THIS JUST IN PSYCHOLOGY Reviewed by Term meta View Psychology RELATIONSHIPS Reviewed by Term meta View Relationships SELF CARE Reviewed by Term meta View All Self Care Explore by CATEGORY Dating Tips Emotions A-Level Psychology
Combining magnetic properties relied on in traditional Chinese medicine with contemporary knowledge about the gut microbiome, researchers have developed a novel oral treatment to prevent and repair hearing loss caused by noise exposure.
Learn about the nervous system - central nervous system and peripheral nervous system function. What are common nervous system diseases.
Interactions between central glial cells and neurons in the pain circuitry are critical contributors to the pathogenesis of chronic pain. In the central nervous system (CNS), two major glial cell types predominate: astrocytes and microglia. Injuries or pathological conditions which evoke pain are concurrently associated with the presence of a reactive microglia or astrocyte state, which is characterized by a variety of changes in the morphological, molecular, and functional properties of these cells. In this review, we highlight the changes that reactive microglia and astrocytes undergo following painful injuries and insults and discuss the critical and interactive role these two cell types play in the initiation and maintenance of chronic pain. Additionally, we focus on several crucial mechanisms by which microglia and astrocytes contribute to chronic pain and provide commentary on the therapeutic promise of targeting these pathways. In particular, we discuss how the inflammasome in activated microglia drives maturation and release of key pro-inflammatory cytokines, which drive pain through neuronal- and glial regulations. Moreover, we highlight several potentially-druggable hemichannels and proteases produced by reactive microglia and astrocytes in pain states and discuss how these pathways regulate distinct phases during pain pathogenesis. We also review two emerging areas in chronic pain research: 1) sexually dimorphic glial cell signaling and 2) the role of oligodendrocytes. Finally, we highlight important considerations for potential pain therapeutics targeting glial cell mediators as well as questions that remain in our conceptual understanding of glial cell activation in pain states.
Beim JetPeel schleusen wir mit einem hochfokussierten Wasserstrahl hochwirksame Seren unter die Haut ein. Wissenschaftlich bewiesene Wirkung.
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MYELINATION OF CNS AND PNS AXONS Central myelination of axons is provided by oligodendroglia. Each oligodendroglial cell can myelinate a single segment of several separate central axons. In the PNS, sensory, motor, and preganglionic autonomic axons are myelinated by Schwann cells. A Schwann cell myelinates only a single segment of one axon. Unmyelinated sensory and autonomic postganglionic autonomic axons are ensheathed by a Schwann cell, which provides a single enwrapping arm of cytoplasm around each of several such axons. The space between adjacent myelin segments of an axon is called a node of Ranvier; this site of axon membrane contains sodium channels and allows the reinitiation of action potentials in the course of propagation down the axon, a process called saltatory conduction. CLINICAL POINT The integrity of the myelin sheath is essential for proper neuronal function in both the CNS and the PNS. Disruption of the myelin sheath around axons in either system results in the inability of the formerly myelinated axons to carry out their functional activities. In the CNS, the myelin sheath of central axons can be attacked in an autoimmune disease such as multiple sclerosis, resulting in a variety of symptoms, such as blindness, diplopia caused by discoordinated eye movements, loss of sensation, loss of coordination, paresis, and others. This condition may occur episodically, with intermittent remyelination occurring as the result of oligodendroglia proliferation and remyelination. In the PNS, a wide variety of insults, including exposure to toxins and the presence of diabetes or autoimmune Guillain-Barré syndrome, result in peripheral axonal demyelination, which is manifested mainly as sensory loss and paralysis or weakness. Remyelination also can occur around peripheral axons, initiated by the Schwann cells. Clinically, the status of axonal conduction is assessed by examining sensory evoked potentials in the CNS and by conduction velocity studies in the PNS.
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Emotion, Motivation And Drug Addiction Emotion Initial attempts to understand the brain bases of emotions focused on the limbic system (see Chapter 45), with the amygdala as the key component in the system thought to be central to emotional processing. The evidence to support such an association has already been discussed in part (in Chapter 45), but it is also worth mentioning the Klüver–Bucy syndrome. This condition is seen with bilateral amygdala damage and is characterized by, among other phenomena, an apparent absence of the normal fear response and by marked placidity. In addition, functional neuroimaging studies in humans have been consistent with animal studies, implicating the amygdala in the processing of emotional stimuli and, notably, in fear conditioning (wherein a previously neutral stimulus can, through association with an unpleasant outcome, produce a fear response when presented alone). It is proposed that the amygdala is the critical site in which: the necessary associations between the stimuli are formed using a process akin to the long-term potentiation (LTP) seen in the hippocampus (see Chapter 45); and the origin of the broad series of phenomena that constitute a fear response through its efferent projections. Motivation Emotions are potentially useful in that they are allied with, and perhaps consist of, behavioural responses. They may be critical in helping us choose between competing behavioural possibilities and to guide behaviours that maximize rewarding and minimize punishing outcomes. The relationship between emotion and motivation is therefore an important one. In this respect, the dopamine systems, most notably the mesolimbic system (see also Chapters 19 and 58), which has connections with the amygdala, appear critical. A series of hypotheses have been put forward concerning the dopaminergic contribution to motivation. · Hedonia hypothesis: whilst dopamine has been thought to be critical to the experience of pleasure. There is increasing evidence against this view. · Learning hypothesis: dopamine is critical to learning the relationship between stimuli and rewards. Dopamine acts as a ‘teaching signal’ for stimuli that predict rewards and thus is the origin of behaviour that makes the reward manifest. · Activation hypothesis: dopamine is required for the actual engagement in work that must be done to obtain the reward. It is important for both the attentional and the locomotor components of the work involved in reward-seeking and consumption. · Incentive salience: dopamine is important in imbuing certain stimuli with motivational or incentive properties. It would be simplistic to express motivational processes solely in terms of the input of the mesolimbic dopamine system to the amygdala but it is nevertheless a useful model by which to explain drug addiction. In addition to the motivational properties of specific stimuli, in many circumstances we must consider motivational states that appear stimulus independent. Feeding behaviours, for example, arise not solely from the motivational properties of foods (sight, smell, taste) but also from a drive state (hunger) dependent on a number of homeostatic factors, for example endocrine signals (levels of insulin, and of the hormones leptin and ghrelin which, respectively, reduce and promote feeding behaviour) acting predominantly through the hypothalamus (see Chapter 11). A comprehensive description of a motivational state would require several levels of description together with an understanding of the interactions inherent in the state; for example, the extent to which motivational properties of stimuli themselves influence, and/or are influenced by, the drive state of the individual. An additional, important concern is when individuals are motivated towards behaviours that are at odds with their homeostatic requirements and consequently detrimental to health, as is the case with addictive behaviours. Drug addiction Using some recreational drugs can be rewarding, but the evidence is that addictive behaviours (and associated withdrawal phenomena) are determined by how the brain adapts in response to repeated drug administration rather than as a direct result of the fact that drugs may be intensely pleasurable. Conversely, although the reward properties of the drug are insufficient to explain addictive behaviours, it is simplistic, too, to consider addiction solely as behaviours aimed towards avoiding withdrawal symptoms. In addition to considering addiction in terms of the pursuit of pleasurable states (drug-induced euphoria) or the avoidance of withdrawal states (an array of physical and psychological symptoms which may actually be produced simply by a stimulus or environment that has become associated with previous withdrawal), we must also take into account what may be considered a markedly augmented state of motivation to taking the drug – referred to as craving. Important in this respect is the fact that a craving may be precipitated by a drug-related stimulus or environment long after the individual has recovered from the withdrawal symptoms. Other important phenomena that need to be explained are tolerance (a requirement for increased frequency and/or dose of the drug with repeated usage) and sensitization (in contrast to tolerance effects, some of the consequences of the drug may actually increase with repeated ingestion). Interestingly, neither tolerance nor sensitization are explicable in purely pharmacological terms because both phenomena also show certain features suggesting that they are conditioned responses. One view that has been put forward to account for the simultaneous occurrence of tolerance and sensitization is that while the pleasurable effects of the drug diminish with repeated administration (leading to tolerance), the drug and related environments and paraphernalia become, over time, more likely to capture attention and to precipitate the associated behaviours (sensitization). While the neurobiological basis of drug addiction is still not fully understood, there is increasing evidence that it involves mesolimbic dopamine systems and genetic susceptibilities, which may in turn affect the normal functioning of this pharmacological system. An example of this is the recent recognition that some patients with Parkinson’s disease develop abnormal behaviours with their dopaminergic therapies–the so-called dopamine dysregulation syndrome which can involve pathological gambling and hypersexuality.
The bacteriophage is the deadliest being on earth, specialized in killing bacteria. On the October page of the 12,023 calendar is a phage attacking an E.Coli bacterium. As antibiotic-resistant bacteria are a major threat to us, phages could become our allies in fighting them.