Imaging the Integrated Neural Network Reward Responses in
Transgenic Fragile X Rats
Social deficits and anxiety, involving abnormalities in communication and social relations, are often key features of both fragile X syndrome and autism. There is a common notion that those with autism show a lack of processing social rewards. Therefore, we hypothesized that the transgenic Fmr1 knock-out rats would display normal and or a lack of interest responses to reward stimuli. Within the study, control and Fmr1 knock-out rats were imaged, using functional magnetic resonance imaging (fMRI), for changes in BOLD signal intensity responses to the odor of almond, a stimulus to elicit an innate reward response. The BOLD signal changes had been registered into a three-dimensional reconstruction of the different brain regions making up the Papez circuit, which is the primary limbic circuitry that is involved in processing emotional experiences. However, not as expected, the odor of almond had shown a pronounced negative BOLD response, while the positive BOLD signal reduced at this time. The intense negative BOLD response, as not limited, hypothesized, to the Papez circuit, but included the basal ganglia as well. Therefore, our hypothesis had been incorrect, in the sense of the Papez circuit but proved that there is a deficit in reward processing within those with fragile X syndrome.
Fragile X syndrome is a neurodevelopmental brain disorder that is associated with an unstable expansion of a cytosine-guanine-guanine (CGG) polymorphism within the 5’-untranslated region of the Fmr1 gene that is located in the X chromosome . Based upon the number of CGG repeats, the allele may be classified as normal (5-45 repeats), intermediate or gray zone (46-54 repeats), premutation (55-199 repeats), or full mutation (more than 200 repeats) . There are some psychiatric and...