Chronic ethanol treatment also affected genes that are associated with neurotransmission. Dopamine signaling was increased, including DDC which produces dopamine from l-dopa, but DBH, which converts dopamine to norepinephrine, is also increased in expression. Increased expression of ADRA2C, one of the α2-adrenergic autoreceptors, could attenuate norepinephrine release, an effect that could be amplified by the increased expression of the norepinephrine transporter, SLC6A2. Increases in the glycine transporter SLC6A9 and serine transporter SLC1A4 could dampen glutamate signaling via the NMDA receptor, because glycine and or D-serine act as co-agonists of that receptor; the dampening could be amplified because the glutamate transporter SLC1A2 is also increased. Glycine can also act as a neurotransmitter. GRIA2, the glutamate ionotropic receptor AMPA type subunit 2, was decreased. The GABA pathway was affected; although the analysis did not predict a direction, the GABA transporter SLC6A11 was decreased, which could mean less uptake of GABA and more activity. Decreased expression of SLC6A11/GAT3 in sweet drinking rats caused them to increase their intake of ethanol, and SLC6A11 was decreased in expression in the amygdala of post-mortem brains (Augier
