Lombardi Aniello, Wang Qiang, Stüttgen Maik C, Mittmann Thomas, Luhmann Heiko J, Kilb Werner
Institute of Physiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Institute of Pathophysiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Front Cell Neurosci. 2023 Sep 25;17:1254776. doi: 10.3389/fncel.2023.1254776. eCollection 2023.
Short-term synaptic plasticity (STP) is a widespread mechanism underlying activity-dependent modifications of cortical networks.
To investigate how STP influences excitatory and inhibitory synapses in layer 2/3 of mouse barrel cortex, we combined whole-cell patch-clamp recordings from visually identified pyramidal neurons (PyrN) and parvalbumin-positive interneurons (PV-IN) of cortical layer 2/3 in acute slices with electrical stimulation of afferent fibers in layer 4 and optogenetic activation of PV-IN.
These experiments revealed that electrical burst stimulation (10 pulses at 10 Hz) of layer 4 afferents to layer 2/3 neurons induced comparable short-term depression (STD) of glutamatergic postsynaptic currents (PSCs) in PyrN and in PV-IN, while disynaptic GABAergic PSCs in PyrN showed a stronger depression. Burst-induced depression of glutamatergic PSCs decayed within <4 s, while the decay of GABAergic PSCs required >11 s. Optogenetically-induced GABAergic PSCs in PyrN also demonstrated STD after burst stimulation, with a decay of >11 s. Excitatory postsynaptic potentials (EPSPs) in PyrN were unaffected after electrical burst stimulation, while a selective optogenetic STD of GABAergic synapses caused a transient increase of electrically evoked EPSPs in PyrN.
In summary, these results demonstrate substantial short-term plasticity at all synapses investigated and suggest that the prominent STD observed in GABAergic synapses can moderate the functional efficacy of glutamatergic STD after repetitive synaptic stimulations. This mechanism may contribute to a reliable information flow toward the integrative layer 2/3 for complex time-varying sensory stimuli.
短期突触可塑性（STP）是一种广泛存在的机制，是皮层网络活动依赖性修饰的基础。
为了研究STP如何影响小鼠桶状皮层第2/3层的兴奋性和抑制性突触，我们将急性脑片中皮层第2/3层经视觉识别的锥体神经元（PyrN）和小白蛋白阳性中间神经元（PV-IN）的全细胞膜片钳记录与第4层传入纤维的电刺激以及PV-IN的光遗传学激活相结合。
这些实验表明，对第2/3层神经元的第4层传入纤维进行电爆发刺激（10赫兹下10个脉冲），在PyrN和PV-IN中诱导出相当的谷氨酸能突触后电流（PSC）短期抑制（STD），而PyrN中的双突触GABA能PSC表现出更强的抑制。爆发诱导的谷氨酸能PSC抑制在<4秒内衰减，而GABA能PSC的衰减需要>11秒。光遗传学诱导的PyrN中的GABA能PSC在爆发刺激后也表现出STD，衰减时间>11秒。电爆发刺激后，PyrN中的兴奋性突触后电位（EPSP）不受影响，而GABA能突触的选择性光遗传学STD导致PyrN中电诱发EPSP短暂增加。
总之，这些结果表明在所研究的所有突触中都存在显著的短期可塑性，并表明在GABA能突触中观察到的显著STD可以在重复突触刺激后调节谷氨酸能STD的功能效力。这种机制可能有助于向整合性第2/3层可靠地传递复杂时变感觉刺激的信息流。
