Neuroscience
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Affective disorders (i.e. anxiety and depression) are commonly observed in patients with epilepsy and induce seizure aggravation. Animal models of epilepsy that exhibit affective disorder features are essential in developing new neuromodulatory treatments. GEAS-W rats (Generalized Epilepsy with Absence Seizures, Wistar background) are an inbred model of generalized epilepsy showing spontaneous spike-wave discharges concomitant with immobility. ⋯ We observed a main effect of treatment and a significant treatment by strain interaction on anxiety-like and depressive-like behaviours, with active-tDCS GEAS-W rats entering the center of the open field more often and showing less immobility in the forced swimming test. Furthermore, there was a main effect of treatment on corticosterone with active-tDCS animals showing marked reduction in plasmatic levels. This study described preclinical evidence to support tDCS treatment of affective disorders in epilepsy and highlights corticosterone as a possible mechanism of action.
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Spectrotemporal integration is a key function of our auditory system for discriminating spectrotemporally complex sounds, such as words. Response latency in the auditory cortex is known to change with the millisecond time-scale depending on acoustic parameters, such as sound frequency and intensity. The functional significance of the millisecond-range latency difference in the integration remains unclear. ⋯ The nonlinear effect measured in the high-frequency region of the A1 linearly changed depending on the millisecond difference of the response onset-times, which were estimated from the spatially-local response latencies and spectral onset-times. In contrast, the low-frequency region of the A1 had no significant sensitivity to the millisecond difference. The millisecond-range latency difference may have functional significance in the spectrotemporal integration with the millisecond time-scale sensitivity at the high-frequency region of A1 but not at the low-frequency region.
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The role of normal sensory inputs in the development of sensory cortices is well known, however, their impacts on the hippocampus, an integrator of sensory modalities with important roles in cognitive functions, has received much less attention. Here, we applied a long-term sensory deprivation paradigm by trimming the rats' whiskers bilaterally, from postnatal day 3 to 59. Female sensory-deprived (SD) rats showed more on-wall rearing and visits to the center of the open-field box, shorter periods of grooming, less defecation and less anxiety-like behaviors in the elevated plus-maze compared to controls, who had their intact whiskers brushed. ⋯ Sholl analysis of CA3 neurons in SD animals also disclosed significantly more branched apical dendrites in males and basal dendrites in females. Sensory deprivation also led to a considerable spine loss and variation of different spine types in a sex-dependent manner. Our findings suggest that experience-dependent structural plasticity is capable of spreading far beyond the manipulated sensory zones and the inevitable functional alterations can be expressed in a multifactorial sex-dependent manner.
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Obesity and depression tend to co-occur, and obese patients with chronic low-grade inflammation have a higher risk of developing depression. However, mechanisms explaining these connections have not been fully elucidated. Here, an animal model of comorbid obesity and depression induced by high-fat diet (HFD) combined with chronic unpredictable mild stress (CUMS) was used, and sucrose preference, open field, elevated plus maze and Morris water maze tests were used to detected depression-and anxiety-like behaviors and spatial memory. ⋯ The HFD and CUMS alone and combination of them increased levels of IL-1β, IL-6 and TNF-α in the hippocampus and prefrontal cortex, which was significantly related to depression-like behaviors. Further, NF-κB protein and mRNA levels and microglial activation in the hippocampus and prefrontal cortex significantly increased in stressed, obese and comorbid groups, with animals in comorbid group having the highest NF-κB mRNA levels in the hippocampus and level of NF-κB proteins in the prefrontal cortex, and the highest microglial activation in both brain areas. The study concluded that HFD and CUMS alone and combination induce depression-like symptoms, abnormal serum lipid levels, microglial activation and increased inflammatory cytokines in the brain, effects that are possibly mediated by TLR4-NF-κB signaling.