Neuroscience
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Incorporation of a tool into the body schema is well established. Here, we assessed whether visual signals originating from the tool provide relevant cues for the perception of arm movements, as would signals originating from the arm holding it. Kinesthetic illusions were investigated by passively moving one arm (via a robotized manipulandum) and therefore the tool (a rake), using the mirror paradigm, with the reflected part being limited to the tool, the arm, or both. ⋯ Results showed that mirror vision of the moving tool was not sufficient for mirror illusions to occur, the same tool in the two hands being an essential condition. Finally, in Experiment 3, we showed that neither prior practice nor active tool use was necessary for the tool mirror illusion to occur. Altogether, these results demonstrate that the visual cues originating from the held-tool are integrated for sensing arm movement.
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Stress is a contributing factor in the etiology of several mood and anxiety disorders, and social defeat models are used to investigate the biological basis of stress-related psychopathologies. Male Syrian hamsters are highly aggressive and territorial, but after social defeat they exhibit a conditioned defeat (CD) response which is characterized by increased submissive behavior and a failure to defend their home territory against a smaller, non-aggressive intruder. Hamsters with dominant social status show increased c-Fos expression in the infralimbic (IL) cortex following social defeat and display a reduced CD response at testing compared to subordinates and controls. ⋯ Furthermore, dominants display more c-Fos-positive cells in both the IL and PL, but not vHPC, compared to subordinates. These findings suggest that dominant hamsters selectively activate IL and PL, but not vHPC, projections to the amygdala during social defeat, which may be responsible for their reduced CD response. This project extends our understanding of the neural circuits underlying resistance to social stress, which is an important step toward delineating a circuit-based approach for the prevention and treatment of stress-related psychopathologies.
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Short-term plasticity enables synaptic strength to be dynamically regulated by input timing. Excitatory synapses arising from the same axon can have profoundly different presynaptic forms of short-term plasticity onto inhibitory and excitatory neurons. We previously showed that Schaffer collateral synapses onto most hippocampal CA1 stratum radiatum interneurons have less paired-pulse facilitation than synapses onto CA1 pyramidal cells, but little difference in steady-state short-term depression. ⋯ These target-cell specific differences in short-term plasticity reduce the strength of excitatory input onto interneurons relative to pyramidal cells, and of depression interneurons relative to facilitation interneurons, during high frequency portions of the train. This occurs to a similar extent at 25 °C and at 33 °C, and is even greater at physiological extracellular calcium. Target-cell specific differences in short-term plasticity enable synapses to have different temporal filtering characteristics, which may help to dynamically regulate the balance of inhibition and excitation in CA1.
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Considerable work in recent years has examined the relationship between cortical thickness (CT) and general intelligence (IQ) in healthy individuals. It is not known whether specific IQ variables (i.e., perceptual reasoning [PIQ], verbal comprehension IQ [VIQ], and full-scale IQ [FSIQ]) are associated with multiple cortical measures (i.e., CT, cortical volume (CV), cortical surface area (CSA) and cortical gyrification (CG)) within the same individuals. Here we examined the association between these neuroimaging metrics and IQ in 56 healthy adults. ⋯ We did not observe statistically significant relationships between IQ and either CSA or CG. Our findings suggest that the neural basis of IQ extends beyond previously observed relationships with fronto-parietal regions. We also conclude that CT and CV may be more useful metrics than CSA or CG in the study of intellectual abilities.
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Anxiety disorder is a major psychiatric disorder characterized by fear, worry, and excessive rumination. However, the molecular mechanisms underlying neural plasticity and anxiety remain unclear. Here, we utilized a mouse model of anxiety-like behaviors induced by the chronic administration of corticosterone (CORT) to determine the exact mechanism of each region of the fear circuits in the anxiety disorders. ⋯ Immunoblot analyses revealed that autophosphorylation of Ca2+/calmodulin-dependent protein kinase (CaMK) IIα at threonine 286 and phosphorylation of cyclic-adenosine-monophosphate response-element-binding protein (CREB) at serine 133 were markedly increased in the BLA of chronic CORT-treated mice after tone stimulation. The protein and mRNA levels of brain-derived neurotrophic factor (BDNF) also significantly increased. Our findings suggest that increased CaMKII activity and synaptic plasticity in the BLA likely account for the aberrant amygdala-dependent fear memory in chronic CORT-treated mice.