The thalamocortical (TC) neurones of the sensory thalamic nuclei receive three excitatory inputs: two are the ascending input from the sensory pathway and the descending input from the cortex, and the third is the modulatory input from the brainstem activating system (Jones, 1985). The sensory and cortical inputs form synapses at different locations on the dendritic arbors of TC neurones, with the sensory input more proximal to the soma and the cortical input more distal. The sensory input to auditory, somatosensory and visual thalamic nuclei has been well characterized as being mediated by both non-NMDA and NMDA ionotropic glutamate receptors both in vitro (Scharfman, Lu, Guido, Adams & Sherman, 1990; Turner, Leresche, Guyon, Soltesz & Crunelli, 1994;Hu, Senatorov & Mooney, 1994;Kao & Coulter, 1997) and in vivo (Salt, 1986;Sillito, Murphy & Salt, 1990a;Sillito, Murphy, Salt & Moody, 1990b;Salt & Eaton, 1991). However, while the contribution of these ionotropic glutamate receptors to corticothalamic synaptic transmission has been established both in vitro and in vivo (Deschênes & Hu, 1990;Scharfman et al. 1990;Eaton & Salt, 1996;Kao & Coulter, 1997) 1. Using an in vitro slice preparation of the rat dorsal lateral geniculate nucleus (dLGN), the properties of retinogeniculate and corticothalamic inputs to thalamocortical (TC) neurones were examined in the absence of GABAergic inhibition. 2. The retinogeniculate EPSP evoked at low frequency (û 0·1 Hz) consisted of one or two fastrising (0·8 ± 0·1 ms), large-amplitude (10·3 ± 1·6 mV) unitary events, while the corticothalamic EPSP had a graded relationship with stimulus intensity, owing to its slower-rising (2·9 ± 0·4 ms), smaller-amplitude (1·3 ± 0·3 mV) estimated unitary components. 3. The retinogeniculate EPSP exhibited a paired-pulse depression of 60·3 ± 5·6 % at 10 Hz, while the corticothalamic EPSP exhibited a paired-pulse facilitation of > 150 %. This frequency-dependent depression of the retinogeniculate EPSP was maximal after the second stimulus, while the frequency-dependent facilitation of the corticothalamic EPSP was maximal after the fourth or fifth stimulus, at interstimulus frequencies of 1-10 Hz. 4. There was a short-term enhancement of the û 0·1 Hz corticothalamic EPSP (64·6 ± 9·2 %), but not the retinogeniculate EPSP, following trains of stimuli at 50 Hz. 5. The û 0·1 Hz corticothalamic EPSP was markedly depressed by the non-NMDA antagonist 1-(4-amino-phenyl)-4-methyl-7,8-methylene-dioxy-5H-2,3-benzodiazepine (GYKI 52466), but only modestly by the NMDA antagonist 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid ((RS)-CPP), and completely blocked by the co-application of GYKI 52466, 6_cyano-7-nitroquinoxaline-2,3-dione (CNQX), (RS)-CPP and (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK_801). Likewise, the corticothalamic responses to trains of stimuli (1-500 Hz) were greatly reduced by this combination of ionotropic glutamate receptor antagonists. 6. In the presence of GYKI 52466, CNQX, (RS)-CPP and MK_801, res...