonistic encounters in several species . Here we report that dopaminergic antagonism in healthy male volunteers , following acute administration of the dopamine D2-class receptor antagonist sulpiride , leads to a selective disruption in the recognition of facial expressions of anger ( signals of appetitive aggression in humans ) , but leaves intact recognition of other emotions and the matching of unfamiliar faces Amphetamine , a potent monoaminergic agonist , has pronounced effects on emotional behavior in humans , including the generation of fear and anxiety . Recent animal studies have demonstrated the importance of monoamines , especially dopamine , in modulating the response of the amygdala , a key brain region involved in the perception of fearful and threatening stimuli , and the generation of appropriate physiological and behavioral responses . We have explored the possibility that the anxiogenic effect of amphetamine in humans reflects the drug 's influence on the activity of the amygdala . In a double-blind placebo controlled study , fMRI revealed that dextroamphetamine potentiated the response of the amygdala during the perceptual processing of angry and fearful facial expressions . Our results provide the first evidence of a specific neural substrate for the anxiogenic effects of amphetamine and are consistent with animal models of dopaminergic activation of the amygdala Recent findings point to a perceptive impairment of emotional facial expressions in patients diagnosed with Parkinson disease ( PD ) . In these patients , administration of dopamine can modulate emotional facial recognition . We used fMRI to investigate differences in the functional activation in response to emotional and nonemotional gestures between PD patients and age-matched healthy controls ( HC ) . In addition , we used PET to evaluate the striatal dopamine transporter availability ( DAT ) with [11C]d-threo-methylpheni date in the patient group . Patients showed an average decrease to 26 % in DAT when compared to age-corrected healthy references . Reduction in the DAT of the left putamen correlated not only with motor impairment but also with errors in emotional gesture recognition . In comparison to HC , PD patients showed a specific decrease in activation related to emotional gesture observation in the left ventrolateral prefrontal cortex ( VLPFC ) and the right superior temporal sulcus . Moreover , the less DAT present in the left putamen , the lower the activation in the left VLPFC . We conclude that a loss of dopaminergic neurotransmission in the putamen results in a reduction of ventrolateral prefrontal access involved in the recognition of emotional gestures In this study , individuals with Parkinson ’s disease were tested as a model for basal ganglia dysfunction to infer how these structures contribute to the processing of emotional speech tone ( emotional prosody ) .  Nondemented individuals with and without Parkinson ’s disease ( n = 21/group ) completed neuropsychological tests and tasks that required them to process the meaning of emotional prosody in various ways ( discrimination , identification , emotional feature rating ) . Individuals with basal ganglia disease exhibited abnormally reduced sensitivity to the emotional significance of prosody in a range of context s , a deficit that could not be attributed to changes in mood , emotional-symbolic processing , or estimated frontal lobe cognitive re source limitations in most conditions . On the basis of these and broader findings in the literature , it is argued that the basal ganglia provide a critical mechanism for reinforcing the behavioral significance of prosodic patterns and other temporal representations derived from cue sequences ( Lieberman , 2000 ) , facilitating cortical elaboration of these events In addition to classic motor signs and symptoms , Parkinson 's disease ( PD ) is characterized by neuropsychological and emotional deficits , including a blunted emotional response . In the present study , we explored both the neural basis of abnormal emotional behavior in PD and the physiological effects of dopaminergic therapy on the response of the amygdala , a central structure in emotion processing . PD patients and matched normal controls ( NCs ) were studied with blood oxygenation level-dependent functional magnetic resonance imaging during a paradigm that involved perceptual processing of fearful stimuli . PD patients were studied twice , once during a relatively hypodopaminergic state ( i.e. , ≥12 hr after their last dose of dopamimetic treatment ) and again during a dopamine-replete state . The imaging data revealed a robust bilateral amygdala response in NCs that was absent in PD patients during the hypodopaminergic state . Dopamine repletion partially restored this response in PD patients . Our results demonstrate an abnormal amygdala response in PD that may underlie the emotional deficits accompanying the disease . Furthermore , consistent with findings in experimental animal paradigms , our results providein vivo evidence of the role of dopamine in modulating the response of the amygdala to sensory information in human subjects The amygdala exhibits significant pathological changes in Parkinson 's disease , including atrophy and Lewy body ( LB ) formation . Amygdala pathology has been suggested to contribute to some clinical features of Parkinson 's disease , including deficits of olfaction and facial expression . The degree of neuronal loss in amygdala subnuclei and the relationship with LB formation in non-demented Parkinson 's disease cases have not been examined previously . Using stereological methods , the volume of neurones and the number of neurones in amygdala subdivisions were estimated in 18 prospect ively studied , non-demented patients with Parkinson 's disease and 16 age- and sex-matched controls . Careful exclusion ( all cortical disease ) and inclusion ( non-demented , levodopa-responsive , idiopathic Parkinson 's disease or controls ) criteria were applied . Seven Parkinson 's disease cases experienced well-formed visual hallucinations many years after disease onset , while nine Parkinson 's disease cases and three controls were treated for depression . Anatomically , the amygdala was subdivided into the lateral nucleus , the basal ( basolateral and basomedial ) nuclei and the corticomedial ( central , medial and cortical nuclei ) complex . LB and Lewy neurites were identified by immunohistochemistry for alpha-synuclein and ubiquitin and were assessed semiquantitatively . LB were found throughout the amygdala in Parkinson 's disease , being present in approximately 4 % of neurones . Total amygdala volume was reduced by 20 % in Parkinson 's disease ( P = 0.02 ) and LB concentrated in the cortical and basolateral nuclei . Lewy neurites were present in most cases but did not correlate with any structural or functional variable . Amygdala volume loss was largely due to a 30 % reduction in volume ( P = 0.01 ) and the total estimated number of neurones ( P = 0.007 ) in the corticomedial complex . The degree of neurone loss and the proportion of LB-containing neurones in the cortical nucleus within this complex were constant across Parkinson 's disease cases and neither variable was related to disease duration ( R(2 ) < 0.03 ; P > 0.5 ) . The cortical nucleus has major olfactory connections and its degeneration is likely to contribute to the early selective anosmia common in Parkinson 's disease . There was a small reduction in neuronal density in the basolateral nucleus in all Parkinson 's disease cases , but no consistent volume or cell loss within this region . However , the proportion of LB-containing neurones in the basolateral nucleus was nearly doubled in cases that exhibited visual hallucinations , suggesting that neuronal dysfunction in this nucleus contributes to this late clinical feature . Detailed quantitation of the other amygdala subdivisions failed to reveal any other substantial anomalies or any associations with depression . Thus , the impact of Parkinson 's disease on the amygdala is highly selective and correlates with both early and late clinical features Impaired social cognition is a core feature of autism . There is much evidence showing people with autism use a different cognitive style than controls for face-processing . We tested if people with autism would show differential activation of social brain areas during a face-processing task .  Thirteen adults with high-functioning autism or Asperger Syndrome ( HFA/AS ) and 13 matched controls . We used fMRI to investigate ' social brain ' activity during perception of fearful faces . We employed stimuli known to reliably activate the amygdala and other social brain areas , and ROI analyses to investigate brain areas responding to facial threat as well as those showing a linear response to varying threat intensities . We predicted : ( 1 ) the HFA/AS group would show differential activation ( as opposed to merely deficits ) of the social brain compared to controls and ( 2 ) that social brain areas would respond to varied intensity of fear in the control group , but not the HFA/AS group . Both predictions were confirmed . The controls showed greater activation in the left amygdala and left orbito-frontal cortex , while the HFA/AS group showed greater activation in the anterior cingulate gyrus and superior temporal cortex . The control group also showed varying responses in social brain areas to varying intensities of fearful expression , including differential activations in the left and right amygdala . This response in the social brain was absent in the HFA/AS group . HFA/AS are associated with different patterns of activation of social brain areas during fearful emotion processing , and the absence in the HFA/AS brain of a response to varying emotional intensity We previously found that patients with Parkinson 's disease ( PD ) were impaired with respect to recognition of fear and disgust in facial expressions . To investigate the neural mechanisms that underlie this impairment , we recorded visual event-related potentials ( ERPs ) in response to the viewing of fearful facial expressions .  Ten normal elderly volunteers and nine patients with PD were studied .  Fearful , surprised , and neutral facial expressions were presented r and omly for 500 ms each , with a probability of 0.1 , 0.1 , and 0.8 , respectively . The locations of the components of the ERPs were analyzed using a scalp-skull-brain/dipole tracing method . The ERPs elicited in response to the facial stimuli consisted of a negative peak ( N1 ) , two positive peaks , and a subsequent slow negative shift . For N1 , the equivalent current dipoles were concentrated in the fusiform gyrus , right superior temporal gyrus , parahippocampal gyrus , cingulate cortex , and cerebellum , in normal subjects . In response to the fearful stimulus , dipoles were also generated from the amygdala in seven out of 10 normal subjects . In contrast , in patients with PD , N1 was centered bilaterally in the angular gyrus and supramarginal gyrus , and there was no neuronal activity in the amygdala . After N1 , dipoles moved toward the frontal region in normal subjects , whereas they remained in the parietal lobes in patients with PD . These results suggest that neither the amygdala nor the temporal visual-associated cortices are involved in responding to fearful expressions in patients with PD . Corticostriatal connections may be variably affected by a lack of dopamine or by pathological changes in the amygdala . Thus , somatosensory recruitment may overcome the mild cognitive emotional deficits that are present in patients with PD owing to a dysfunction of the amygdala Recent neuroimaging studies have demonstrated abnormal central emotional processing in psychiatric disorders . The dopamine ( DA ) systems and serotonin ( 5-HT ) systems are the main target of psychopharmacotherapy . DA D2 receptor antagonists and selective serotonin reuptake inhibitors ( SSRIs ) are widely used in psychiatric practice . Investigating the effects of these drugs on emotional processing should lead to a better underst and ing of the pathophysiology and pharmacotherapy of neuropsychiatric disorders . We aim ed to examine effects of dopaminergic and serotonergic manipulation on neural responses to unpleasant pictures in healthy volunteers using pharmacological fMRI .  Thirteen healthy male subjects participated in a single-blind , r and omized , placebo-controlled design study . Each subject participated in three fMRI sessions . In each session , participants were orally administered either 25 mg of sultopride or 50 mg of fluvoxamine or placebo prior to scanning , and neural responses to unpleasant and neutral pictures were recorded . Despite no significant differences being found in the subjective ratings of affective pictures across three sessions , compared to placebo , acute treatments of DA D2 receptor antagonists and SSRIs commonly attenuated the amygdala activity , although both treatments had slightly different modulatory effects on other components of the neural circuit of emotional processing . This study has shown that even acute treatment of drugs that manipulate neurotransmitter systems could affect brain activation associated with emotional processing in human brain . At the same time , our findings suggest that pharmacological fMRI could be a powerful tool for investigating the neurophysiological properties of drugs targeting neuropsychiatric disorders Objective : A link between the brain dopaminergic ( DA ) system and emotional processing seems to be supported by the DA nature of neural systems surrounding emotional recognition , the occurrence of emotional deficits in medical disorders involving a DA dysfunction , and the effect of DA agonists or antagonists on emotional processing . The authors tested the influence of levodopa administration on emotional processing in a functional MRI ( fMRI ) study of 10 elderly volunteers . Methods : A placebo-controlled , cross-over experimental design was used . Subjects received either levodopa ( 100 mg ) or placebo in 2 fMRI sessions . Performance was evaluated with a passive facial emotion perception test . Results : During the placebo situation , the region-of-interest ( ROI ) analysis showed that emotional processing activated the bilateral amygdala . In levodopa volunteers , this activation was missing . The statistical comparison between the 2 situations ( 
    Output:
    
We then discuss the functional roles of the striato-thalamo-cortical and mesolimbic circuits , ending with the conclusion that both these pathways are indeed involved in emotional processing