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. This evidence concerns the gene HRH3 and Hyperammonemia.