Gabaa and Gabab Receptors

Since the introduction of the alpha function by Rall in 1967 12], there has been signii-cant progress in our understanding of the molecular events underlying synaptic transmission. Particular receptor types have been identiied and their activation kinetics characterized. It is now possible to develop models of these receptors, using a formalism similar to that introduced by Hodgkin and Huxley 9]. In this paper, we present recently-introduced models obtained by simplifying more detailed biophysical models of postsynaptic receptors 7]. The simpliied models are fully compatible with the Hodgkin-Huxley formalism, are very ee-cient to simulate, and account for important phenomena such as synaptic summation and desensitization. These models should be useful in large-scale network simulations. In a previous paper 7], we developed a model of synaptic transmission that incorporated the kinetics of voltage-dependent channels, the kinetics of exo-cytosis of neurotransmitter in the synapse, diiusion of the neurotransmitter and binding to postsynaptic receptors, and nally the kinetics of activation of these receptors. It was shown that introducing simplifying assumptions leads to much simpler kinetic models for a variety of receptor types, including fast transmission and neuromodulation. Synaptic receptors activate or deactivate ion channels located in the postsy-naptic cell. In the case of \fast" synaptic transmission, the receptor and the channel are part of the same protein complex. In these so-called ionotropic receptors, the ligand is a neurotransmitter and its binding to the complex leads to the opening of the associated ionophore. Ionotropic receptors include the glutamate AMPA/kainate and NMDA types, the fast GABAergic receptors 9