Neuroscience
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Ocular dominance has been extensively studied, often with the goal to understand neuroplasticity, which is a key characteristic within the critical period. Recent work on monocular deprivation, however, demonstrates residual neuroplasticity in the adult visual cortex. After deprivation of patterned inputs by monocular patching, the patched eye becomes more dominant. ⋯ However, binocular rivalry reflects the result of direct interocular competition that strongly weights the contour information transmitted along each monocular pathway. Monocular phase deprivation may not change the weights in the integration (fusion) mechanism much, but alters the balance in the rivalry (competition) mechanism. Our work suggests that ocular dominance plasticity may occur at different stages of visual processing, and that homeostatic compensation also occurs for the lack of phase regularity in natural scenes.
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Striatal-enriched phosphatase 61 (STEP61) is a member of intracellular protein tyrosine phosphatases, which is involved in the regulation of synaptic plasticity and a line of neuropsychiatric disorders. This protein tyrosine phosphatase is also abundant in pain-related spinal cord dorsal horn neurons. However, whether and how this tyrosine phosphatase modulates the nociceptive plasticity and behavioral hypersensitivity remain largely unknown. ⋯ To reinstate STEP61 activity, we overexpressed wild-type STEP61 [STEP61(WT)] in spinal dorsal horn, finding that STEP61(WT) completely blunted LTP induction. Behavioral tests showed that LTP blockade by STEP61(WT) correlated with a long-lasting alleviation of thermal hypersensitivity and mechanical allodynia induced by chronic constriction injury of sciatic nerves. These data implicated that STEP61 exerted a negative control over spinal nociceptive plasticity, which might have therapeutic benefit in pathological pain.
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Premature or ill full-term infants are subject to a number of noxious procedures as part of their necessary medical care. Although we know that human infants show neural changes in response to such procedures, we know little of the sensory or affective brain circuitry activated by pain. In rodent models, the focus has been on spinal cord and, more recently, midbrain and medulla. ⋯ Formalin induced the oft-reported biphasic response at this age and induced a conditioned aversion to cues associated with its injection, thus demonstrating the aversiveness of the stimulation. Morphometric analyses, structural equation modeling and co-expression analysis showed that limbic and sensory paths were activated, the most prominent of which were the prefrontal and anterior cingulate cortices, nucleus accumbens, amygdala, hypothalamus, several brainstem structures, and the cerebellum. Therefore, both sensory and affective circuits, which are activated by pain in the adult, can also be activated by noxious stimulation in 12-day-old rat pups.
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Since Ebbinghaus' classical work on oblivion and saving effects, we know that declarative memories may become at first spontaneously irretrievable and only subsequently completely extinguished. Recently, this time-dependent path toward memory-trace loss has been shown to correlate with different patterns of brain activation. Environmental enrichment (EE) enhances learning and memory and affects system memory consolidation. ⋯ At day 21 SC mice do not show preferential exploration of novel object, irrespective of the retraining, while EE mice are still capable to benefit from retraining, even if they were not able to spontaneously recover the trace. Analysis of c-fos expression 20days after learning shows a different pattern of active brain areas in response to the retraining session in EE and SC mice, with SC mice recruiting the same brain network as naïve SC or EE mice following de novo learning. This suggests that EE promotes formation of longer lasting object recognition memory, allowing a longer time window during which saving is present.
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Few minutes of focal vibration (FV) on limb muscles can improve motor control in neurological (stroke, Parkinson) patients for unknown underlying neurophysiological mechanisms. Here we hypothesized that in healthy volunteers this FV would increase excitability in the primary sensorimotor cortex (S1-M1) during an isometric contraction of the stimulated muscle. The design included an initial control condition with no FV stimulation (Baseline) as well as three short experimental sessions of FV and a Sham (fake) session in a pseudo-random order. ⋯ Results showed that, compared to the Baseline (no FV) or Sham stimulation, the first two FV sessions showed a cumulative increase in alpha (but not beta) MRPD at C3 electrode, suggesting a specific effect of vibration on the excitability of contralateral S1-M1 generating EEG "mu" rhythms. FV over limb muscles modulates neurophysiological oscillations enhancing excitability of contralateral S1-M1 in healthy volunteers. The proposed mechanism may explain the clinical effects of vibratory rehabilitation in neurological patients with motor deficits.