Neuroscience
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In both perceptual and motor learning, numerous studies have shown specificity of learning to the trained eye or hand and to the physical features of the task. However, generalization of learning is possible in both perceptual and motor domains. Here, I review evidence for perceptual and motor learning generalization, suggesting that generalization patterns are affected by the way in which the original memory is encoded and consolidated. ⋯ Such generalization may be supported by sleep, involving functional interactions between low and higher-order brain areas. Repeated exposure to the task may alter generalization patterns of learning and overall offline learning. Development of unifying frameworks across learning modalities and better understanding of the conditions under which learning can generalize may enable to gain insight regarding the neural mechanisms underlying procedural learning and have useful clinical implications.
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It is widely known that prenatal stress (PS) exposure causes depression-like behaviour to offspring, as well as maladaptive responses including neurobiological and physiological changes. However, the underlying mechanism of PS induced juvenile-onset depression remains largely unravelled. The inadequacies of monoamine deficiency hypothesis, the emerging evidence of altered glutamate neurotransmission in mood disorders, as well as our previous studies inspired us to assess the potential role of glutamatergic system in the pathogenesis of juvenile depression. ⋯ We also detected that PS significantly altered the expression of glutamate receptor and glutamate transporters of these depressed rats. In brief, the changes of phosphorylated GluR1 subunit of AMPAR protein level in the hippocampus and frontal cortex, as well as markedly decreased EAAT2 mRNA expression in the hippocampus, striatum and frontal cortex and EAAT3 mRNA expression in the hippocampus of stressed rats were both observed. These results underpinned that glutamate receptors and glutamate transporters might be involved in the progress of depression-like behaviour in juvenile rat offspring induced by PS.
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Postural support alters anticipatory postural adjustments (APAs). Efficient adaptation to changes in postural support in reactive and centrally initiated postural synergies is impaired in Parkinson's disease (PD). This study examined whether APAs are affected differently by familiar and novel supports in people with PD, ON and OFF levodopa. ⋯ Controls and PD patients in the OFF state further refined the postural strategy with practice as evidenced by changes in amplitude of vertical ground reaction forces and forces applied to support apparatus within conditions between the initial and final trials. In the ON state, people with PD failed to refine the use of postural supports in any condition. The results suggest that immediate postural adaptation is intact in people with PD and unaffected by levodopa administration but the ability to refine postural adaptations with task experience is compromised by dopamine therapy.
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Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE). This gas has been involved in the pain processing and insulin resistance produced during diabetes development. However, there is no evidence about its participation in the peripheral neuropathy induced by this metabolic disorder. ⋯ Paradoxically, H2S levels were decreased in nerve sciatic, dorsal root ganglion and spinal cord, but not paw nor blood plasma, during diabetes-associated peripheral neuropathy development. Collectively, results suggest that H2S synthesized by CBS and CSE participate in formalin-induced nociception in diabetic and non-diabetic rats, as well as; in tactile allodynia in streptozotocin-injected rats. In addition, data seems to indicate that diabetic rats are more sensible to H2S-induced hyperalgesia than normoglycemic rats.
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Here, we have translated from the rat to the non-human primate a unilateral lumbosacral injury as a model for cauda equina injury. In this morphological study, we have investigated retrograde effects of a unilateral L6-S2 ventral root avulsion (VRA) injury as well as the long-term effects of Wallerian degeneration on avulsed ventral roots at 6-10 months post-operatively in four adult male rhesus monkeys. Immunohistochemistry for choline acetyl transferase and glial fibrillary acidic protein demonstrated a significant loss of the majority of the axotomized motoneurons in the affected L6-S2 segments and signs of an associated astrocytic glial response within the ventral horn of the L6 and S1 spinal cord segments. ⋯ In summary, a lumbosacral VRA injury resulted in retrograde motoneuron loss and astrocytic glial activation in the ventral horn. Surprisingly, the Wallerian degeneration of motor axons in the avulsed ventral roots was followed by a repopulation of the avulsed roots by small myelinated and unmyelinated fibers. We speculate that the small axons may represent sprouting or axonal regeneration by primary afferents or autonomic fibers.