Background: Chronic pain conditions may result from peripheral nerve injury, chronic peripheral inflammation, or sensory ganglia inflammation. However, inflammatory processes may also contribute to peripheral nerve injury responses. To isolate the contribution of local inflammation of sensory ganglia to chronic pain states, the authors previously developed a rat model in which long-lasting pain is induced by inflaming sensory ganglia without injuring the neurons. This results in prolonged mechanical pain, local increases in proinflammatory cytokines, increased neuronal hyperexcitability, and abnormal spontaneous activity.
Methods: The authors used whole cell patch clamp in acutely isolated small-diameter neurons to determine how localized inflammation (3-5 days) of L4 and L5 ganglia altered voltage-gated K+ and Na+ currents.
Results: Tetrodotoxin-sensitive Na+ currents increased twofold to threefold in neurons from inflamed ganglia. Tetrodotoxin-resistant Na+ currents increased more than twofold, but only in cells that bound isolectin B4. These increases occurred without shifts in voltage dependence of activation and inactivation. Similar results are seen in models of peripheral inflammation, except for the large magnitudes. Unlike most pain models, localized inflammation increased rather than decreased voltage-gated K+ currents, due to increased amplitudes of the sustained (delayed rectifier) and fast-inactivating transient components. The overall effect in current clamp experiments was an increase in excitability as indicated by decreased rheobase and lower action potential threshold. 相似文献
According to traditional teaching mode, the courses in preclinical medicine including pharmacology are separately run. This mode causes a series of disadvantages including loose connection between knowledge in different disciplines and weak ability to bridge basic preclinical knowledge and clinical practice. In order to overcome the disadvantages and promote the teaching efficiency, we constructed a new integrated course-Course of Basic Medical Sciences, which includes 6 traditional courses, anatomy, histology and embryology, physiology, pathology, pathophysiology and pharmacology. We integrated these courses based on the human organ systems and according to the principle-" From macro to micro, From morphological to functional, From normal to abnormal and From disease to drug therapy" and published the series of textbook in 2004. The contents of pharmacology are taught just after pathology and pathophysiology in every organ system. In comparison with the traditional teaching mode, teachers of pharmacology need not spend a lot of time to review preceding knowledge of anatomy and histology, physiology, pathophysiology and pathology. This is helpful in saving time and improving the teaching efficiency. 相似文献