Neuroscience
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Accumulating evidence has accrued demonstrating that inflammatory processes in the central nervous system (CNS) are associated with various neurological disorders including depression. However, whether inflammation-mediated neuronal damage is involved in depression-like behaviors induced by chronic stress and, in particular, whether suppression of inflammation could then serve as a potential strategy in depression therapy remains largely unknown. The present study aimed to investigate the neuronal mechanisms and signaling pathways through which inflammation results in neuronal deterioration in a rat model of depression and thus identify agents with potential roles as antidepressant treatments. ⋯ In contrast, chronic administration of either IL-1β or nuclear factor κB (NF-κB) antagonists significantly ameliorated this dysregulation of neuronal structure and biochemical parameters such as SSH1 and phospho-cofilin within the mPFC, as well as the display of depression-like behaviors induced by CUMS exposure. More importantly, pretreatment with curcumin (40 mg/kg, i.p., 5 weeks), produced antidepressant-like actions and repressed the inflammatory responses and neuronal structural abnormalities. These findings reveal some of the molecular neuroinflammation pathways associated with depression and suggest new avenues of investigation for the development of potential antidepressant therapies in the treatment of inflammation-related neuronal deterioration in this disorder.
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This study aims to investigate the value of diffusion kurtosis imaging (DKI) in assessing microstructural changes associated with cognitive impairment in chronic traumatic brain injury (TBI). At 7 months, six TBI rats and six control rats underwent Morris water maze (MWM) tests, followed by DKI examinations. DKI parameters were measured in bilateral cortex, hippocampus, and callosum. ⋯ Further correlational study showed a positive relationship between MK and NeuN, MD and MBP in ipsilateral cortex, and a negative relationship between MK and Iba-1, MBP in ipsilateral cortex and hippocampus (P < 0.05). The MK in ipsilateral cortex and hippocampus were also correlated with MWM test results (P < 0.05). Our study suggests that DKI could be used to assess the microstructural changes associated with cognitive impairment in chronic TBI.
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Auditory-evoked potentials (AEPs) can be modified by associative learning, where the appearance of learned compensatory responses (CCRs) may result in the emergence of drug withdrawal symptoms and relapse. Although CCRs' influence on later attentive and cognitive domains has been extensively examined, contextual conditioned tolerance occurring in preattentive mechanisms operating at earlier stages of information processing has remained largely unexplored. To extend our knowledge on this subject, compensatory changes on the motor and emotional aspects of behavior evoked by contextual cues were investigated with an electronic open field in morphine-pretreated rats challenged with two morphine overdoses (40 and 80 mg/kg). ⋯ Electrophysiological data revealed increases in the amplitude of AEPs evoked in a non-familiar context. Our results indicate that behavioral learning responses emerge following Pavlovian conditioning even with the use of low and regular doses of morphine over a short-term treatment. Changes in the CIC electrophysiology may indicate that the development of drug dependence occurs covertly in the early stages of sensory information processing.
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The human brain is known by its ability to modify and update existing memories, mediated by underlying neuronal plasticity. This ability is facilitated by two main phenomena, interference and generalization. ⋯ While each of these two phenomena may be well known separately, we review recent evidence primarily in perceptual and motor skill memory, spanning synaptic, neural systems-level, and behavioral research, suggesting that although the outcomes are different, the underlying neural and behavioral processes responsible for their inducements share numerous commonalities. The reviewed literature may imply a common mechanism underlying these two phenomena, and suggests a unified framework of memory and learning in the human brain.
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The successful recovery from affective loss (i.e., bereavement, relationship breakup) has been linked to adult attachment style (AAS), a personality trait. Up to now, the association between AAS, affective loss experiences and brain gray matter volume is unclear. In 192 healthy subjects we investigated the association between MRI brain gray matter volume, applying voxel based morphometry, AAS (Relationship Scales Questionnaire (RSQ), subscales "avoidance" (AV) and "anxiety" (ANX)), and number of affective losses within the last 5 years (AL; List of Threatening Experiences Questionnaire). ⋯ In additional region-of-interest (ROI) analyses (p < 0.05 FWE-corrected), based on previously reported findings, no significant associations were observed. ANX and AV differently correlate with local volumes of the left insula and pars opercularis of the left inferior frontal gyrus, which are implicated in emotion processing, empathy and emotion regulation among other functions. Our results support the notion that individual attachment styles, which develop in the interplay of genes and social environment, differ in their correlation with brain structure.