Alone did not induce significant increases in ACTH. ACTH(11?4) and astressin blocked EA anti-edema but not EA anti-hyperalgesia. EA induced phosphorylation of NR1, an essential subunit of the N-methyl-D-aspartic acid (NMDA) receptor, in CRH-containing neurons of the paraventricular nucleus. Conclusion: The data demonstrate that EA activates CRH neurons to significantly increase plasma ACTH levels