Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]....Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor （BDNF） [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] （Fig. 1C）. To determine the rela- tionship between the gliogenic LTP and high frequency stimulation （HFS）-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP （Fig. 1A）. Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP （Fig. 1B）.展开更多
文摘Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor （BDNF） [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] （Fig. 1C）. To determine the rela- tionship between the gliogenic LTP and high frequency stimulation （HFS）-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP （Fig. 1A）. Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP （Fig. 1B）.
