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Human Prefrontal Cortex (human + prefrontal_cortex)
Selected AbstractsSubjective neuronal coding of reward: temporal value discounting and riskEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2010Wolfram Schultz Abstract A key question in the neurobiology of reward relates to the nature of coding. Rewards are objects that are advantageous or necessary for the survival of individuals in a variety of environmental situations. Thus reward appears to depend on the individual and its environment. The question arises whether neuronal systems in humans and monkeys code reward in subjective terms, objective terms or both. The present review addresses this issue by dealing with two important reward processes, namely the individual discounting of reward value across temporal delays, and the processing of information about risky rewards that depends on individual risk attitudes. The subjective value of rewards decreases with the temporal distance to the reward. In experiments using neurophysiology and brain imaging, dopamine neurons and striatal systems discount reward value across temporal delays of a few seconds, despite unchanged objective reward value, suggesting subjective value coding. The subjective values of risky outcomes depend on the risk attitude of individual decision makers; these values decrease for risk-avoiders and increase for risk-seekers. The signal for risk and the signal for the value of risky reward covary with individual risk attitudes in regions of the human prefrontal cortex, suggesting subjective rather than objective coding of risk and risky value. These data demonstrate that important parameters of reward are coded in a subjective manner in key reward structures of the brain. However, these data do not rule out that other neurons or brain structures may code reward according to its objective value and risk. [source] Changes in alternative brain-derived neurotrophic factor transcript expression in the developing human prefrontal cortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2009Jenny Wong Abstract In this study, we determined when and through which promoter brain-derived neurotrophic factor (BDNF) transcription is regulated during the protracted period of human frontal cortex development. Using quantitative real-time polymerase chain reaction, we examined the expression of the four most abundant alternative 5, exons of the BDNF gene (exons I, II, IV, and VI) in RNA extracted from the prefrontal cortex. We found that expression of transcripts I,IX and VI,IX was highest during infancy, whereas that of transcript II,IX was lowest just after birth, slowly increasing to reach a peak in toddlers. Transcript IV,IX was significantly upregulated within the first year of life, and was maintained at this level until school age. Quantification of BDNF protein revealed that levels followed a similar developmental pattern as transcript IV,IX. In situ hybridization of mRNA in cortical sections showed the highest expression in layers V and VI for all four BDNF transcripts, whereas moderate expression was observed in layers II and III. Interestingly, although low expression of BDNF was observed in cortical layer IV, this BDNF mRNA low-zone decreased in prominence with age and showed an increase in neuronal mRNA localization. In summary, our findings show that dynamic regulation of BDNF expression occurs through differential use of alternative promoters during the development of the human prefrontal cortex, particularly in the younger age groups, when the prefrontal cortex is more plastic. [source] Normal human aging and early-stage schizophrenia share common molecular profilesAGING CELL, Issue 3 2009Bin Tang Summary We examined genome-wide expression datasets from human prefrontal cortex of normal and schizophrenic individuals ranging from 19 to 81 years of age. We found that changes in gene expression that are correlated with aging in normal subjects differ dramatically from those observed with aging in schizophrenic subjects. Only 2.5% of genes were correlated with age in both groups. Surprisingly, we also found a significant overlap (29,34%) between those genes whose expression was correlated with aging in normal subjects and those significantly altered in subjects with early-stage schizophrenia (within 4 years of diagnosis). This suggests that schizophrenia onset anticipates the normal aging process, and further, that some symptoms of aging, i.e. dementia and psychosis, might be explained by these common molecular profiles. [source] Transmembrane signaling through phospholipase C-, in the developing human prefrontal cortexJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2006Iñigo Ruiz de Azúa Abstract To investigate changes in muscarinic receptor-stimulated phospholipase C-, (PLC-,) activity during brain development, we examined the functional coupling of each of the three major protein components of the phosphoinositide system (M1, M3, and M5 muscarinic receptor subtypes; Gq/11 proteins; PLC-,1,4 isoforms) in membrane preparations from post-mortem human prefrontal cerebral cortex collected at several stages of prenatal and postnatal development. In human prenatal brain membranes, PLC was found to be present and could be activated by calcium, but the ability of guanosine-5,-o-3 thiotriphosphate (GTP,S) or carbachol (in the presence of GTP,S) to modulate prenatal PLC-, was significantly weaker than that associated with postnatal PLC-,. Western blot analysis revealed that the levels of G,q/11 did not change significantly during development. In contrast, dramatically higher levels of expression of PLC-,1,4 isoforms and of M1, M3, and M5 muscarinic receptors were detected in the child vs. the fetal brain, a finding that might underlie the observed increased activity of PLC. Thus, inositol phosphate production may be more efficiently regulated by altering the amount of effectors (PLC-,1,4) and receptors (M1,3,5 subtypes) than by altering the level of G,q/11 subunits. These results demonstrate that different PLC isoforms are expressed in the prefrontal cortex of the developing human brain in an age-specific manner, suggesting specific roles not only in synaptic transmission but also in the differentiation and maturation of neurons in the developing brain. © 2006 Wiley-Liss, Inc. [source] | ||||||||||