Otis T, Zhang S, Trussell L O
Department of Neurophysiology, University of Wisconsin, Madison 53706, USA.
J Neurosci. 1996 Dec 1;16(23):7496-504. doi: 10.1523/JNEUROSCI.16-23-07496.1996.
Although almost all ionotropic neurotransmitter receptors undergo desensitization, the onset and recovery of desensitization at a synapse have never been observed directly. We have found changes in postsynaptic AMPA receptor sensitivity in neurons of the chick cochlear nucleus, the nucleus magnocellularis (nMAG), by photolysis of caged glutamate immediately after activation of a single synaptic input. Additionally, synaptic desensitization was demonstrated via competition between synaptically released glutamate and an exogenous nondesensitizing agonist, kainate. Both approaches indicated that at least 35-40% of the receptors were desensitized after a single synaptic stimulus. Miniature synaptic currents were depressed after an evoked synaptic current, indicating that desensitization led to a reduction in the response to individual transmitter quanta. Stimulation of adjacent glutamatergic inputs to the same cell demonstrated that nearby terminals did not depress one another, suggesting that the desensitizing level of glutamate is restricted to each axon terminal. These findings confirm that postsynaptic neurons may use desensitization to regulate the strength of transmission on a synapse-specific basis.
尽管几乎所有离子型神经递质受体都会发生脱敏，但在突触处脱敏的起始和恢复从未被直接观察到。我们通过在激活单个突触输入后立即光解笼锁型谷氨酸，发现了鸡耳蜗核大细胞神经元（nMAG）中突触后AMPA受体敏感性的变化。此外，通过突触释放的谷氨酸与外源性非脱敏激动剂 kainate 之间的竞争证明了突触脱敏。两种方法均表明，单次突触刺激后至少35 - 40%的受体发生了脱敏。诱发的突触电流后，微小突触电流受到抑制，表明脱敏导致对单个递质量子的反应降低。对同一细胞相邻谷氨酸能输入的刺激表明，附近的终末彼此之间不会相互抑制，这表明谷氨酸的脱敏水平仅限于每个轴突终末。这些发现证实，突触后神经元可能利用脱敏在突触特异性基础上调节传递强度。
