In this issue of Neurology , two studies report changes in serotonergic function in the epileptic hippocampus of patients with temporal lobe epilepsy (TLE). In the first, Toczek et al.1 report decreased binding of the PET tracer [18F]FCWAY to the 5HT1A receptor in both medial and lateral temporal regions ipsilateral to the epileptic focus, as well as in the brain stem, of patients with TLE. In the second, Natsume et al.2 explored the role of serotonin synthesis in TLE with the PET tracer alpha[11C]methyl-L-tryptophan (AMT). They report increased AMT uptake in the hippocampus ipsilateral to the seizure focus of TLE patients with normal hippocampal volumes but not in patients with hippocampal atrophy. When examining the relationship between the results of AMT PET to glucose metabolism PET in the TLE group as a whole, Natsume et al.2 found decreased glucose metabolism in the lateral temporal and frontal lobes correlated with an increase in the regional uptake constant (K*) for AMT in the hippocampus. Conversely, they report higher ipsilateral lenticular nucleus and cingulate cortex glucose metabolism, which was correlated with increased hippocampal AMT K*. Both reports build upon previous basic studies exploring serotonergic mechanisms in …