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Hyperpolarisation rectification in cat lateral geniculate neurons modulated by intact corticothalamic projections.
D A Nita1, M Steriade, F Amzica
1Laboratoire de neurophysiologie, Faculté de médecine, Université Laval, Quebec, Canada G1K 7P4.
The Journal of Physiology
|August 26, 2003
Summary
Corticothalamic projections regulate the hyperpolarization-activated cation current (Ih) in thalamic neurons. Ih is expressed during cortical disfacilitation but absent during active cortical states, suggesting intact corticothalamic loops prevent delta oscillations.
Area of Science:
- Neuroscience
- Cellular Electrophysiology
Background:
- Thalamic neuron intrinsic properties are shaped by synaptic inputs and neuromodulators.
- Corticothalamic projections significantly influence thalamic neuronal activity.
Purpose of the Study:
- To investigate the impact of corticothalamic projections on the hyperpolarization-activated cation current (Ih) in dorsal lateral geniculate (dLG) nucleus neurons.
- To determine how cortical network states affect Ih expression in dLG neurons.
Main Methods:
- Intracellular recordings from dLG neurons in anesthetized cats, preserving intact corticothalamic loops.
- Photic stimulation via optic tract and light-emitting-diodes to identify dLG neurons.
- Application of concentrated K+ solution to the visual cortex to induce cortical depression.
Main Results:
- The expression of Ih, a depolarizing sag current, in dLG neurons was dependent on the cortical network state.
- Ih was detected during cortical disfacilitation (slow oscillations) but absent during active (depolarized) cortical periods.
- Inducing cortical depression with K+ enabled Ih expression in previously non-expressing dLG neurons.
Conclusions:
- Intact corticothalamic projections prevent the generation of thalamic clock-like delta oscillations in dLG neurons.
- The interplay between Ih and low-threshold calcium current (IT) for delta oscillations is modulated by cortical activity.
- Cortical states dynamically regulate the intrinsic excitability of thalamic neurons via Ih.