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Figure 5 | Molecular Pain

Figure 5

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

Figure 5

Endogenous and applied NAAG inhibit synaptic transmission in the CeLC of the mouse amygdala. (A) Representative current traces recorded from two neurons in the CeLC region of brain slices from untreated control mice following stimulation of the spinoparabrachial amygdaloid afferents in the absence and presence of MgCl2 in the ACSF. ZJ43 (0.1 μM) inhibits inactivation of endogenously released NAAG and significantly reduces the amplitude of the evoked excitatory current. This effect is reversed by the group II mGluR antagonist LY341495 (1 μM). (B) Bar graph showing average data in each recording condition (n = 7, Mg2+ free ACSF; n = 6, standard ACSF). (C) Representative current traces from cells treated with NAAG (1 μM, n = 4) or group II mGluR agonist SLx-3095-1 (0.5 μM, n = 7). Both agonists inhibit the evoked current in the CeLC. (D) Bar graph showing average values from each drug treatment in the recording conditions. (E and F) Group II antagonist does not significantly affect evoked eEPSCs in control CeLC presented as mean ± SEM of percent control values. *p ≤ 0.05 vs. control, paired Student's t-test.

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