Temporal Lobe Epilepsy (TLE) is often triggered by a brain insult (meningitis, brain trauma, etc.). The insult induces network modifications during epileptogenesis (the process leading to epilepsy), and when seizures are recurrent. Since these modifications are extremely diverse, it is essential to determine their causal relationship with respect to the construction of epileptic networks. These issues have been addressed in animal models of TLE. In this chapter we present the state of our current knowledge regarding the time-dependent reorganizations of GABAergic and glutamatergic circuits - at the synaptic level - during epileptogenesis. We will discuss the possible functional consequences of these alterations. We will focus particularly on the fate of GABAergic circuits. Does the loss of interneurons many days before the first occurrence of a spontaneous seizure suggest that decreased inhibition is not pro-epileptic per se? We will discuss the role of interneuron loss in the construction of epileptic circuits. Synaptic reorganizations at GABAergic and glutamatergic synapses not only enable seizure occurrence, they also modify the normal information processing performed by these networks. We will also discuss how modifications in GABAergic and glutamatergic circuits can negatively impact cognitive functions. Strategies have been designed to prevent these reorganizations or to repair the circuitry; their efficiency is discussed.