Neuroscience
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Intrauterine growth restriction (IUGR) associates with increased preference for palatable foods and altered insulin sensitivity. Insulin modulates the central dopaminergic response and changes behavioral responses to reward. We measured the release of dopamine in the accumbens during palatable food intake in IUGR rats both at baseline and in response to insulin. ⋯ FR rats showed metabolic alterations and a delay in the dopaminergic response to palatable foods. This could explain the increased palatable food intake and behavioral entropy found in FR rats. IUGR may lead to binge eating, obesity and its metabolic consequences by modifying the central dopaminergic response to sweet food.
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Lactating female mice nurture their pups and attack intruders in their territory. When an intruder invades a dam's territory, she needs to switch her behavior from care to aggression to protect her pups and territory. Although the neuronal mechanisms underlying each distinct behavior have been studied, it is unclear how these behaviors are displayed alternatively. ⋯ Injections of N-methyl-d-aspartic acid (NMDA) receptor antagonists or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonists into the DRN inhibited biting behavior but not nurturing behavior. In contrast, injections of NMDA or AMPA into the DRN inhibited nurturing behavior. These results suggest that glutamatergic signals in the DRN, which may originate from the mPFC and/or LHb, regulate the preferential display of biting behavior over nurturing behavior in dams.
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Alterations in central extended amygdala (EAc) function have been linked to anxiety, depression, and anxious temperament (AT), the early-life risk to develop these disorders. The EAc is composed of the central nucleus of the amygdala (Ce), the bed nucleus of the stria terminalis (BST), and the sublenticular extended amygdala (SLEA). Using a non-human primate model of AT and multimodal neuroimaging, the Ce and the BST were identified as key AT-related regions. ⋯ Triple-labeling immunofluorescence staining revealed that SST protein-expressing cell bodies are a small proportion of the total CeL and BSTL neurons and have considerable co-labeling with CRF. The SLEA exhibited strong SST mRNA and protein expression, suggesting a role for SST in mediating information transfer between the CeL and BSTL. These data provide the foundation for mechanistic non-human primate studies focused on understanding EAc function in neuropsychiatric disorders.
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Since the first report of noise-induced synaptic damage in animals without permanent threshold shifts (PTSs), the concept of noise-induced hidden hearing loss (NIHHL) has been proposed to cover the functional deficits in hearing associated with noise-induced synaptopathy. Moreover, the potential functional deficit associated with the noise-induced synaptopathy has been largely attributed to the loss of auditory nerve fibers (ANFs) with a low spontaneous spike rate (SSR). As this group of ANFs is critical for coding at suprathreshold levels and in noisy background, coding-in-noise deficit (CIND) has been considered to be main consequence of the synaptopathy. ⋯ However, no such reduction was seen in the scalp-recorded envelope following response (EFR), suggesting a compensation due to increased central gain. Moreover, there was no significant difference in masking effect between the control and noise groups. The results suggest that either there is no significant CIND after the synaptopathy we created, or the AM response tested with our protocol was not sufficiently sensitive to detect such a deficit; far-field EFR is not sensitive to cochlear pathology.
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Motor neuron damage caused by diseases, traumatic insults or de-afferentation of the spinal cord is often incurable due to the poor intrinsic regenerative capacity. Moreover, regenerated peripheral nerves often do not reach normal functionality. Here, we investigated cardiolipin in the process of neuro-differentiation, since cardiolipin is closely linked to the mitochondrial energy supply in cells. ⋯ The positive correlation between neuro-differentiation and concentration of those molecular cardiolipin species containing palmitic and oleic acid implied a link between differentiation of NSC-34 cells and cardiolipin metabolism. We further demonstrated the impact of cellular lipid metabolism, and particularly cardiolipin metabolism, during and NSC-34 neuritogenesis. Thus, cardiolipin may represent a new therapeutic target for axon regeneration after peripheral nerve injuries or when axon sprouting is required to compensate for motor neuron loss in response to aging and/or disease.