National Institute for Medical Research, London, UK.
Clinics (Sao Paulo). 2011;66 Suppl 1(Suppl 1):3-17. doi: 10.1590/s1807-59322011001300002.
Long-term potentiation and long-term depression are enduring changes in synaptic strength, induced by specific patterns of synaptic activity, that have received much attention as cellular models of information storage in the central nervous system. Work in a number of brain regions, from the spinal cord to the cerebral cortex, and in many animal species, ranging from invertebrates to humans, has demonstrated a reliable capacity for chemical synapses to undergo lasting changes in efficacy in response to a variety of induction protocols. In addition to their physiological relevance, long-term potentiation and depression may have important clinical applications. A growing insight into the molecular mechanisms underlying these processes, and technological advances in non-invasive manipulation of brain activity, now puts us at the threshold of harnessing long-term potentiation and depression and other forms of synaptic, cellular and circuit plasticity to manipulate synaptic strength in the human nervous system. Drugs may be used to erase or treat pathological synaptic states and non-invasive stimulation devices may be used to artificially induce synaptic plasticity to ameliorate conditions arising from disrupted synaptic drive. These approaches hold promise for the treatment of a variety of neurological conditions, including neuropathic pain, epilepsy, depression, amblyopia, tinnitus and stroke.
长时程增强和长时程压抑是突触强度的持久变化，由特定的突触活动模式诱导，它们作为中枢神经系统信息存储的细胞模型受到了广泛关注。许多脑区的研究，从脊髓到大脑皮层，以及许多动物物种，从无脊椎动物到人类，都证明了化学突触具有可靠的能力，可以根据各种诱导方案对功效进行持久的改变。除了具有生理相关性外，长时程增强和压抑可能具有重要的临床应用。对这些过程的分子机制的深入了解，以及对大脑活动的非侵入性操纵的技术进步，使我们处于利用长时程增强和压抑以及其他形式的突触、细胞和电路可塑性来操纵人类神经系统中突触强度的门槛。药物可用于消除或治疗病理性突触状态，非侵入性刺激设备可用于人工诱导突触可塑性，以改善因突触驱动中断而产生的状况。这些方法有望治疗多种神经疾病，包括神经病理性疼痛、癫痫、抑郁、弱视、耳鸣和中风。
