How do network and neurotransmitters interact in epileptogenesis?

It is difficult to understand when the process of epileptogenesis is complete and which mechanisms develop with time-course that produces clinically detectable epileptiform activity. Changes in network characteristics and functional connectivity are shown to be associated with epilepto-genesis. Excessive neuronal synchronization is also the hallmark of epileptic discharges. Several mechanisms have been implicated in the initiation of epileptic synchronization. Hyper-synchronous synaptic transmission can spread epileptiform activity from a single neuron to different regions of the brain by recruiting local area neurons as well as distant neurons. These neurotransmitter-mediated activities will convert a normal neuronal network to an epileptogenic network. The widely accepted principle that is applied to the process of epileptogenesis is disruption of mechanisms that normally create a balance between excitation and inhibition. Any alteration in the glutamatergic and GABAergic synaptic transmission can create a micro-environment of epileptic activity which can propagate to other cortical regions. Measurement of excitatory and inhibitory postsynaptic currents, using patch-clamp technique, in slice preparations of resected brain specimens assist in investigating modulation of neurotrans-mission. The comparison of GABA and glutamate-mediated synaptic transmission in specimens obtained from two different regions will throw light on the magnitude of change in epileptic activity. Understanding the propagation and maintenance of the functional connectivity and network configurations through neurotransmitter mediated abnormal synaptic activity in complex brain regions in epilepsy may open avenues for novel surgical interventions as well as for the accurate localization of the epileptic focus, thus resulting in a better surgical outcome.