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Long-term memory is believed to depend on long-lasting changes in the strength of synaptic transmission known as synaptic plasticity. Understanding the molecular mechanisms of long-term synaptic plasticity is one of the principle goals of neuroscience. Among the most powerful tools being brought to bear on this question are genetically modified mice with changes in the expression or biological activity of genes thought to contribute to these processes. This article reviews how strains of mice with alterations in the cyclic adenosine monophosphate/protein kinase A/cyclic adenosine monophosphate-response element-binding protein signaling pathway have advanced our understanding of the biological basis of learning and memory.
This chapter discusses traditional metabolic genes that contribute to sleep regulation as well as candidate genes that may govern the systems independently. Inadequate sleep simultaneously modulates the level of multiple hormones that govern metabolism. In general, with sleep deprivation, the following hormones are decreased: insulin, growth hormone (GH), growth hormone releasing hormone (GHRH), and leptin levels. Even though starvation appears to confer fewer detrimental effects with extended waking than sleep deprivation, this response may come with consequences of its own. There are increasing number of proteins that affect sleep and metabolism, but are not classical metabolic genes. One class of genes that links metabolism and sleep is the circadian rhythm genes. It is interesting to note how often the effect of sleep deprivation invokes a starvation-like response from the body and how a starvation or a starvation-like state results in decreased sleep.
This chapter focuses on the biologically driven strategies that are being developed to enhance that recovery following neural injury. It is beyond the scope of this chapter to review the entire field of neurologic rehabilitation, much of which involves orthotic, prosthetic, behavioural, psychological and sociological approaches. Many of these approaches are accumulating substantial evidence for their effectiveness and their omission here should not be interpreted as an indication of lack of importance. Several recent monographs on neurologic rehabilitation cover them in greater detail (Dobkin, 1996; Lazar, 1998; Ozer, 2000). Here, the behavioural, physiological and structural mechanisms by which the nervous system adapts spontaneously to injury will be reviewed. Then some promising current approaches to optimizing recovery by utilizing the nervous system's own adaptive processes will be discussed. Finally the mechanisms that limit the ability of the nervous system to reconstitute the lost neural circuitry will be examined, and strategies that are being developed to overcome these limitations will be summarized.
Mechanisms of spontaneous recovery
Following injury to the nervous system, it is usual for patients to recover to a variable degree. This is a consequence of three processes. First, depending on the type of injury, an ischemic/traumatic penumbra (Heiss & Graf, 1994; Tator, 1995) results in temporary dysfunction of neuronal elements due to pressure from edema, excitotoxicity with intracellular (intramitochondrial) calcium accumulation (Stout et al., 1998), extracellular accumulation of potassium and magnesium, and inflammation (Carlson et al., 1998) (Fig. 6.1). If they do not kill the neurons, these changes eventually resolve and neuronal function is restored. Secondly, patients can employ a variety of behavioural adaptations to restore equivalent functions to those lost as a consequence of the structural and physiological alterations brought about by the injury. Thirdly, physiological changes and short distance anatomic rearrangements in spared neural pathways may result in compensatory enhancement in transmission through those pathways to reproduce or substitute for lost functions. A fourth mechanism, frank regeneration of injured axons and replacement of lost neurons to reconstitute the interrupted synaptic circuits, is currently believed not to occur to a significant degree in the mammalian CNS. Strategies to promote such neural repair are discussed later in the chapter.
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