Progress in brain research
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Synaptic plasticity has often been argued to play an important role in learning and memory. The discovery of long-term potentiation (LTP) and long-term depression (LTD), the two most widely cited cellular models of synaptic plasticity, significantly spurred research in this field. ⋯ In this review, we discuss a number of recent advancements in the understanding of the mechanisms that mediate LTP and LTD in the rodent hippocampus and focus on the use of subunit-specific N-methyl-d-aspartate receptor antagonists and interference peptides as potential tools to study the role of synaptic plasticity in learning and memory. By using the modulation of synaptic plasticity and hippocampal-dependent learning and memory by acute stress as an example, we review a large body of convincing evidence indicating that alterations in synaptic plasticity underlie the changes in learning and memory produced by acute stress.
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Post-traumatic stress disorder (PTSD) is a well-recognized complication of severe illness. PTSD has been described in patients after multiple trauma, burns, or myocardial infarction with a particularly high incidence in survivors of acute pulmonary failure (Acute Respiratory Distress Syndrome) or septic shock. Many patients with evidence of PTSD after critical illness have been treated in intensive care units (ICUs). ⋯ This can possibly be explained by a cortisol-induced temporary impairment in traumatic memory retrieval that has previously been demonstrated in both rats and humans. ICU therapy of critically ill patients can serve as a stress model that allows the delineation of stress hormone effects on traumatic memory and PTSD development. This could also result in new approaches for prophylaxis and treatment of stress-related disorders.
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Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, hypothyroidism, glucocorticoid and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the non-osmotic stimulation of arginine vasopressin release with upregulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. ⋯ They may involve several factors, such as impaired counter-current concentration secondary to downregulation of Na-K-2Cl co-transporter. Vasopressin-resistant downregulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.
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In primate, the M-group is a cell cluster in the rostral mesencephalon which contains premotor neurons for the levator palpebrae (LP) and upward-pulling eye muscles. It is therefore thought to play a role in lid-eye coupling during vertical saccades. To further elucidate its role, the afferents to the M-group and LP motoneurons were studied in monkeys. ⋯ This connectivity pattern supports the hypothesis that the M-group mediates lid-eye coupling during vertical upgaze, but is indirectly driven by collaterals of saccadic burst neurons in the RIMLF during lid saccades. A selective projection from the OPN area to the LP motoneurons, but not to other oculomotor neurons is reported here for the first time. The result is supported by the presence of glycinergic terminals only over LP motoneurons, and implies that a subset of OPNs may directly trigger saccade-related blinks.
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Traumatic brain injury (TBI) and traumatic spinal cord injury (SCI) are acquired when an external physical insult causes damage to the central nervous system (CNS). Functional disabilities resulting from CNS trauma are dependent upon the mode, severity, and anatomical location of the mechanical impact as well as the mechanical properties of the tissue. Although the biomechanical insult is the initiating factor in the pathophysiology of CNS trauma, the anatomical loading distribution and the resulting cellular responses are currently not well understood. ⋯ Correlation of insult parameters with cellular changes and subsequent deficits may lead to refined tolerance criteria and facilitate the development of improved protective gear. In addition, advancements in the understanding of injury biomechanics are essential for the development and interpretation of experimental studies at both the in vitro and in vivo levels and may lead to the development of new treatment approaches by determining injury mechanisms across the temporal spectrum of the injury response. Here we discuss basic concepts relevant to the biomechanics of CNS trauma, injury models used to experimentally simulate TBI and SCI, and novel multilevel approaches for improving the current understanding of primary damage mechanisms.