DRD1 and Hyperammonemia: A recent study in cortical cultures showed that glutamate release can be stimulated through D1Rs, an effect abolished in the presence of the protein kinase A inhibitor KT5720 (200nM).49 We took advantage of the slightly upregulated D1R expression in LGS‐KO mice27 and studied the influence of a D1R agonist on H3R‐mediated plasticity: a D1R agonist, which stimulates cAMP production29, 48 counteracted LLDhist in LGS‐KO but not in WT mice indicating stronger signaling through D1R in mice with inborn hyperammonemia.