Discussion
The present results demonstrate that (i) endogenous synthesis of KYNA, a glutamate receptor inhibitor, was lowered in the hippocampal samples obtained from patients with MTLE-HS, possibly due to reduced levels of the enzyme KAT II and its co-factor PLP. (ii) Reduced endogenous KYNA levels may contribute to the maintenance of enhanced synaptic glutamatergic activity on to the pyramidal neurons in slice preparations of the resected hippocampal samples obtained from patients with MTLE-HS. (iii) Under resting conditions, the effect of the reduced endogenous KYNA levels could be attributed to both pre- as well as post-synaptic regulation of glutamatergic activity. (iv) Endogenous synthesis of QUIN was elevated in the hippocampal samples obtained from patients with MTLE-HS. These concepts can help explain the potential contribution of TKP metabolites to hyperexcitability associated with MTLE-HS.