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Figure 2 | Molecular Pain

Figure 2

From: Endogenous N-acetylaspartylglutamate (NAAG) inhibits synaptic plasticity/transmission in the amygdala in a mouse inflammatory pain model

Figure 2

Enhanced synaptic transmission in the CeLC nucleus of control and formalin brain slices. Enhanced evoked current was observed in the central amygdala, laterocapsular part (CeLC) neurons 6 and 24 hours after peripheral inflammation. Input-output experiments were conducted to examine neurotransmission changes in the CeLC as a result of peripheral inflammation (QX-314 [5 mM] local anesthetic was included in the pipette solution). (A) Representative trace depicting evoked response at maximal stimulation intensity in cells from untreated control and formalin treated animals 1 and 6 hours post inflammation (standard ACSF).(B) An increase in current output was observed at 6 hours (n = 6) and not 1 hour (n = 9-13) in the CeLC post inflammation.(C) Representative trace depicting evoked response at maximal stimulation intensity in cells from untreated control and formalin treated animals 6 and 24 hours post inflammation (Mg2+ Free ACSF). (D) There was a significant gain in the current output at 6 (n = 13) and 24 hours (n = 12) in the CeLC following inflammation. (E) Representative trace depicts how NMDA/AMPA ratio was obtained. NMDAR antagonist, CPP (10 μM), was used to determine the relative contribution of the NMDA and AMPA components of the evoked current response during input-output experiments (Mg2+ Free ACSF). (F) NMDA/AMPA ratio was unchanged in the CeLC 24 hours after inflammation [control (n = 6), formalin 24 hours (n = 11)]. Data presented as mean ± SEM, *p ≤ 0.05 vs. control, Student's t-test.

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