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J Physiol Volume 552, Number 1, 325-332, October 1, 2003 DOI: 10.1113/jphysiol.2003.050310
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J Physiol (2003), 552.1, pp. 325-332
© Copyright 2003 The Physiological Society
DOI: 10.1113/jphysiol.2003.050310

Hyperpolarisation rectification in cat lateral geniculate neurons modulated by intact corticothalamic projections

D. A. Nita, M. Steriade and F. Amzica

Laboratoire de neurophysiologie, Faculté de médecine, Université Laval, Quebec, Canada G1K 7P4

The intrinsic properties of thalamic neurons are influenced by synaptic activities in ascending pathways and corticofugal projections, as well as by the actions of neurotransmitters released by generalised modulatory systems. We focused on the effects of corticothalamic projections on the hyperpolarisation-activated cation current Ih. Intracellular recordings of thalamocortical neurons in the dorsal lateral geniculate (dLG) nucleus were performed in cats under ketamine-xylazine anaesthesia. At variance with the conventional way of recording intracellularly from thalamic neurons after partial or total ablation of the grey and white matter overlying the dLG, we preserved intact corticothalamic neuronal loops. Stimulating electrodes inserted into the optic tract and light-emitting-diodes as photic stimulation were used to identify the dLG neurons. The expression of the depolarising sag due to Ih depended on the state of cortical networks. Thalamic dLG Ih, induced by hyperpolarising current steps, was detected during the periods of cortical disfacilitation that occur during the cortical slow (< 1 Hz) oscillation, whereas Ih was absent during the active (depolarised) periods. The possibility that the excitatory corticothalamic projections could preclude the generation of the Ih was tested by applying a concentrated K+ solution (3 M) to the primary visual cortex. The same dLG neurons that did not display Ih before application of K+ were able to produce hyperpolarisation-activated depolarising sags during K+-induced cortical depression. Our data suggest that the thalamic clock-like delta oscillation, which results from an interplay between Ih and the low-threshold calcium current (IT), as described in preparations without cerebral cortex, is prevented in dLG neurons when corticothalamic loops are intact.






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