TNF-α Differentially Regulates Synaptic Plasticity in the Hippocampus and Spinal Cord by Microglia-Dependent Mechanisms after Peripheral Nerve Injury

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Figure 2.
Figure 2.

SNI induces differential changes in synaptic transmission. A, Representative mEPSCs of CA1 pyramidal neurons, their amplitude, cumulative probability, and frequency in WT mice from the sham and SNI groups (n = 12, amplitude, p = 0.659; frequency, p = 0.008; 12 neurons from 6 mice per group). B, Representative mEPSCs of spinal NK1-PNs, their amplitude, cumulative probability, and frequency in WT mice from the sham and SNI groups (n = 10, amplitude, p = 0.819; frequency, p = 0.012; 10 neurons from 5 mice per group). C, NMDA/AMPA current ratios at CA3–CA1 synapses in the indicated groups (n = 15, p = 0.021; 15 neurons from 6 mice per group). Evoked AMPA receptor EPSC (bottom traces) and evoked NMDA receptor EPSC (top traces) were recorded at membrane potentials of −70 and +50 mV, respectively. Circles indicate the time at which the amplitudes of AMPA or NMDA receptor currents were measured. D, NMDA/AMPA current ratio in spinal NK1-PNs in the different groups (n = 16, p = 0.022; 16 neurons from 6 mice per group). Values are the mean ± SEM. *p < 0.05, **p < 0.01 versus sham groups. Data for all bar graphs were analyzed using Student's t test.

  1. The Journal of Neuroscience vol. 37 no. 4 871-881
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