CHARACTERIZATION OF SENSORY AND CORTICOTHALAMIC EXCITATORY INPUTS TO RAT THALAMOCORTICAL NEURONS IN-VITRO

1. Using an in vitro slice preparation of the rat dorsal lateral genic ulate nucleus (dLGN), the properties of retinogeniculate and corticoth alamic inputs to thalamocortical (TC) neurones were examined in the ab sence of GABAergic inhibition. 2. The retinogeniculate EPSP evoked at low frequency (less than or equal to 0.1 Hz) consisted of one or two f ast-rising (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), smal ler-amplitude (1.3 +/- 0.3 mV) estimated unitary components. 3. The re tinogeniculate EPSP exhibited a paired-pulse depression of 60.3 +/- 5. 6% at 10 Hz, while the corticothalamic EPSP exhibited a paired-pulse f acilitation of > 150%. This frequency-dependent depression of the reti nogeniculate EPSP was maximal after the second stimulus, while the fre quency-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 less than or equal to 0.1 Hz corticothalamic EPSP (64.6 +/- 9.2%), but not the retinogen iculate EPSP, following trains of stimuli at 50 Hz. 5. The less than o r equal to 0.1 Hz corticothalamic EPSP was markedly depressed by the n on-NMDA antagonist -4-methyl-7,8-methylene-dioxy-5H-2,3-benzodiazepin (GYKI 52466), but only modestly by the NMDA antagonist 3-((RS)-2-carbo xypiperazin-4-yl)-propyl-1- phosphonic acid ((RS)-CPP), and completely blocked by the co-application of GYKI 52466, 6-cyano-7-nitroquinoxali ne-2,3-dione (CNQX), (RS)-CPP and thyl-10,11-dihydro-5H-dibenzo[a,d]cy clohepten-5,10 -imine (MK-801). Likewise, the corticothalamic response s to trains of stimuli (1-500 Hz) were greatly reduced by this combina tion of ionotropic glutamate receptor antagonists. 6. In the presence of GYKI 52466, CNQX, (RS)-CPP and MK-801, residual corticothalamic res ponses and slow EPSPs, with a time to peak of 2-10 s, could be generat ed following trains of five to fifty stimuli. Neither of these respons es were occluded by 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1 ,S,3R-ACPD), suggesting they are not mediated via group I and II metab otropic glutamate receptors.