Dendritic depolarization efficiently attenuates low-threshold calcium spikes in thalamic relay cells.

Thalamic relay cells respond in two distinct modes, burst and tonic, that depend on a voltage-dependent, low-threshold, transient Ca(2+) current (I(T)), and these modes relay different forms of information to cortex. I(T) activation evokes a low-threshold spike (LTS), producing a burst of action potentials. Modulatory inputs from cortex and brainstem are known to activate metabotropic receptors on relay cell dendrites at which the T channels underlying I(T) may be concentrated. We thus investigated the influence of activating these receptors on the LTS, using current-clamp intracellular recording in an in vitro slice preparation of the cat's lateral geniculate nucleus. We found a strong correlation between LTS amplitude and the number of action potentials evoked in the burst. We then found that activation of either metabotropic glutamate or muscarinic receptors produced a hyperpolarizing shift in the sigmoid relationship between LTS amplitude and the initial holding potential without affecting the maximum LTS amplitude or slope of the relationship. This hyperpolarizing shift in the voltage dependency of LTS amplitude is best explained by space-clamp limitations and significantly more depolarization of T channels near the dendritic location of activated receptors than at the soma. Thus, nonretinal modulatory inputs may have a stronger influence on I(T) and number of action potentials generated in a burst than previously imagined from somatic recording, because the EPSP amplitudes generated by these inputs at the dendritic location of most T channels are greater than after their electrotonic decay recorded at the soma.