Neuroscience
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An absence of reward in chronic stress may impair the reward circuit in the brain, resulting in major depressive disorder (MDD). In a part of chronically stressed individuals, MDD is not present, i.e., there is resilience, implying endogenous anti-depressive mechanisms in the brain. We studied social defeat model mice and analyzed the mRNA maps of the hippocampus from a control group and social defeat (SD)-susceptible and SD-resilient mice using high-throughput sequencing techniques. ⋯ In our study, minocycline inhibited the activation of microglia, thereby improving the depressive state of CSDS mice. In addition, minocycline combined with fluoxetine enhanced the efficacy of fluoxetine. Thus, our results propose the most probable mechanism underlying different responses to CSDS and indicate the potential of a combination of anti-inflammatory drugs and antidepressants in treating refractory depression.
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Predictions of incoming words performed during reading have an impact on how the reader moves their eyes and on the electrical brain potentials. Eye tracking (ET) experiments show that less predictable words are fixated for longer periods of times. Electroencephalography (EEG) experiments show that these words elicit a more negative potential around 400 ms (N400) after the word onset when reading one word at a time (foveated reading). ⋯ Our results show that the N400 potential disappear when the reader recognises the sentence. Furthermore, time-frequency analyses show a larger alpha lateralisation and a beta power increase for memory-encoded sentences. This suggests a more distributed attention and an active maintenance of the cognitive set, in concordance to the predictive coding framework.
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Abnormal N-methyl-D-aspartate receptor (NMDAr) function has been linked to oscillopathies, psychosis, and cognitive dysfunction in schizophrenia (SCZ). Here, we investigate the role of NMDAr hypofunction in pathological oscillations and behavior. We implanted mice with tetrodes in the dorsal/intermediate hippocampus and medial prefrontal cortex (mPFC), administered the NMDAr antagonist MK-801, and recorded oscillations during spontaneous exploration in an open field and in the y-maze spatial working memory test. ⋯ In the mPFC, MK-801 increased the power of theta and gamma, generated high-frequency oscillations (HFO 155-185 Hz), and disrupted theta/gamma coupling. Moreover, the performance of mice in the spatial working memory version of the y-maze was strongly correlated with CA1-PFC theta/gamma co-modulation. Thus, theta/gamma mediated by NMDAr function might explain several of SCZ's cognitive symptoms and might be crucial to explaining hippocampal-PFC interaction.
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The present study aimed to investigate the relationship between olfactory sulcus (OS) depth and olfactory function considering age and gender and to provide normative data on OS depth in a population with normal olfactory function. ⋯ Considering the limited resolution of the presently used T1 weighted MR scans and the nature of the olfactory screening test, OS depth explained only minor portions of the variance of olfactory function, which was largely determined by age. Age-related normative data of OS depth are presented as a reference for future work.
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Neonatal pain experiences including traumatic injury influence negatively on development of nociceptive circuits, resulting in persistent pain hypersensitivity in adults. However, the detailed mechanism is not yet well understood. In the present study, to clarify the pathogenesis of orofacial pain hypersensitivity associated with neonatal injury, the involvement of the voltage-gated sodium channel (Nav) 1.8 and the C-C chemokine ligand 2 (CCL2)/C-C chemokine receptor 2 (CCR2) signaling in the trigeminal ganglion (TG) in facial skin incisional pain hypersensitivity was examined in 190 neonatal facial-injured and sham male rats. ⋯ Blockages of Nav1.8 in the incised region and CCR2 in the TG suppressed the enhancement of mechanical hypersensitivity in the Incision-Incision group. Administration of CCL2 into the TG enhanced mechanical hypersensitivity in the Sham-Sham, Incision-Sham and Sham-Incision group. Our results suggest that neonatal facial injury accelerates the TG neuronal hyperexcitability following orofacial skin injury in adult in association with Nav1.8 overexpression via CCL2 signaling, resulting in the enhancement of orofacial incisional pain hypersensitivity in the adulthood.