Neuroscience
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Kainic acid (KA), an analogue of the excitatory neurotransmitter glutamate, when administered systemically can trigger seizures and neuronal loss in a manner that mirrors the neuropathology of human mesial temporal lobe epilepsy (mTLE), which affects ∼50 million people globally. Evidence suggests that changes in astrocytes which precede neuronal damage play an important role in the degeneration of neurons and/or development of seizures in TLE pathogenesis. Additionally, a role for microtubule associated tau protein, involved in various neurodegenerative diseases including Alzheimer's disease, has also been suggested in the development of seizure and/or neurodegeneration in TLE pathogenesis. ⋯ Concurrently, the total (Tau1 and Tau5) and phospho-tau (AT270 and PHF1) levels are transiently enhanced following KA administration. Furthermore, the level/expression of cleaved-tau, which is apparent in a subset of GFAP-, S100B- and A2-positive astrocytes, are increased in KA-treated rats. These results, taken together, suggest a differential role for various astrocytic subpopulations and tau protein in the development of seizure and/or loss of neurons in KA model of TLE and possibly in human mTLE pathogenesis.
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The unpredictable chronic mild stress (UCMS) model has been used to induce depressive-like symptoms in animal models, showing adequate predictive validity. Our work aims to evaluate the effects of environmental enrichment (EE) on resilience in this experimental model of depression. We also aim to assess changes in brain connectivity using cytochrome c oxidase histochemistry in cerebral regions related to cognitive-affective processes associated with depressive disorder: dorsal hippocampus, prefrontal cortex, amygdala, accumbens, and habenula nuclei. ⋯ EE induced a functional reorganization of brain activity. The EE + UCMS and UCMS groups showed different patterns of connections between brain regions. Our results showed that EE favors greater resilience and could reduce vulnerability to disorders such as depression and anxiety, modifying metabolic brain activity.
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There are numerous clinical reports that youth with cerebral palsy (CP) have proprioceptive, stereognosis and tactile discrimination deficits. The growing consensus is that the altered perceptions in this population are attributable to aberrant somatosensory cortical activity seen during stimulus processing. It has been inferred from these results that youth with CP likely do not adequately process ongoing sensory feedback during motor performance. ⋯ Furthermore, the strength of the somatosensory cortical responses during the passive condition were positively associated with the strength of somatosensory cortical responses during the haptic condition (r = 0.75, P = 0.004). This indicates that the aberrant somatosensory cortical responses seen in youth with CP during rest are a good predictor of the extent of somatosensory cortical dysfunction during the performance of motor actions. These data provide novel evidence that aberrations in somatosensory cortical function in youth with CP likely contribute to the difficulties in sensorimotor integration and the ability to effectively plan and execute motor actions.