Synaptic basis for whisker deprivation- induced synaptic depression in rat somatosensory cortex
Synaptic basis for whisker deprivation- induced synaptic depression in rat somatosensory cortex
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DOI:
10.1523/jneurosci.0175-06.2006
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发表时间:
2006-04-19
影响因子:
5.3
通讯作者:
Feldman, DE
中科院分区:
文献类型:
--
作者:
Bender, KJ;Allen, CB;Feldman, DE
Whisker deprivation weakens excitatory layer 4 (L4) inputs to L2/3 pyramidal cells in rat primary somatosensory (S1) cortex, which is likely to contribute to whisker map plasticity. This weakening has been proposed to represent long- term depression (LTD) induced by sensory deprivation in vivo. Here, we studied the synaptic expression mechanisms for deprivation- induced weakening of L4-L2/3 inputs and assessed its similarity to LTD, which is known to be expressed presynaptically at L4-L2/3 synapses. Whisker deprivation increased the paired pulse ratio at L4-L2/3 synapses and slowed the use- dependent block of NMDA receptor currents by MK- 801[(5S, 10R)-(+)-5methyl-10,11- dihydro-5H- dibenzo[a, d] cyclohepten-5,10- imine maleate], indicating that deprivation reduced transmitter release probability at these synapses. In contrast, deprivation did not alter either miniature EPSC amplitude in L2/3 neurons or the amplitude of quantal L4-L2/3 synaptic responses measured in strontium, indicating that postsynaptic responsiveness was unchanged. In young postnatal day 12 (P12) rats, at least 4 d of deprivation were required to significantly weaken L4-L2/3 synapses. Similar weakening occurred when deprivation began at older ages ( P20), when synapses are mostly mature, indicating that weakening is unlikely to represent a failure of synaptic maturation but instead represents a reduction in the strength of existing synapses. Thus, whisker deprivation weakens L4-L2/3 synapses by decreasing presynaptic function, similar to known LTD mechanisms at this synapse.