Sáez Ignacio, Friedlander Michael J
Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
J Neurosci. 2009 Dec 2;29(48):15286-98. doi: 10.1523/JNEUROSCI.2980-09.2009.
In neocortex, the induction and expression of long-term potentiation (LTP) and long-term depression (LTD) vary depending on cortical area and laminae of presynaptic and postsynaptic neurons. Layer 4 (L4) is the initial site of sensory afference in barrel cortex and primary visual cortex (V1) in which excitatory inputs from thalamus, L6, and neighboring L4 cells are integrated. However, little is known about plasticity within L4. We studied plasticity at excitatory synaptic connections between pairs and triplets of interconnected L4 neurons in guinea pig V1 using a fixed delay pairing protocol. Plasticity outcomes were heterogeneous, with some connections undergoing LTP (n = 7 of 42), some LTD (n = 19 of 42), and some not changing (n = 16 of 42). Although quantal analysis revealed both presynaptic and postsynaptic plasticity expression components, reduction in quantal size (a postsynaptic property) contributing to LTD was ubiquitous, whereas in some cell pairs, this change was overridden by an increase in the probability of neurotransmitter release (a presynaptic property) resulting in LTP. These changes depended on the initial reliability of the connections: highly reliable connections depressed with contributions from presynaptic and postsynaptic effects, and unreliable connections potentiated as a result of the predominance of presynaptic enhancement. Interestingly, very strong, reliable pairs of connected cells showed little plasticity. Pairs of connected cells with a common presynaptic or postsynaptic L4 cell behaved independently, undergoing plasticity of different or opposite signs. Release probability of a connection with initial 100% failure rate was enhanced after pairing, potentially avoiding silencing of the presynaptic terminal and maintaining L4-L4 synapses in a broader dynamic range.
在新皮层中，长时程增强（LTP）和长时程抑制（LTD）的诱导和表达因皮层区域以及突触前和突触后神经元的层而异。第4层（L4）是桶状皮层和初级视觉皮层（V1）中感觉传入的初始位点，来自丘脑、第6层和相邻L4细胞的兴奋性输入在此整合。然而，关于L4内的可塑性知之甚少。我们使用固定延迟配对方案研究了豚鼠V1中相互连接的L4神经元对和三联体之间兴奋性突触连接的可塑性。可塑性结果是异质性的，一些连接经历LTP（42个中有7个），一些经历LTD（42个中有19个），还有一些没有变化（42个中有16个）。尽管量子分析揭示了突触前和突触后可塑性表达成分，但导致LTD的量子大小减小（一种突触后特性）普遍存在，而在一些细胞对中，这种变化被神经递质释放概率的增加（一种突触前特性）所抵消，从而导致LTP。这些变化取决于连接的初始可靠性：高度可靠的连接在突触前和突触后效应的作用下发生抑制，而不可靠的连接由于突触前增强占主导而增强。有趣的是，非常强且可靠的连接细胞对几乎没有可塑性。具有共同突触前或突触后L4细胞的连接细胞对表现独立，经历不同或相反方向的可塑性。初始失败率为100%的连接在配对后释放概率增加，这可能避免突触前终末沉默，并在更广泛的动态范围内维持L4 - L4突触。
