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Figure 1 | Molecular Pain

Figure 1

From: Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex

Figure 1

No difference in neuronal excitability or excitatory neurotransmissions in ACC pyramidal neurons from WT and Ap oa 1 mice. (A) Diagram illustrating the experimental design and procedures. Ap oa1 receptor is a Gs-coupled receptor from Aplysia. Transgenic mice expressing Ap oa1 receptors were used for slice electrophysiology and inflammatory pain behaviors. (B) Representative traces and pooled results showing neuronal responses to current injections from -200 pA to 200 pA with 100 pA step for 400 ms. Action potentials were induced in neurons from both WT and transgenic mice. (C) Sample trances and pooled results showing no difference in input-output curve of AMPA receptor-mediated EPSCs between WT and Ap oa1 mice. (D) No difference in I-V curve of AMPA receptor-mediated EPSCs between WT and transgenic mice.

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